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<title>Heart</title>
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<title><![CDATA['Warm-up Angina': harnessing the benefits of exercise and myocardial ischaemia]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304187v1?rss=1</link>
<description><![CDATA[<p>The phenomenon of warm-up angina was first noted over 200&nbsp;years ago. It describes the curious observation whereby exercise-induced ischaemia on second effort is significantly reduced or even abolished if separated from first effort by a brief rest period. However, the precise mechanism via which this cardio-protection occurs remains uncertain. Three possible explanations for reduced myocardial ischaemia on second effort include: first, an improvement in myocardial perfusion; second, increased myocardial resistance to ischaemia similar to ischaemic preconditioning; and third, reduced cardiac work through better ventricular&ndash;vascular coupling. Obtaining accurate coronary physiological measurements in the catheter laboratory throughout exercise demands a complex research protocol. In the 1980s, studies into warm-up angina relied on great cardiac vein thermo-dilution to estimate coronary blood flow. This technique has subsequently been shown to be inaccurate. However exercise physiology in the catheter laboratory has recently been resurrected with the advent of coronary artery wires that allow continuous measurement of distal coronary artery pressure and blood flow velocity. This review summarises the intriguing historical background to warm-up angina, and provides a concise critique of the important studies investigating mechanisms behind this captivating cardio-protective phenomenon.</p>]]></description>
<dc:creator><![CDATA[Williams, R. P., Manou-Stathopoulou, V., Redwood, S. R., Marber, M. S.]]></dc:creator>
<dc:date>2013-06-18T00:00:57-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304187</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304187</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA['Warm-up Angina': harnessing the benefits of exercise and myocardial ischaemia]]></dc:title>
<prism:publicationDate>2013-06-18</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303490v1?rss=1">
<title><![CDATA[Ivabradine in heart failure: NICE guidance]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303490v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Heart rate and the funny channel</st><p>In the normal heart the sinus node determines the heart rate.<cross-ref type="bib" refid="R1">1</cross-ref> Sino-atrial myocytes are characterised by a poorly developed contractile system and self-generating repetitive action potentials, a feature not found in the myocytes of cardiac muscle. At the end of the action potential, depolarisation of the membrane voltage continues, during phase four, until this triggers another action potential. While sino-atrial myocytes are heavily innervated by both sympathetic and vagal nerves, the spontaneous activity is independent of innervation. The mechanisms controlling, or modifying, these spontaneous diastolic depolarisations are central to interventions that might be employed to modify heart rate. Early thinking attributed pacemaker activity to the decay of an outward K+ current, but in the late 1970s Brown <I>et al</I> identified, to their surprise, a new likely inward current accordingly described as a &lsquo;funny current or I<I><sup>f</sup></I>&rsquo;.<cross-ref type="bib" refid="R2">2</cross-ref></p><p>Although many questions remain unanswered,<cross-ref...]]></description>
<dc:creator><![CDATA[Hardman, S. M. C.]]></dc:creator>
<dc:date>2013-06-18T00:00:57-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303490</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303490</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Acute coronary syndromes]]></dc:subject>
<dc:title><![CDATA[Ivabradine in heart failure: NICE guidance]]></dc:title>
<prism:publicationDate>2013-06-18</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304117v1?rss=1">
<title><![CDATA[The divergence between European STEMI guidelines and evidence: a potential threat to optimising reperfusion therapy for patients with ST-elevation myocardial infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304117v1?rss=1</link>
<description><![CDATA[<p>The 2012 European Society of Cardiology (ESC) ST-Elevation Myocardial Infarction (STEMI) guideline acknowledges that STEMI patients should receive reperfusion therapy as soon as possible, and that prehospital fibrinolysis or field-triage directly to Primary Percutaneous Coronary Intervention (PPCI) centres is the preferred reperfusion strategy.<cross-ref type="bib" refid="R1">1</cross-ref> However, when recommending fibrinolytic therapy (FT) within 30&nbsp;min from First Medical Contact (FMC), if PPCI cannot be performed &lsquo;within 60&nbsp;min of FMC in patients presenting early, with a large amount of myocardium at risk&rsquo;, the guidelines imply that only 30&nbsp;min extra may be expended to perform PPCI instead of administering FT (&lsquo;PCI-related delay&rsquo;) (<cross-ref type="fig" refid="HEARTJNL2013304117F1">figure 1</cross-ref>).</p><p><fig loc="float" id="HEARTJNL2013304117F1"><no>Figure&nbsp;1</no><caption><p>Various delays when treating patients with ST-Elevation Myocardial Infarction (STEMI) with fibrinolysis or primary percutaneous coronary intervention (PPCI). &lsquo;Healthcare system delay&rsquo; is the total delay from emergency medical service (EMS) call to PPCI. &lsquo;PCI-related delay&rsquo; is the extra delay that one may use to perform PPCI instead...]]></description>
<dc:creator><![CDATA[Terkelsen, C. J., Pinto, D., Thiele, H., Clemmensen, P., Nikus, K., Lassen, J. F., Hildick-Smith, D., Christiansen, E. H., Aaroe, J., Hansen, H.-H. T., Stankovic, G., Junker, A., Sianos, G., Olivecrona, G., Botker, H. E., Gibson, C. M., Boersma, E.]]></dc:creator>
<dc:date>2013-06-17T22:18:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304117</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304117</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The divergence between European STEMI guidelines and evidence: a potential threat to optimising reperfusion therapy for patients with ST-elevation myocardial infarction]]></dc:title>
<prism:publicationDate>2013-06-17</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304068v1?rss=1">
<title><![CDATA[Creating transparency in UK adult cardiac surgery data]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304068v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Brief summary</st><p>Cardiac surgeons in the UK have openly published their outcome data at hospital and individual surgeon levels since 2005. Publication of these data has been associated with a decreased risk of inhospital mortality following cardiac surgery despite more high risk patients undergoing surgery. Cardiac surgeons in the UK have now developed a series of different tools with the aim of further improving transparency, facilitating access to clinical data and driving quality improvement. These tools make contemporary high quality data from the National Adult Cardiac Surgery Audit (NACSA) database available to various different interest groups. This article describes the tools that have been developed and details how they can be accessed.</p><p>The National Health Service (NHS) commissioning Board has recently announced that results for 10 specialties will be published at an individual team level by Summer 2013.<cross-ref type="bib" refid="R1">1</cross-ref> The public inquiry into the events at the Mid Staffordshire NHS...]]></description>
<dc:creator><![CDATA[Grant, S. W., Hickey, G. L., Cosgriff, R., Cooper, G., Deanfield, J., Roxburgh, J., Bridgewater, B.]]></dc:creator>
<dc:date>2013-06-17T00:30:38-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304068</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304068</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Creating transparency in UK adult cardiac surgery data]]></dc:title>
<prism:publicationDate>2013-06-17</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304132v1?rss=1">
<title><![CDATA[Multiple giant right coronary artery aneurysms associated with a fistula to the left ventricular]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304132v1?rss=1</link>
<description><![CDATA[<sec><p>A 49-year-old man presented with progressive exertional dyspnoea associated with palpitations for 4&nbsp;months&rsquo; duration. Physical examination was notable for marked jugular venous distention and a to-and-fro murmur was heard at the apex. A chest x-ray showed significant cardiomegaly with a bulging contour over the right cardiac border (<cross-ref type="fig" refid="HEARTJNL2013304132F1">figure 1</cross-ref>A). Transthoracic echocardiography revealed the right coronary artery (RCA) was obviously dilated with a huge aneurysm and a fistula draining into the LV, moreover, the right heart chamber was significantly collapsed due to extrinsic compression of the aneurysm (<cross-ref type="fig" refid="HEARTJNL2013304132F1">figure 1</cross-ref>B). Selective RCA angiography confirmed the presence of two giant saccular aneurysms located in the middle and distal portions of the RCA, associated with an extremely tortuous, diffusely dilated fistula draining into the LV (<cross-ref type="fig" refid="HEARTJNL2013304132F1">figure 1</cross-ref>C, online supplementary video 1). The cardiac CT angiography images highlighted the multiple and giant size of these aneurysms (<cross-ref type="fig" refid="HEARTJNL2013304132F1">figure...]]></description>
<dc:creator><![CDATA[Tang, L., Fang, Z.-f., Zhou, S.-h.]]></dc:creator>
<dc:date>2013-06-13T00:02:15-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304132</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304132</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Multiple giant right coronary artery aneurysms associated with a fistula to the left ventricular]]></dc:title>
<prism:publicationDate>2013-06-13</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304036v1?rss=1">
<title><![CDATA[Alcohol intake and prognosis of atrial fibrillation patients]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304036v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To assess alcohol intake as a risk factor for adverse events among patients with incident atrial fibrillation (AF).</p></sec><sec><st>Design</st><p>Prospective cohort study.</p></sec><sec><st>Setting</st><p>Population based cohort study and nationwide Danish registries.</p></sec><sec><st>Patients</st><p>The Danish Diet, Cancer and Health study included 57&nbsp;053 participants (27&nbsp;178 men and 29&nbsp;875 women) aged between 50 and 64&nbsp;years. The study population for this study included the 3107 participants (1999 men, 1108 women) who developed incident AF after inclusion.</p></sec><sec><st>Main outcome measures</st><p>A composite of thromboembolism or death.</p></sec><sec><st>Results</st><p>During a median follow-up of 4.9&nbsp;years 608 deaths and 211 thromboembolic events occurred. Of those who developed AF, 690 (35%) men and 233 (21%) women had a high intake of alcohol (&gt;20 drinks/week for men and &gt;13 drinks/week for women). After adjustment for use of oral anticoagulation and components of the CHA<SUB>2</SUB>DS<SUB>2</SUB>-VASc score, men with an intake of &gt;27 drinks/week had a higher risk for thromboembolism or death (hazard ratio (HR) 1.33, 95% CI 1.08 to 1.63) than men with an intake of &lt;14 drinks/week. Women with an intake of &gt;20 drinks/week also had a higher risk (HR 1.23, 95% CI 0.78 to 1.96) than women in the low intake category. The higher risk among men was primarily driven by mortality (HR 1.51, 95% CI 1.20 to 1.89), whereas the risk found among women was driven by thromboembolism (HR 1.71, 95% CI 0.81 to 3.60).</p></sec><sec><st>Conclusions</st><p>High alcohol intake predicts thromboembolism or death, even after adjustment for established clinical risk factors, and may help identify high risk AF patients who could be targeted for stroke and cardiovascular prevention strategies.</p></sec>]]></description>
<dc:creator><![CDATA[Overvad, T. F., Rasmussen, L. H., Skjoth, F., Overvad, K., Albertsen, I. E., Lane, D. A., Lip, G. Y. H., Larsen, T. B.]]></dc:creator>
<dc:date>2013-06-13T00:02:15-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304036</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304036</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Alcohol intake and prognosis of atrial fibrillation patients]]></dc:title>
<prism:publicationDate>2013-06-13</prism:publicationDate>
<prism:section>Heart rhythm disorders</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304220v1?rss=1">
<title><![CDATA[Utility of real-time three-dimensional intracardiac echocardiography for patent foramen ovale closure]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304220v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Recently, many interventional centres have adopted intracardiac echocardiography (ICE) in preference to transoesophageal echocardiography to guide percutaneous patent foramen ovale (PFO) closure. ICE obviates the need for general anaesthesia, facilitating earlier hospital discharge, and gives superior imaging capability, particularly of the inferior interatrial septum.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref></p><p>The advent of real-time three-dimensional (RT3D) echocardiography has been a major technological advance in transoesophageal echocardiography; however until very recently ICE has been limited to two-dimensional (2D) imaging. RT3D imaging allows for more comprehensive anatomical assessment of complex intracardiac structures, including valves and congenital defects, compared with 2D imaging. Moreover, RT3D imaging is extremely useful in the periprocedural setting as it allows immediate detailed feedback on the effectiveness of catheter-based interventions.</p><p>We report the first use of RT3D ICE for PFO closure. A 50-year-old woman underwent PFO closure via the right femoral vein. An ACUSON AcuNav 3D ultrasound catheter (Siemens AG, Germany)...]]></description>
<dc:creator><![CDATA[Cunnington, C., Hampshaw, S. A., Mahadevan, V. S.]]></dc:creator>
<dc:date>2013-06-13T00:02:15-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304220</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304220</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Utility of real-time three-dimensional intracardiac echocardiography for patent foramen ovale closure]]></dc:title>
<prism:publicationDate>2013-06-13</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303813v1?rss=1">
<title><![CDATA[Primary angiosarcoma of the heart]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303813v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>A 67-year-old cachectic patient presented with a 6-week history of increasing breathlessness, loss of weight and appetite. Examination showed peripheral oedema and signs of cardiac tamponade. Transthoracic echocardiography demonstrated a thick walled cystic mass in the anterior pericardium (see online <A HREF="http://heart.bmj.com/lookup/suppl/doi:10.1136/heartjnl-2013-303813/-/DC1">supplementary video 1</A>), compressing the right ventricle (RV) and right atrium (RA). Further evaluation, including bubble contrast echocardiography, suggested a haematogenous connection between the RA and tumour cavity (see online supplementary video 2). This was confirmed on a contrast enhanced CT scan, with late contrast enhancement of the tumour cavity (<cross-ref type="fig" refid="HEARTJNL2013303813F1">figures&nbsp;1</cross-ref><cross-ref type="fig" refid="HEARTJNL2013303813F2"></cross-ref>&ndash;<cross-ref type="fig" refid="HEARTJNL2013303813F3">3</cross-ref>). In view of these unusual findings, histological diagnosis was considered important. Open biopsy was undertaken due to the potential hazards of percutaneous biopsy. Histology revealed pleomorphic spindle shaped cells (<cross-ref type="fig" refid="HEARTJNL2013303813F4">figure&nbsp;4</cross-ref>) expressing CD31 and CD34 markers confirming the diagnosis of angiosarcoma. A trial of chemotherapy was considered, but the...]]></description>
<dc:creator><![CDATA[Rao, U., Curtin, J., Ryding, A.]]></dc:creator>
<dc:date>2013-06-13T00:02:15-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303813</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303813</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Primary angiosarcoma of the heart]]></dc:title>
<prism:publicationDate>2013-06-13</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303688v1?rss=1">
<title><![CDATA[The role of salt intake and salt sensitivity in the management of hypertension in South Asian people with chronic kidney disease: a randomised controlled trial]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303688v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>The effectiveness of salt restriction to lower blood pressure (BP) in Bangladeshi patients with chronic kidney disease (CKD) is uncertain.</p></sec><sec><st>Objective</st><p>To test the hypothesis that a tailored intervention intended to reduce salt intake in addition to standard care will achieve a greater reduction in BP in UK Bangladeshi patients with CKD than standard care alone.</p></sec><sec><st>Design</st><p>A randomised parallel-group controlled trial conducted over a 6&nbsp;month period.</p></sec><sec><st>Setting</st><p>A tertiary renal unit based in acute care hospital in East London.</p></sec><sec><st>Participants</st><p>56 adult participants of Bangladeshi origin with CKD and BP &gt;130/80&nbsp;mm&nbsp;Hg or on antihypertensive medication.</p></sec><sec><st>Intervention</st><p>Participants were randomly allocated to receive a tailored low-salt diet or the standard low-salt advice. BP medication, physical activity and weight were monitored.</p></sec><sec><st>Main outcome measures</st><p>The primary outcome was change in ambulatory BP. Adherence to dietary advice was assessed by measurement of 24&nbsp;h urinary salt excretion.</p></sec><sec><st>Results</st><p>Of 56 participants randomised, six withdrew at the start of the study. During the study, one intervention group participant died, one control group participant moved to Bangladesh. Data were available for the primary endpoint on 48 participants. Compared with control group the intervention urinary sodium excretion fell from 260 mmol/d to 103&nbsp;mmol/d (&ndash;131 to &ndash;76, p&lt;0.001) at 6&nbsp;months and resulted in mean (95% CI) falls in 24&nbsp;h systolic/diastolic BP of &ndash;8&nbsp;mm&nbsp;Hg (&ndash;11 to &ndash;5)/2 (&ndash;4 to &ndash;2) both p&lt;0.001.</p></sec><sec><st>Conclusions</st><p>A tailored intervention can achieve moderate salt restriction in patients with CKD, resulting in clinically meaningful falls in BP independent of hypertensive medication.</p></sec><sec><st>Trial Registration</st><p>ClinicalTrials.gov NCT00702312.</p></sec>]]></description>
<dc:creator><![CDATA[de Brito-Ashurst, I., Perry, L., Sanders, T. A. B., Thomas, J. E., Dobbie, H., Varagunam, M., Yaqoob, M. M.]]></dc:creator>
<dc:date>2013-06-13T00:02:14-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303688</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303688</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The role of salt intake and salt sensitivity in the management of hypertension in South Asian people with chronic kidney disease: a randomised controlled trial]]></dc:title>
<prism:publicationDate>2013-06-13</prism:publicationDate>
<prism:section>Hypertension and renovascular disease</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303605v1?rss=1">
<title><![CDATA[Paradoxically lower prevalence of peripheral arterial disease in South Asians: a systematic review and meta-analysis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303605v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>While people of South Asian (SA) descent have higher rates of cardiovascular disease compared with people of White European (WE) descent, a lower prevalence of lower extremity peripheral arterial disease (PAD) has been suggested in SA. Our intent was to systematically review the literature on PAD prevalence in people of SA descent and to conduct a meta-analysis to identify differences in PAD prevalence between SA and WE.</p></sec><sec><st>Methods</st><p>Standard Cochrane systematic review methodology was used for conducting a literature review of published research. Population prevalence studies of PAD in SA with a WE comparison group were included. Full text studies were selected and reviewed by two authors with independent data extraction. Prevalence differences between SA and WE were analysed using ORs.</p></sec><sec><st>Findings</st><p>129 studies were initially identified and ultimately 15 (n=240&nbsp;003 patients) studies were included. Only one study reported direct comparative general PAD prevalence between SA and WE (OR=0.26, 95%CI 0.17 to 0.38, p&lt;0.001, n=77&nbsp;855). Fourteen studies with comparative prevalence data between SA and WE in high-risk populations confirm significantly lower odds of PAD in SA with coronary artery disease (CAD) (OR=0.47, 95%CI 0.39 to 0.56, p&lt;0.001, n=139&nbsp;313) and diabetes (OR=0.44; 95% CI 0.30 to 0.63, p&lt;0.001, n=22&nbsp;835).</p></sec><sec><st>Interpretation</st><p>Reported PAD prevalence is significantly lower in SA than WE for both the CAD and diabetes populations. Explanations for these findings, if true, are unclear. These results underscore the need for further study to clarify mechanisms of ethnic divergence in PAD prevalence.</p></sec>]]></description>
<dc:creator><![CDATA[Sebastianski, M., Makowsky, M. J., Dorgan, M., Tsuyuki, R. T.]]></dc:creator>
<dc:date>2013-06-11T00:01:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303605</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303605</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Paradoxically lower prevalence of peripheral arterial disease in South Asians: a systematic review and meta-analysis]]></dc:title>
<prism:publicationDate>2013-06-11</prism:publicationDate>
<prism:section>Systematic review</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303798v1?rss=1">
<title><![CDATA[Risk factors for atrial fibrillation and their population burden in postmenopausal women: the Women's Health Initiative Observational Study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303798v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>Atrial fibrillation (AF) is the most common arrhythmia in women. Large studies evaluating key AF risk factors in older women are lacking. We aimed to identify risk factors for AF in postmenopausal women and measure population burden of modifiable risk factors.</p></sec><sec><st>Design</st><p>Prospective observational study.</p></sec><sec><st>Setting</st><p>The Women's Health Initiative (WHI) Observational Study.</p></sec><sec><st>Patients</st><p>93&nbsp;676 postmenopausal women were followed for an average of 9.8&nbsp;years for cardiovascular outcomes. After exclusion of women with prevalent AF or incomplete data, 8252 of the remaining 81&nbsp;892 women developed incident AF.</p></sec><sec><st>Main outcome measures</st><p>Incident AF was identified by WHI-ascertained hospitalisation records and diagnosis codes from Medicare claims. Multivariate Cox hazard regression analysis identified independent risk factors for incident AF.</p></sec><sec><st>Results</st><p>Age, hypertension, obesity, diabetes, myocardial infarction and heart failure were independently associated with incident AF. Hypertension and overweight status accounted for 28.3% and 12.1%, respectively, of the population attributable risk. Hispanic and African&ndash;American participants had lower rates of incident AF (HR 0.58, 95% CI 0.47 to 0.70 and HR 0.59, 95% CI 0.53 to 0.65, respectively) than Caucasians.</p></sec><sec><st>Conclusions</st><p>Caucasian ethnicity, traditional cardiovascular risk factors and peripheral arterial disease were independently associated with higher rates of incident AF in postmenopausal women. Hypertension and overweight status accounted for a large proportion of population attributable risk. Measuring burden of modifiable AF risk factors in older women may help target interventions.</p></sec>]]></description>
<dc:creator><![CDATA[Perez, M. V., Wang, P. J., Larson, J. C., Soliman, E. Z., Limacher, M., Rodriguez, B., Klein, L., Manson, J. E., Martin, L. W., Prineas, R., Connelly, S., Hlatky, M., Wassertheil-Smoller, S., Stefanick, M. L.]]></dc:creator>
<dc:date>2013-06-11T00:01:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303798</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303798</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Health policy, Drugs: cardiovascular system, Hypertension, Acute coronary syndromes]]></dc:subject>
<dc:title><![CDATA[Risk factors for atrial fibrillation and their population burden in postmenopausal women: the Women's Health Initiative Observational Study]]></dc:title>
<prism:publicationDate>2013-06-11</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304058v1?rss=1">
<title><![CDATA[Swinging heart and vector alternans: signs of impending doom]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304058v1?rss=1</link>
<description><![CDATA[<sec><p>An 80-year-old man with history of atrial flutter and tachy-brady syndrome presented to our hospital with dyspnoea and hypotension. Two days prior, he had undergone atrial flutter ablation and permanent pacemaker placement, and was discharged on dabigatran. Physical examination was remarkable for hypotension, tachycardia, elevated jugular venous pressure (JVP) and pulsus paradoxus. 12-lead ECG revealed atrial flutter and QRS electrical alternans (amplitude and vector alternans) (<cross-ref type="fig" refid="HEARTJNL2013304058F1">figure 1</cross-ref>). Echocardiogram revealed a large pericardial effusion with swinging heart sign and early diastolic collapse of the right ventricle, consistent with cardiac tamponade (see online supplementary video 1). He underwent emergency pericardiocentesis revealing haemopericardium which occurred as a likely complication from pacemaker placement and anticoagulation.</p><p><fig loc="float" id="HEARTJNL2013304058F1"><no>Figure&nbsp;1</no><caption><p>12-lead ECG reveals atrial flutter and QRS electrical alternans. QRS-amplitude alternans is seen in most of the leads; however, QRS-vector alternans is seen most prominently in precordial leads V3 and V4.</p></caption><link locator="heartjnl2013304058f01"></fig></p><p>Though QRS-amplitude electrical alternans (ie,...]]></description>
<dc:creator><![CDATA[Chhabra, L., Spodick, D. H.]]></dc:creator>
<dc:date>2013-06-08T00:01:59-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304058</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304058</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Swinging heart and vector alternans: signs of impending doom]]></dc:title>
<prism:publicationDate>2013-06-08</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304138v1?rss=1">
<title><![CDATA[The impact of smoking on clinical efficacy and pharmacodynamic effects of clopidogrel: a systematic review and meta-analysis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304138v1?rss=1</link>
<description><![CDATA[<sec><st>Context</st><p>Previous findings regarding the relationship between smoking and clopidogrel effects were considerably discrepant.</p></sec><sec><st>Objective</st><p>To assess the impact of smoking on clinical and pharmacodynamic response to clopidogrel.</p></sec><sec><st>Data sources</st><p>Medline, EMBASE and the Cochrane Library through January 2013 were searched. Reference lists of pertinent literatures and abstracts of major cardiovascular conferences were screened.</p></sec><sec><st>Study selection</st><p>Clinical and laboratory studies, which reported major adverse cardiovascular events and on-clopidogrel platelet reactivity categorised by smoking status respectively, were selected.</p></sec><sec><st>Data extraction</st><p>Descriptive and quantitative data were extracted. The main analyses were performed under a random-effects model. For clinical studies, HR estimates were synthesised according to smoking status; for laboratory studies, standardised mean difference (SMD) of on-clopidogrel platelet reactivity and OR for high on-clopidogrel platelet reactivity were pooled. Heterogeneity was quantified by computing I<sup>2</sup> statistic.</p></sec><sec><st>Results</st><p>Of the 1869 citations retrieved, seven clinical studies and 12 laboratory studies involving 111&nbsp;132 patients with established cardiovascular disease and 6658 patients with acute coronary syndrome and/or stent deployment, respectively, were included for meta-analysis. Pooled clinical results showed that an intensified antiplatelet regimen involving clopidogrel was associated with 10% reduced risk for major adverse cardiovascular events among non-current smokers (HR 0.90; 95% CI 0.85 to 0.96), while this clinical benefit was enhanced by 2.9-fold among current smokers (HR 0.71; 95% CI 0.62 to 0.80). Pooled analysis of laboratory studies revealed that current smokers had significantly lower on-clopidogrel platelet reactivity (SMD &ndash;0.30; 95% CI &ndash;0.46 to &ndash;0.15) but, notably, there was considerable inter-study heterogeneity (I<sup>2</sup> 76.2%; p=0.000). The analysis based on four studies (n=1423) suggested a significantly lower odds of high on-clopidogrel platelet reactivity among current smokers than those among never smokers (OR 0.33; 95% CI 0.22 to 0.43).</p></sec><sec><st>Conclusions</st><p>Smoking appears to positively modify the relative clinical efficacy and pharmacodynamic effects of clopidogrel.</p></sec>]]></description>
<dc:creator><![CDATA[Zhao, Z.-g., Chen, M., Peng, Y., Chai, H., Liu, W., Li, Q., Ren, X., Wang, X.-q., Luo, X.-l., Zhang, C., Huang, D.-j.]]></dc:creator>
<dc:date>2013-06-08T00:01:59-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304138</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304138</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Clinical diagnostic tests, Tobacco use]]></dc:subject>
<dc:title><![CDATA[The impact of smoking on clinical efficacy and pharmacodynamic effects of clopidogrel: a systematic review and meta-analysis]]></dc:title>
<prism:publicationDate>2013-06-08</prism:publicationDate>
<prism:section>Systematic review</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303945v1?rss=1">
<title><![CDATA[An association between gestational diabetes mellitus and long-term maternal cardiovascular morbidity]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303945v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To investigate whether a diagnosis of gestational diabetes mellitus (GDM) is a risk factor for subsequent long-term cardiovascular morbidity.</p></sec><sec><st>Design</st><p>A population-based study.</p></sec><sec><st>Setting</st><p>Soroka University Medical Center, a tertiary centre in the southern region of Israel.</p></sec><sec><st>Patients</st><p>A cohort of women with and without a diagnosis of GDM who delivered during the years 1988&ndash;1999 with a follow-up period until 2010.</p></sec><sec><st>Interventions</st><p>A comparison of the incidence of cardiovascular morbidity.</p></sec><sec><st>Results</st><p>Of 47&nbsp;909 deliveries that met the inclusion criteria, 4928 (10.3%) occurred in patients who were diagnosed with GDM. During a follow-up period of more than 10&nbsp;years, compared with women who gave birth at the same time period, after adjustment for age and ethnicity, patients with GDM had higher rates of cardiovascular morbidity including non-invasive cardiac diagnostic procedures (OR=1.8; 95% CI 1.4 to 2.2), simple cardiovascular events (OR=2.7; 95% CI 2.4 to 3.1) and total cardiovascular hospitalisations (OR=2.3; 95% CI 2.0 to 2.5). In a Cox proportional hazards model, adjusted for comorbidities such as pre-eclampsia and obesity, GDM was independently associated with cardiovascular hospitalisations (adjusted HR 2.6, 95% CI 2.3 to 3).</p></sec><sec><st>Conclusions</st><p>GDM is an independent risk factor for long-term cardiovascular morbidity in a follow-up period of more than a decade.</p></sec>]]></description>
<dc:creator><![CDATA[Kessous, R., Shoham-Vardi, I., Pariente, G., Sherf, M., Sheiner, E.]]></dc:creator>
<dc:date>2013-06-08T00:01:59-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303945</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303945</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[An association between gestational diabetes mellitus and long-term maternal cardiovascular morbidity]]></dc:title>
<prism:publicationDate>2013-06-08</prism:publicationDate>
<prism:section>Diabetes, lipids and metabolism</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303825v1?rss=1">
<title><![CDATA[Resting heart rate and physical activity as risk factors for lone atrial fibrillation: a prospective study of 309 540 men and women]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303825v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To study the impact of resting heart rate and leisure time physical activity at middle age on long term risk of drug treated lone atrial fibrillation (AF).</p></sec><sec><st>Design</st><p>Longitudinal cohort study of 309&nbsp;540 Norwegian men and women aged 40&ndash;45&nbsp;years examined during 1985&ndash;1999 followed from 2005 through 2009.</p></sec><sec><st>Setting</st><p>Data from a national health screening programme were linked to the Norwegian Prescription Database (NorPD).</p></sec><sec><st>Patients</st><p>The cohort comprised 162&nbsp;078 women and 147&nbsp;462 men; 575 (0.4%) men and 288 women (0.2%) received flecainide and 568 men and 256 women sotalol and were defined as patients with AF.</p></sec><sec><st>Interventions</st><p>No interventions.</p></sec><sec><st>Main outcome measures</st><p>The outcome was lone fibrillation defined by having at least one prescription of flecainide or sotalol registered in NorPD between 2005 and 2009. Cox proportional hazard regression models were used to assess time to first prescription.</p></sec><sec><st>Results</st><p>The risk for being prescribed these drugs increased with decreasing baseline resting heart. Adjusted hazard ratio (HR) per 10 beats/min decrease in resting heart rate for flecainide prescription was 1.26 in men (95% CI 1.17 to 1.35) and 1.15 (95% CI 1.05 to 1.27) in women. Similar effects were seen for sotalol in men, but not in women. Men who reported intensive physical activity were more often prescribed flecainide than those in the sedentary group (adjusted HR=3.14, 95% CI 2.17 to 4.54).</p></sec><sec><st>Conclusions</st><p>This population based study supports the hypothesis that the risk of drug treated lone AF increases with declining resting heart rate in both sexes, and with increasing levels of self-reported physical activity in men.</p></sec>]]></description>
<dc:creator><![CDATA[Thelle, D. S., Selmer, R., Gjesdal, K., Sakshaug, S., Jugessur, A., Graff-Iversen, S., Tverdal, A., Nystad, W.]]></dc:creator>
<dc:date>2013-06-08T00:01:59-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303825</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303825</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Resting heart rate and physical activity as risk factors for lone atrial fibrillation: a prospective study of 309 540 men and women]]></dc:title>
<prism:publicationDate>2013-06-08</prism:publicationDate>
<prism:section>Heart rhythm disorders</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304274v1?rss=1">
<title><![CDATA[Percutaneous valve-in-valve implantations: importance of knowing the effective internal diameter of bioprosthetic valves]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304274v1?rss=1</link>
<description><![CDATA[<sec><p>Valve-in-valve (VIV) implantation with the transcatheter aortic valve implantation (TAVI) technology has been used to treat dysfunctional bioprosthetic valves. A factor that determines a patient's suitability is the valve size of the previously implanted bioprosthetic valve. A 64-year-old lady with previous tricuspid valve replacement (33&nbsp;mm stented tissue valve, model: ESP100-33M-00 Epic, St Jude Medical, Minnesota, USA), was referred for treatment of her dysfunctional tricuspid valve due to severe tricuspid regurgitation. She had a cardiac resynchronisation therapy device implanted where the ICD lead was placed outside the bioprosthetic valve during her previous tricuspid valve surgery. Her calculated Euroscore II was 37%. A percutaneous tricuspid VIV implantation was proposed. As per the product literature, the internal diameter of her 33&nbsp;mm bioprosthetic valve was 31&nbsp;mm (<cross-ref type="fig" refid="HEARTJNL2013304274F1">figure 1</cross-ref>), so we were reluctant to consider a VIV implantation as the largest commercially available valve technology was a 29&nbsp;mm (Sapien XT, Edwards Lifesciences, Irvine,...]]></description>
<dc:creator><![CDATA[Gopalamurugan, A. B., Reinthaler, M., Mullen, M. J.]]></dc:creator>
<dc:date>2013-06-07T00:03:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304274</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304274</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Percutaneous valve-in-valve implantations: importance of knowing the effective internal diameter of bioprosthetic valves]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304292v1?rss=1">
<title><![CDATA[Could tranexamic acid use in surgery reduce perioperative myocardial infarction?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304292v1?rss=1</link>
<description><![CDATA[<sec><p><b>To the Editor</b> Endogenous plasmin produced during trauma and surgery reduces clot stability and worsens bleeding. Plasmin production can be inhibited with tranexamic acid, a competitive antagonist of the lysine binding sites on plasminogen. Although caution is urged in patients at high risk of arterial occlusive events, due to the possibility that tranexamic acid might precipitate myocardial infarction, results from clinical trials show that tranexamic acid decreases rather than increases the risk of myocardial infarction.</p><p>The clinical randomisation of antifibrinolytic in significant haemorrhage 2 (CRASH-2) trial was a multicentre randomised controlled trial of early (within 8&nbsp;h of injury) administration of tranexamic acid (1&nbsp;g intravenous, loading dose followed by 1&nbsp;g infusion over 8&nbsp;h) or placebo in 20&nbsp;211 patients with traumatic bleeding. Tranexamic acid significantly reduced mortality due to bleeding. All-cause mortality was also reduced.<cross-ref type="bib" refid="R1">1</cross-ref> These results are consistent with the fibrinolytic role of plasmin and the antifibrinolytic effect of tranexamic...]]></description>
<dc:creator><![CDATA[Roberts, I.]]></dc:creator>
<dc:date>2013-06-07T00:03:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304292</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304292</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Could tranexamic acid use in surgery reduce perioperative myocardial infarction?]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304245v1?rss=1">
<title><![CDATA[Unprotected single coronary artery main-stem angioplasty]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304245v1?rss=1</link>
<description><![CDATA[<sec><p>An 84-year-old female presented with exertional angina. Coronary angiography demonstrated an anomalous coronary artery with a single ostium arising from the right coronary sinus with a calcified stenosis of the &lsquo;common right main-stem&rsquo; (CRMS), and only mild plaque disease distally in the left coronary artery (LCA) (<cross-ref type="fig" refid="HEARTJNL2013304245F1">figure 1</cross-ref>A). CT coronary angiography confirmed the anatomy (<cross-ref type="fig" refid="HEARTJNL2013304245F1">figure 1</cross-ref>B), and the heart team discussion recommended intervention.</p><p><fig loc="float" id="HEARTJNL2013304245F1"><no>Figure&nbsp;1</no><caption><p>Preintervention imaging. (A) Coronary angiogram showing an anomalous solitary ostium of a single coronary artery from the right coronary sinus with a calcified stenosis (arrow) of the &lsquo;common right main-stem&rsquo; (CRMS)). (B) CT angiogram confirming a single origin with calcific disease. (C) Intravascular ultrasound stills of a pullback from the right coronary artery (RCA) into the (CRMS) prior to percutaneous coronary intervention.</p></caption><link locator="heartjnl2013304245f01"></fig></p><p>Intravascular ultrasound (IVUS) interrogation of both major branches revealed calcified disease of the CRMS ostium and further significant disease of...]]></description>
<dc:creator><![CDATA[Patel, N., Sabharwal, N., Banning, A. P.]]></dc:creator>
<dc:date>2013-06-07T00:03:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304245</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304245</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Unprotected single coronary artery main-stem angioplasty]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304263v1?rss=1">
<title><![CDATA[Right coronary artery 'diverticulosis' 4 years after sirolimus-eluting stent implantation associated with very late stent thrombosis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304263v1?rss=1</link>
<description><![CDATA[<sec><p>A 55-year-old female patient with diabetes was admitted with an acute inferior ST-elevation myocardial infarction. Three years previously, she had undergone elective percutaneous coronary intervention&nbsp;to the proximal and mid-segments of her right coronary artery (RCA) (<cross-ref type="fig" refid="HEARTJNL2013304263F1">figure 1</cross-ref>A) with two overlapping sirolimus-eluting stents (Cypher Select Plus 2.75<FONT FACE="arial,helvetica">x</FONT>33&nbsp;mm and 3.0<FONT FACE="arial,helvetica">x</FONT>33&nbsp;mm).</p><p><fig loc="float" id="HEARTJNL2013304263F1"><no>Figure&nbsp;1</no><caption><p>Angiography (A&ndash;D) and frequency domain optical coherence tomography (FD-OCT) (E and F) images of the right coronary artery including: (A) after sirolimus-eluting stent implantation, (B) following presentation with thrombotic occlusion, (C) post-recanalisation with marked outpouchings in the proximal vessel, (D) post-intervention with everolimus-eluting stents highlighting (yellow arrowheads) residual outpouchings corresponding to the FD-OCT images, (E) evaginations (maximum 0.4&nbsp;mm) at the site of initial mid-vessel occlusion and (F) multiple large (maximum 1.4&nbsp;mm) proximal evaginations.</p></caption><link locator="heartjnl2013304263f01"></fig></p><p>Emergency coronary angiography revealed a thrombotic occlusion of the previous RCA stents (<cross-ref type="fig" refid="HEARTJNL2013304263F1">figure 1</cross-ref>B). Following aspiration thrombectomy, angiography revealed residual thrombus and moderate in-stent...]]></description>
<dc:creator><![CDATA[Good, R. I. S., Kalra, S., Lee, T. C.]]></dc:creator>
<dc:date>2013-06-07T00:03:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304263</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304263</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Right coronary artery 'diverticulosis' 4 years after sirolimus-eluting stent implantation associated with very late stent thrombosis]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303849v1?rss=1">
<title><![CDATA[Exercise training improves activity in adolescents afflicted with congenital heart disease]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303849v1?rss=1</link>
<description><![CDATA[<sec><st>Objectives</st><p>To ascertain if motivational techniques and a structured exercise programme can increase activity in adolescents afflicted with congenital heart disease (CHD).</p></sec><sec><st>Design</st><p>Prospective randomised controlled trial.</p></sec><sec><st>Setting</st><p>One hundred and forty-three patients aged 12&ndash;20&nbsp;years attending the tertiary centre for paediatric cardiology in Northern Ireland.</p></sec><sec><st>Main outcome measures</st><p>Increase in exercise capacity as assessed by duration of exercise stress test, and number of minutes spent in moderate to vigorous physical activity (MVPA) per day.</p></sec><sec><st>Results</st><p>Eighty-six patients were men (60%), mean age was 15.60&plusmn;2.27&nbsp;years. Seventy-three percent were considered to have major CHD. Seventy-two participants were randomised to the intervention group. Following intervention, duration of exercise test increased by 1&nbsp;min 5&nbsp;s for the intervention group (p value 0.02) along with increase in predicted VO<SUB>2Max</SUB> (p value 0.02). There was a significant increase in minutes of MVPA per day for the intervention group from baseline to reassessment (p value &lt;0.001) while MVPA remained much the same for the control group. Fourteen patients met the current recommendation for more than 60&nbsp;min MVPA per day at baseline. This doubled to 29 participants at reassessment. There were no adverse effects or mortalities reported.</p></sec><sec><st>Conclusions</st><p>Exercise training is safe, feasible and beneficial in adolescents with CHD. Psychological techniques can be employed to maximise the impact of interventions.</p></sec><sec><st>Trial Registration Number</st><p>ISRCTN27986270.</p></sec>]]></description>
<dc:creator><![CDATA[Morrison, M. L., Sands, A. J., McCusker, C. G., McKeown, P. P., McMahon, M., Gordon, J., Grant, B., Craig, B. G., Casey, F. A.]]></dc:creator>
<dc:date>2013-06-07T00:03:34-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303849</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303849</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Congenital Heart Disease, Congenital heart disease, Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Exercise training improves activity in adolescents afflicted with congenital heart disease]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>Congenital heart disease</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303927v1?rss=1">
<title><![CDATA[Assessment of valve haemodynamics, reverse ventricular remodelling and myocardial fibrosis following transcatheter aortic valve implantation compared to surgical aortic valve replacement: a cardiovascular magnetic resonance study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303927v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To compare the effects of transcatheter aortic valve implantation (TAVI) and surgical aortic valve replacement (SAVR) on aortic valve haemodynamics, ventricular reverse remodelling and myocardial fibrosis (MF) by cardiovascular magnetic resonance (CMR) imaging.</p></sec><sec><st>Design</st><p>A 1.5&nbsp;T CMR scan was performed preoperatively and 6&nbsp;months postoperatively.</p></sec><sec><st>Setting</st><p>University hospitals of Leeds and Leicester, UK.</p></sec><sec><st>Patients</st><p>50 (25 TAVI, 25 SAVR; age 77&plusmn;8&nbsp;years) high-risk severe symptomatic aortic stenosis (AS) patients.</p></sec><sec><st>Main outcome measures</st><p>Valve haemodynamics, ventricular volumes, ejection fraction (EF), mass and MF.</p></sec><sec><st>Results</st><p>Patients were matched for gender and AS severity but not for age (80&plusmn;6 vs 73&plusmn;7&nbsp;years, p=0.001) or EuroSCORE (22&plusmn;14 vs 7&plusmn;3, p&lt;0.001). Aortic valve mean pressure gradient decreased to a greater degree post-TAVI compared to SAVR (21&plusmn;8&nbsp;mm&nbsp;Hg vs 35&plusmn;13&nbsp;mm&nbsp;Hg, p=0.017). Aortic regurgitation reduced by 8% in both groups, only reaching statistical significance for TAVI (p=0.003). TAVI and SAVR improved (p&lt;0.05) left ventricular (LV) end-systolic volumes (46&plusmn;18&nbsp;ml/m<sup>2</sup> vs 41&plusmn;17&nbsp;ml/m<sup>2</sup>; 44&plusmn;22&nbsp;ml/m<sup>2</sup> vs32&plusmn;6&nbsp;ml/m<sup>2</sup>) and mass (83&plusmn;20&nbsp;g/m<sup>2</sup> vs 65&plusmn;15&nbsp;g/m<sup>2</sup>; 74&plusmn;11&nbsp;g/m<sup>2</sup> vs 59&plusmn;8&nbsp;g/m<sup>2</sup>). SAVR reduced end-diastolic volumes (92&plusmn;19&nbsp;ml/m<sup>2</sup> vs 74&plusmn;12&nbsp;ml/m<sup>2</sup>, p&lt;0.001) and TAVI increased EF (52&plusmn;12% vs 56&plusmn;10%, p=0.01). MF reduced post-TAVI (10.9&plusmn;6% vs 8.5&plusmn;5%, p=0.03) but not post-SAVR (4.2&plusmn;2% vs 4.1&plusmn;2%, p=0.98). Myocardial scar (p&le;0.01) and baseline ventricular volumes (p&lt;0.001) were the major predictors of reverse remodelling.</p></sec><sec><st>Conclusions</st><p>TAVI was comparable to SAVR at LV reverse remodelling and superior at reducing the valvular pressure gradient and MF. Future work should assess the prognostic importance of reverse remodelling and fibrosis post-TAVI to aid patient selection.</p></sec>]]></description>
<dc:creator><![CDATA[Fairbairn, T. A., Steadman, C. D., Mather, A. N., Motwani, M., Blackman, D. J., Plein, S., McCann, G. P., Greenwood, J. P.]]></dc:creator>
<dc:date>2013-06-07T00:03:34-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303927</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303927</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Aortic valve disease]]></dc:subject>
<dc:title><![CDATA[Assessment of valve haemodynamics, reverse ventricular remodelling and myocardial fibrosis following transcatheter aortic valve implantation compared to surgical aortic valve replacement: a cardiovascular magnetic resonance study]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>Cardiovascular imaging</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304135v1?rss=1">
<title><![CDATA[Long-term efficacy of percutaneous mitral commissurotomy for recurrent mitral stenosis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304135v1?rss=1</link>
<description><![CDATA[<sec><p>Surgical treatment of mitral stenosis is one of the first heart operations that consistently provided relief of symptoms and improved survival. Two surgeons, Charles Bailey in Philadelphia and Dwight Harken in Boston performed the first successful closed mitral commissurotomy almost simultaneously (4&nbsp;days apart) in June of 1948.<cross-ref type="bib" refid="R1">1</cross-ref> The relief of the inflow obstruction resulted in immediate improvement of patients&rsquo; clinical picture. The initial success led to the refinement of the technique by introduction of a special valve dilatator. Tubbs from the UK perfected the valve dilatator developed by Dr Logan, which is named after him.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> Closed mitral commissurotomy is performed through a left thoracotomy in the beating heart without cardiopulmonary bypass by inserting the dilatator through the left ventricular apex and opening its arms inside the mitral leaflets. The surgeon cannot see, but feel the changes that occur in the valve by the...]]></description>
<dc:creator><![CDATA[Tuzcu, E. M., Kapadia, S. R.]]></dc:creator>
<dc:date>2013-06-07T00:03:34-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304135</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304135</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Echocardiography, Interventional cardiology, Mitral valve disease, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Long-term efficacy of percutaneous mitral commissurotomy for recurrent mitral stenosis]]></dc:title>
<prism:publicationDate>2013-06-07</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303761v1?rss=1">
<title><![CDATA[A rare complication of coronary angiography: 'iodide mumps']]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303761v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Iodide &lsquo;mumps&rsquo;: a rare side effect of iodine-based contrast use</st><p>A 70-year-old male patient with coronary artery disease underwent coronary angiography using 50&nbsp;ml of iopromide contrast (370&nbsp;mg/ml). His comorbid illnesses included hypertension, type 2 diabetes mellitus, psoriasis, duodenal ulcer and iron deficiency anaemia. Around 10&nbsp;h postprocedure, he complained of puffiness of the face. He had no associated dryness of mouth, fever, swelling of lips or breathing difficulty. Physical examination revealed swelling of bilateral parotid, submandibular and left periorbital regions without erythema, rubor or tenderness (<cross-ref type="fig" refid="HEARTJNL2013303761F1">figure 1</cross-ref>). Blood investigations including renal and liver function tests were normal. An ultrasound of the salivary glands revealed bilateral bulky submandibular glands with thickened septae and capsule. Parotid glands were enlarged for age with overlying subcutaneous oedema. A diagnosis of contrast-induced sialadenitis was made. He was observed for 5&nbsp;days by which time the swellings had completely resolved (<cross-ref type="fig" refid="HEARTJNL2013303761F2">figure 2</cross-ref>).</p><p><fig loc="float" id="HEARTJNL2013303761F1"><no>Figure&nbsp;1</no><caption><p>Swelling...]]></description>
<dc:creator><![CDATA[Sajeev, C. G., Mohanan, S., Gopalakrishnapillai, A., Muneer, K.]]></dc:creator>
<dc:date>2013-06-06T00:00:43-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303761</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303761</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[A rare complication of coronary angiography: 'iodide mumps']]></dc:title>
<prism:publicationDate>2013-06-06</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303878v2?rss=1">
<title><![CDATA[The effect of dual-chamber closed-loop stimulation on syncope recurrence in healthy patients with tilt-induced vasovagal cardioinhibitory syncope: a prospective, randomised, single-blind, crossover study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303878v2?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>The closed-loop stimulation (CLS) pacemaker algorithm is a system that permanently monitors the contractile state of the myocardium and converts the intrinsic information into rate regulation. The role that the CLS algorithm plays in the prevention of syncope recurrences still remains unclear. The aim of our prospective, randomised, single-blind, crossover study was to evaluate the effect of dual-chamber CLS in the prevention of syncope recurrence in patients with refractory vasovagal syncope (VVS) and a cardioinhibitory response to head-up tilt test (HUT) during a 36&nbsp;months follow-up.</p></sec><sec><st>Method sand results</st><p>We studied 50 patients (mean age 53&plusmn;5.1; 33 male) with the indication for permanent dual-chamber cardiac pacing for HUT-induced vasovagal cardioinhibitory syncope. They were randomised after 1&nbsp;month of stabilisation period to CLS algorithm features programmed OFF or ON for 18&nbsp;months each, using a crossover design. The number of syncopal and presyncopal episodes during active treatment was lower than those registered during no treatment (n syncopal episodes: 2 vs 15; p=0.007; n presincopal episodes: 5 vs 30; p = 0.004). Lead parameters remained stable over time, and there were no lead-related complications.</p></sec><sec><st>Conclusions</st><p>Based on these 36&nbsp;months follow-up data, it is concluded that dual-chamber CLS is an effective algorithm for preventing syncope recurrences in healthy patients with tilt-induced vasovagal cardioinhibitory syncope.</p></sec>]]></description>
<dc:creator><![CDATA[Russo, V., Rago, A., Papa, A. A., Golino, P., Calabro, R., Russo, M. G., Nigro, G.]]></dc:creator>
<dc:date>2013-06-06T00:00:21-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303878</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303878</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology]]></dc:subject>
<dc:title><![CDATA[The effect of dual-chamber closed-loop stimulation on syncope recurrence in healthy patients with tilt-induced vasovagal cardioinhibitory syncope: a prospective, randomised, single-blind, crossover study]]></dc:title>
<prism:publicationDate>2013-06-06</prism:publicationDate>
<prism:section>Interventional cardiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304070v1?rss=1">
<title><![CDATA[Mechanism of septal bounce in constrictive pericarditis: a simultaneous cardiac catheterisation and echocardiographic study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304070v1?rss=1</link>
<description><![CDATA[<sec><p>A 71-year-old man complained of dyspnoea on exertion and oedema. Chest radiograph demonstrated calcified pericardium. Echocardiogram and gated CT revealed abnormal septal motion in diastole (septal bounce) as well as a septal shift with inspiration (see online supplementary video 1 and 2).</p><p>A right and left heart catheterisation with high-fidelity manometric catheters was performed simultaneously with M-mode echocardiography. Rapidly changing gradients between right ventricular (RV) and left ventricular (LV) pressures, particularly in early diastole, were seen (<cross-ref type="fig" refid="HEARTJNL2013304070F1">figure 1</cross-ref>). There was evidence of early rapid filling and equalisation of both RV and LV diastolic pressures, findings which are seen in both constrictive and restrictive diseases. However, there was abrupt rise in early diastole of the RV pressure curve, overtaking LV pressure. M-mode showed the septum shifting briskly from the RV into the LV. As RV pressure plateaued, filling of the LV led to increased pressure, shifting the septum back. These...]]></description>
<dc:creator><![CDATA[Coylewright, M., Welch, T. D., Nishimura, R. A.]]></dc:creator>
<dc:date>2013-06-05T00:00:40-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304070</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304070</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Mechanism of septal bounce in constrictive pericarditis: a simultaneous cardiac catheterisation and echocardiographic study]]></dc:title>
<prism:publicationDate>2013-06-05</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303698v1?rss=1">
<title><![CDATA[The efficiency of cardiovascular risk assessment: do the right patients get statin treatment?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303698v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To evaluate targeting of statin prescribing for primary prevention to those with high cardiovascular disease (CVD) risk.</p></sec><sec><st>Design</st><p>Two cohort studies including the general population and initiators of statins aged 35&ndash;74 years.</p></sec><sec><st>Setting</st><p>UK primary care records in the Clinical Practice Research Datalink.</p></sec><sec><st>Patients</st><p>3.8 million general population patients and 300 914 statin users.</p></sec><sec><st>Intervention</st><p>Statin prescribing.</p></sec><sec><st>Main outcome measures</st><p>Statin prescribing by CVD risk; observed 5-year CVD risks; variability between practices.</p></sec><sec><st>Results</st><p>Statin prescribing increased substantially over time to patients with high 10-year CVD risk (&ge;20%): 7.0% of these received a statin prior to 2007, and 30.4% in 2007 onwards. Prescribing to patients with low risk (&lt;15%) also increased (from 1.9% to 5.0%). Only about half the patients initiating statin treatment were high risk according to CVD risk score. The 5-year CVD risks, as observed during statin treatment, reduced over calendar time (from 17.0% to 7.1%). There was a large variation between general practices in the percentage of high-risk patients prescribed a statin in 2007 onwards, ranging from 8.2% to 61.5%. For low-risk patients, these varied from 2.1% to 29.1%.</p></sec><sec><st>Conclusions</st><p>There appeared to be substantive overuse in low CVD risk and underuse in high CVD risk (600&nbsp;000 and 850&nbsp;000 patients, respectively, in the UK since 2007). There is wide variation between practices in statin prescribing to patients at high CVD risk. There is a clear need for randomised trials for the best strategy to target statin treatment and manage CVD risk for primary prevention.</p></sec>]]></description>
<dc:creator><![CDATA[van Staa, T.-P., Smeeth, L., Ng, E. S.-W., Goldacre, B., Gulliford, M.]]></dc:creator>
<dc:date>2013-06-04T00:02:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303698</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303698</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The efficiency of cardiovascular risk assessment: do the right patients get statin treatment?]]></dc:title>
<prism:publicationDate>2013-06-04</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303753v1?rss=1">
<title><![CDATA[Congenital aortopulmonary window; an unusual cause of breathlessness]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303753v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Having recently moved to the UK, a 27-year-old woman with known uncorrected congenital heart disease was referred for cardiovascular MRI (CMRI) due to increased shortness of breath. CMRI revealed a large (40&nbsp;mm) aortopulmonary window (<cross-ref type="fig" refid="HEARTJNL2013303753F1">figure 1</cross-ref>) with complete mixing of the pulmonary and systemic circulations (SaO<SUB>2</SUB> 73%), moderate mixed aortic valve disease and mild-moderate pulmonary valve regurgitation. Left and right ventricular volumes and systolic function were normal.</p><p><fig loc="float" id="HEARTJNL2013303753F1"><no>Figure&nbsp;1</no><caption><p>(A) A coronal view and (B) a transverse view of normal proximal aortic and pulmonary artery anatomy compared with (C) a coronal view and (D) a transverse view of the large congenital aortopulmonary connection marked by an * (RV, Right Ventricle; MPA, Main Pulmonary Artery).</p></caption><link locator="heartjnl2013303753f01"></fig></p><p>An aortopulmonary window is a communication between the ascending aorta and the pulmonary trunk. It is a distinct entity from truncus arteriosus due to the presence of two separate arterial valves rather than a...]]></description>
<dc:creator><![CDATA[Rider, O. J., Bissell, M., Myerson, S. G.]]></dc:creator>
<dc:date>2013-06-04T00:02:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303753</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303753</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Congenital aortopulmonary window; an unusual cause of breathlessness]]></dc:title>
<prism:publicationDate>2013-06-04</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303858v1?rss=1">
<title><![CDATA[A new transventricular aproach for pulmonary valve implantation in a patient with severe valve disease after tetralogy-of-Fallot repair]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303858v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>One-third of all patients with tetralogy-of-Fallot (TOF) repair are developing symptomatic pulmonary regurgitation or stenosis.<sup>1</sup> Percutaneous pulmonary valve (PV) implantation via the femoral vein is an accepted method reducing numbers of repeat operations.<sup>2</sup> We present the case of a 44-year-old man with symptomatic PV regurgitation after TOF repair at the age of 10 years. The right ventricle (RV) was severely dilated. Due to severely impaired RV function, percutaneous approach for valve replacement was chosen. Potential coronary compression was ruled out. As the PV annulus, measuring 26&nbsp;mm in diameter (<cross-ref type="fig" refid="HEARTJNL2013303858F1">figure 1</cross-ref>A and B), was too large for currently available transcatheter pulmonary valves, a SAPIEN-XT 29&nbsp;mm designed for transapical aortic valve implantation was used. First, a vascular stent (AS48XXL, Andramed) was implanted in the PV annulus with a 28&nbsp;mm balloon under fluoroscopy and 3D-transoesophageal echocardiography (TEE) guidance (<cross-ref type="fig" refid="HEARTJNL2013303858F1">figure 1</cross-ref>C and D) via transapical access. However, correct placement...]]></description>
<dc:creator><![CDATA[Duerr, G. D., Breuer, J., Schiller, W.]]></dc:creator>
<dc:date>2013-06-04T00:02:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303858</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303858</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[A new transventricular aproach for pulmonary valve implantation in a patient with severe valve disease after tetralogy-of-Fallot repair]]></dc:title>
<prism:publicationDate>2013-06-04</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303921v1?rss=1">
<title><![CDATA[Comparing the decline in coronary heart disease and stroke mortality in neighbouring countries with different healthcare systems]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303921v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To examine age and gender specific trends in coronary heart disease (CHD) and stroke mortality in two neighbouring countries, the Republic of Ireland (ROI) and Northern Ireland (NI).</p></sec><sec><st>Design</st><p>Epidemiological study of time trends in CHD and stroke mortality.</p></sec><sec><st>Setting/patients</st><p>The populations of the ROI and NI, 1985&ndash;2010.</p></sec><sec><st>Interventions</st><p>None.</p></sec><sec><st>Main outcome measures</st><p>Directly age standardised CHD and stroke mortality rates were calculated and analysed using joinpoint regression to identify years where the slope of the linear trend changed significantly. This was performed separately for specific age groups (25&ndash;54, 55&ndash;64, 65&ndash;74 and 75&ndash;84&nbsp;years) and by gender. Annual percentage change (APC) and 95% CIs are presented.</p></sec><sec><st>Results</st><p>There was a striking similarity between the two countries, with percentage change between 1985 and 1989 and between 2006 and 2010 of 67% and 69% in CHD mortality, and 64% and 62% in stroke mortality for the ROI and NI, respectively. However, joinpoint analysis identified differences in the pace of change between the two countries. There was an accelerated pace of decline (negative APC) in mortality for both CHD and stroke in both countries from the mid-1990s (APC ROI &ndash;8% (95% CI &ndash;9.5 to 6.5) and NI &ndash;6.6% (&ndash;6.9 to &ndash;6.3)), but the accelerated decrease started later for CHD mortality in the ROI. In recent years, a levelling off in CHD mortality was observed in the 25&ndash;54 year age group in NI and in stroke mortality for men and women in the ROI.</p></sec><sec><st>Conclusions</st><p>While differences in the pace of change in mortality were observed at different time points, similar, substantial decreases in CHD and stroke mortality were achieved between 1985 and 1989 and between 2006 and 2010 in the ROI and NI despite important differences in health service structures. There is evidence of a levelling in mortality rates in some groups in recent years.</p></sec>]]></description>
<dc:creator><![CDATA[Bennett, K., Hughes, J., Jennings, S., Kee, F., Shelley, E.]]></dc:creator>
<dc:date>2013-06-04T00:02:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303921</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303921</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Comparing the decline in coronary heart disease and stroke mortality in neighbouring countries with different healthcare systems]]></dc:title>
<prism:publicationDate>2013-06-04</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303910v1?rss=1">
<title><![CDATA[Progressive rise in red cell distribution width is associated with poor outcome after transcatheter aortic valve implantation]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303910v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To investigate the prognostic value of baseline and temporal changes in red cell distribution width (RDW) in patients undergoing transcatheter aortic valve implantation (TAVI).</p></sec><sec><st>Design</st><p>Single-centre retrospective observational study.</p></sec><sec><st>Setting</st><p>Tertiary cardiac centre.</p></sec><sec><st>Patients</st><p>175 patients undergoing TAVI were included in this study.</p></sec><sec><st>Main outcome measure</st><p>Survival.</p></sec><sec><st>Results</st><p>We analysed data from 175 TAVI patients (mean (&plusmn;SD) age 83&plusmn;7&nbsp;years, 49% men, mean Logistic EuroSCORE 23&plusmn;1, 66% preserved left ventricular ejection fraction (LVEF)). Immediately pre-TAVI, mean RDW was 14.6&plusmn;1.6% with an RDW&gt;15% in 29% of patients. Over median follow-up of 12&nbsp;months, the median rate of change in RDW was 0.2% per month, and 51 (29%) patients died. On multivariate survival analyses, baseline RDW&ge;15.5% predicted death (adjusted HR 2.70, 95% CI 1.40 to 5.22, p=0.003) independently of LVEF, transfemoral approach, baseline pulmonary artery systolic pressure, moderate/severe mitral regurgitation and body mass index. A greater rate of increase in RDW over time was associated with increased mortality (adjusted HR 1.11, 95% CI 1.04 to 1.18, p=0.001) independently of baseline RDW and other significant temporal variables including a change in creatinine, bilirubin, mean cell haemoglobin concentration or urea. An increase in RDW&gt;0.1%/month was associated with a twofold increased risk of mortality.</p></sec><sec><st>Conclusions</st><p>Baseline RDW&ge;15.5% and a rising RDW over time strongly correlate to an increased risk of death post-TAVI, and could be used to refine risk stratification. Investigating and ameliorating the causes of RDW expansion may improve survival.</p></sec>]]></description>
<dc:creator><![CDATA[Aung, N., Dworakowski, R., Byrne, J., Alcock, E., Deshpande, R., Rajagopal, K., Brickham, B., Monaghan, M. J., Okonko, D. O., Wendler, O., MacCarthy, P. A.]]></dc:creator>
<dc:date>2013-06-04T00:02:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303910</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303910</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Drugs: cardiovascular system, Mitral valve disease, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Progressive rise in red cell distribution width is associated with poor outcome after transcatheter aortic valve implantation]]></dc:title>
<prism:publicationDate>2013-06-04</prism:publicationDate>
<prism:section>Interventional cardiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303266v3?rss=1">
<title><![CDATA[Low dietary sodium in heart failure: a need for scientific rigour]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303266v3?rss=1</link>
<description><![CDATA[<p>There is much evidence that higher sodium intake is associated with elevated blood pressure and there is a strong likelihood that the relationship between excess dietary sodium intake and hypertension is causal.<cross-ref type="bib" refid="R1">1&ndash;3</cross-ref><cross-ref type="bib" refid="R2"></cross-ref><cross-ref type="bib" refid="R3"></cross-ref> Corresponding evidence from clinical trials shows that significant reductions in blood pressure can be achieved by lowering dietary sodium consumption in groups with hypertension as well as among normotensive individuals.<cross-ref type="bib" refid="R4">4</cross-ref> With high blood pressure identified as the leading cause of cardiovascular disease in the world, responsible for more than 60% of stroke events and almost 50% of coronary heart disease,<cross-ref type="bib" refid="R5">5</cross-ref> efforts to control blood pressure levels have been a global priority for decades. In addition to very well established clinical hypertension control programmes, many of the world's leading scientific and health organisations recommend the widespread reduction of sodium intake for blood pressure lowering. In the USA, the US...]]></description>
<dc:creator><![CDATA[Jun, M., Neal, B.]]></dc:creator>
<dc:date>2013-06-01T00:00:37-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303266</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303266</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Low dietary sodium in heart failure: a need for scientific rigour]]></dc:title>
<prism:publicationDate>2013-06-01</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304066v1?rss=1">
<title><![CDATA[Complete avulsion of right coronary artery caused by acute type-A aortic dissection]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304066v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>A 49-year-old lady presented to the emergency department with acute onset chest pain and non-specific ECG changes. CT revealed a Stanford type-A aortic dissection (<cross-ref type="fig" refid="HEARTJNL2013304066F1">figure 1</cross-ref>A). She underwent an emergency surgical repair. Intraoperative transoesophageal echocardiogram demonstrated aortic root dissection (<cross-ref type="fig" refid="HEARTJNL2013304066F1">figure 1</cross-ref>B, see online supplementary video 1). At surgery, complete disruption of the right coronary artery (RCA) was found (<cross-ref type="fig" refid="HEARTJNL2013304066F2">figure 2</cross-ref>). The distal RCA was grafted with a vein graft and the proximal RCA was ligated. The ascending aorta, aortic root and aortic valve were replaced with a composite valved conduit. The left coronary artery was reimplanted as a button.</p><p><fig loc="float" id="HEARTJNL2013304066F1"><no>Figure&nbsp;1</no><caption><p>(A) Contrast-enhanced computed tomogram demonstrating Type A aortic dissection with intimal flaps in both the ascending (white arrow) and descending thoracic aorta. (B) Intraoperative transoesophageal echocardiogram demonstrating an intimal flap extending into the aortic root (4 white arrows).</p></caption><link locator="heartjnl2013304066f01"></fig></p><p><fig loc="float" id="HEARTJNL2013304066F2"><no>Figure&nbsp;2</no><caption><p>An intraoperative photograph...]]></description>
<dc:creator><![CDATA[Modi, A., Diprose, P., Tsang, G.]]></dc:creator>
<dc:date>2013-05-31T00:00:41-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304066</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304066</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Complete avulsion of right coronary artery caused by acute type-A aortic dissection]]></dc:title>
<prism:publicationDate>2013-05-31</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304013v1?rss=1">
<title><![CDATA[Gender-specific differences in clinical outcome of primary prevention implantable cardioverter defibrillator recipients]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304013v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To assess differences in clinical outcome of implantable cardioverter-defibrillator (ICD) treatment in men and women.</p></sec><sec><st>Design</st><p>Prospective cohort study.</p></sec><sec><st>Setting</st><p>University Medical Center.</p></sec><sec><st>Patients</st><p>1946 primary prevention ICD recipients (1528 (79%) men and 418 (21%) women). Patients with congenital heart disease were excluded for this analysis.</p></sec><sec><st>Main outcome measures</st><p>All-cause mortality, ICD therapy (antitachycardia pacing and shock) and ICD shock.</p></sec><sec><st>Results</st><p>During a median follow-up of 3.3&nbsp;years (25th&ndash;75th percentile 1.4&ndash;5.4), 387 (25%) men and 76 (18%) women died. The estimated 5-year cumulative incidence for all-cause mortality was 20% (95% CI 18% to 23%) for men and 14% (95% CI 9% to 19%) for women (log rank p&lt;0.01). After adjustment for potential confounding covariates all-cause mortality was lower in women (HR 0.65; 95% CI 0.49 to 0.84; p&lt;0.01). The 5-year cumulative incidence for appropriate therapy in men was 24% (95% CI 21% to 28%) as compared with 20% (95% CI 14% to 26%) in women (log rank p=0.07). After adjustment, a non-significant trend remained (HR 0.82; 95% CI 0.64 to 1.06; p=0.13).</p></sec><sec><st>Conclusions</st><p>In clinical practice, 21% of primary prevention ICD recipients are women. Women have lower mortality and tend to experience less appropriate ICD therapy as compared with their male peers.</p></sec>]]></description>
<dc:creator><![CDATA[van der Heijden, A. C., Thijssen, J., Borleffs, C. J. W., van Rees, J. B., Hoke, U., van der Velde, E. T., van Erven, L., Schalij, M. J.]]></dc:creator>
<dc:date>2013-05-30T00:01:56-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304013</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304013</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Congenital heart disease, Drugs: cardiovascular system, Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Gender-specific differences in clinical outcome of primary prevention implantable cardioverter defibrillator recipients]]></dc:title>
<prism:publicationDate>2013-05-30</prism:publicationDate>
<prism:section>Heart rhythm disorders</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303679v1?rss=1">
<title><![CDATA[Multislice CT for assessing in-stent dimensions after left main coronary artery stenting: a comparison with three dimensional intravascular ultrasound]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303679v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To evaluate the agreement between multislice CT (MSCT) and intravascular ultrasound (IVUS) to assess the in-stent lumen diameters and lumen areas of left main coronary artery (LMCA) stents.</p></sec><sec><st>Design</st><p>Prospective, observational single centre study.</p></sec><sec><st>Setting</st><p>A single tertiary referral centre.</p></sec><sec><st>Patients</st><p>Consecutive patients with LMCA stenting excluding patients with atrial fibrillation and chronic renal failure.</p></sec><sec><st>Interventions</st><p>MSCT and IVUS imaging at 9&ndash;12&nbsp;months follow-up were performed for all patients.</p></sec><sec><st>Main outcome measures</st><p>Agreement between MSCT and IVUS minimum luminal area (MLA) and minimum luminal diameter (MLD). A receiver operating characteristic (ROC) curve was plotted to find the MSCT cut-off point to diagnose binary restenosis equivalent to 6&nbsp;mm<sup>2</sup> by IVUS.</p></sec><sec><st>Results</st><p>52 patients were analysed. Passing&ndash;Bablok regression analysis obtained a &beta; coefficient of 0.786 (0.586 to 1.071) for MLA and 1.250 (0.936 to 1.667) for MLD, ruling out proportional bias. The &alpha; coefficient was &ndash;3.588 (&ndash;8.686 to &ndash;0.178) for MLA and &ndash;1.713 (&ndash;3.583 to &ndash;0.257) for MLD, indicating an underestimation trend of MSCT. The ROC curve identified an MLA &le;4.7&nbsp;mm<sup>2</sup> as the best threshold to assess in-stent restenosis by MSCT.</p></sec><sec><st>Conclusions</st><p>Agreement between MSCT and IVUS to assess in-stent MLA and MLD for LMCA stenting is good. An MLA of 4.7&nbsp;mm<sup>2</sup> by MSCT is the best threshold to assess binary restenosis. MSCT imaging can be considered in selected patients to assess LMCA in-stent restenosis.</p></sec>]]></description>
<dc:creator><![CDATA[Roura, G., Gomez-Lara, J., Ferreiro, J. L., Gomez-Hospital, J. A., Romaguera, R., Teruel, L. M., Carreno, E., Esplugas, E., Alfonso, F., Cequier, A.]]></dc:creator>
<dc:date>2013-05-30T00:01:55-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303679</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303679</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Drugs: cardiovascular system, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Multislice CT for assessing in-stent dimensions after left main coronary artery stenting: a comparison with three dimensional intravascular ultrasound]]></dc:title>
<prism:publicationDate>2013-05-30</prism:publicationDate>
<prism:section>Interventional cardiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303631v1?rss=1">
<title><![CDATA[The prevalence and characteristics of coronary atherosclerosis in asymptomatic subjects classified as low risk based on traditional risk stratification algorithm: assessment with coronary CT angiography]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303631v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To evaluate the prevalence and characteristics of coronary atherosclerosis in asymptomatic subjects classified as low risk by National Cholesterol Education Program (NCEP) guideline using coronary CT angiography (CCTA).</p></sec><sec><st>Design</st><p>An observational study.</p></sec><sec><st>Setting</st><p>A single tertiary referral centre.</p></sec><sec><st>Patients</st><p>2133 (49.2%) subjects, who were classified as low risk by the NCEP guideline, of 4339 consecutive middle-aged asymptomatic subjects who underwent CCTA with 64-slice scanners as part of a general health evaluation.</p></sec><sec><st>Main outcome measures</st><p>The incidence of atherosclerosis plaques, significant stenosis.</p></sec><sec><st>Results</st><p>In the subjects at low risk, 11.4% (243 of 2133) of subjects had atherosclerosis plaques, 1.3% (28 of 2133) of subjects had significant stenosis, and 0.8% (18 of 2133) of subjects had significant stenosis caused by non-calcified plaque (NCP). Especially, 75.0% (21 of 28) of subjects with significant stenosis and 94.4% (17 of 18) of subjects with significant stenosis caused by NCP were young adults. Mid-term follow-up (29.3&plusmn;14.9&nbsp;months) revealed four subjects with cardiac events: three subjects with unstable angina requiring hospital stay and one subject with percutaneous coronary intervention.</p></sec><sec><st>Conclusions</st><p>Although an asymptomatic population classified as low risk by the NCEP guideline has been regarded as a minimal risk group, the prevalence of atherosclerosis plaques and significant stenosis were not negligible. However, considering very low event rate for those patients, CCTA should not be performed in low-risk asymptomatic subjects, although CCTA might have the potential for identification of high-risk groups in the selected subjects regarded as a minimal-risk group by NCEP guideline.</p></sec>]]></description>
<dc:creator><![CDATA[Kim, K. J., Choi, S. I., Lee, M. S., Kim, J. A., Chun, E. J., Jeon, C. H.]]></dc:creator>
<dc:date>2013-05-30T00:01:55-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303631</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303631</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Percutaneous intervention, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[The prevalence and characteristics of coronary atherosclerosis in asymptomatic subjects classified as low risk based on traditional risk stratification algorithm: assessment with coronary CT angiography]]></dc:title>
<prism:publicationDate>2013-05-30</prism:publicationDate>
<prism:section>Cardiovascular imaging</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304223v1?rss=1">
<title><![CDATA[Can we improve the detection of heart valve disease?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304223v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Introduction</st><p>The clinical care of patients with valve disease is best organised by multidisciplinary specialist valve teams.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> These supervise inpatient and outpatient care, design protocols and processes and coordinate training and education. However, valve disease may not be detected or, if detected, a referral to a specialist team may not be made. This leads to preventable premature death.<cross-ref type="bib" refid="R3">3</cross-ref> <cross-ref type="bib" refid="R4">4</cross-ref></p><p>A working group was therefore convened by the British Heart Valve Society with representatives of all interested national bodies and a panel of invited international commentators. The overall aim was to produce recommendations to improve the detection, conservative management and interventional treatment of valve disease. This document focuses on the detection of valve disease. This occurs principally, but not exclusively, in the community.</p></sec><sec id="s2"><st>Limitations in current detection rates</st><p>In the USA, the estimated prevalence of moderate or severe valve disease is 2.5% using population...]]></description>
<dc:creator><![CDATA[Arden, C., Chambers, J. B., Sandoe, J., Ray, S., Prendergast, B., Taggart, D., Westaby, S., Grothier, L., Wilson, J., Campbell, B., Gohlke-Barwolf, C., Mestres, C. A., Rosenhek, R., Pibarot, P., Otto, C.]]></dc:creator>
<dc:date>2013-05-30T00:01:54-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304223</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304223</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Echocardiography, Aortic valve disease, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Can we improve the detection of heart valve disease?]]></dc:title>
<prism:publicationDate>2013-05-30</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303767v1?rss=1">
<title><![CDATA[Ethnicity and stroke risk in patients with atrial fibrillation]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303767v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To examine the prevalence of atrial fibrillation (AF) and stroke risk by ethnic group in south and east London; to compare classification with CHA<SUB>2</SUB>DS<SUB>2</SUB>VASc and CHADS<SUB>2</SUB>; to examine the appropriateness of anticoagulant treatment and historic trends in prescribing by gender, age, and ethnicity.</p></sec><sec><st>Design</st><p>Cross-sectional study.</p></sec><sec><st>Setting</st><p>Routine general practice records from south and east London.</p></sec><sec><st>Patients</st><p>Patients aged 18&nbsp;years or over with AF.</p></sec><sec><st>Main outcome measures</st><p>Risk of stroke by CHA<SUB>2</SUB>DS<SUB>2</SUB>VASc and CHADS<SUB>2</SUB> score, and prescription of anticoagulant.</p></sec><sec><st>Results</st><p>In 2011, we identified 6292 patients with AF, with an age adjusted prevalence of 0.63% (1.2% white, 0.4% black African/Caribbean and 0.2% South Asian). 93% of the AF population were at high risk of stroke with a CHA<SUB>2</SUB>DS<SUB>2</SUB>VASc score &ge;1, of whom 54% were on warfarin. South Asian patients were at higher stroke risk than white patients (OR 1.67, 95% CI 1.02 to 2.73). Warfarin under-prescribing in people over 80&nbsp;years of age persisted without improvement throughout 2008&ndash;2011. There were no clear differences in warfarin use by ethnic group.</p></sec><sec><st>Conclusions</st><p>Despite a reduced prevalence of AF among South Asian patients, their risk of stroke is higher than for white patients or black African/Caribbean patients in association with diabetes, cardiovascular disease, and hypertension. Under-prescription of anticoagulation persists in all ethnic groups, a deficit most pronounced in the elderly. Use of the CHA<SUB>2</SUB>DS<SUB>2</SUB>VASc score would enhance optimal management in primary care.</p></sec>]]></description>
<dc:creator><![CDATA[Mathur, R., Pollara, E., Hull, S., Schofield, P., Ashworth, M., Robson, J.]]></dc:creator>
<dc:date>2013-05-29T00:00:44-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303767</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303767</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Ethnicity and stroke risk in patients with atrial fibrillation]]></dc:title>
<prism:publicationDate>2013-05-29</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304244v1?rss=1">
<title><![CDATA[Re: visualising the conducting system]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304244v1?rss=1</link>
<description><![CDATA[<sec><p><b>The Author's reply</b> Dr Anderson&rsquo;s letter in response to this editorial seems to have overinterpreted the phrase &lsquo;naked eye&rsquo;.<sup>1</sup> I used the phrase, in what I had hitherto thought was its typical application, as a figure of speech for visual perception without the aid of a means of a magnification device. I apologise that I was not aware of the apparently common ironic use of the phrase in developmental cardiac anatomy.</p><p>Dr Anderson is correct that without specific stains there are no reliable physical landmarks to identify the majority of the conduction system. However, with the requisite vital dyes or post-vital stains, most of the elements of the conventional conduction system in humans can be observed without magnification aids (eg, in the operating room or in the autopsy suite). Indeed, much of this work is based directly on Anderson's seminal contributions.</p><p>Finally, my description of these structures was intended solely to indicate...]]></description>
<dc:creator><![CDATA[MacRae, C.]]></dc:creator>
<dc:date>2013-05-28T00:01:33-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304244</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304244</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Re: visualising the conducting system]]></dc:title>
<prism:publicationDate>2013-05-28</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303832v1?rss=1">
<title><![CDATA[Invasive measurement of coronary microvascular resistance in patients with acute myocardial infarction treated by primary PCI]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303832v1?rss=1</link>
<description><![CDATA[<p>Up to 40% of patients with acute myocardial infarction develop microvascular obstruction (MVO) despite successful treatment with primary percutaneous coronary intervention (PCI). The presence of MVO is linked to negative remodelling and left ventricular dysfunction, leading to decreased long-term survival, increased morbidity and reduced quality of life. The acute obstruction and dysfunction of the microvasculature can potentially be reversed by pharmacological treatment in addition to the standard PCI treatment. Identifying patients with post-PCI occurrence of MVO is essential in assessing which patients could benefit from additional treatment. However, at present there is no validated method to identify these patients. Angiographic parameters like myocardial blush grade or corrected Thrombolysis In Myocardial Infarction (TIMI) flow do not accurately predict the occurrence of MVO as visualised by MRI in the days after the acute event. Theoretically, acute MVO can be detected by intracoronary measurements of flow and resistance directly following the PCI procedure. In MVO the microvasculature is obstructed or destructed and will therefore display a higher coronary microvascular resistance (CMVR). The methods for intracoronary assessment of CMVR are based on either thermodilution or Doppler-flow measurements. The aim of this review is to present an overview of the currently available methods and parameters for assessing CMVR, with special attention given to their use in clinical practice and information provided by clinical studies performed in patients with acute myocardial infarction.</p>]]></description>
<dc:creator><![CDATA[Amier, R. P., Teunissen, P. F. A., Marques, K. M., Knaapen, P., van Royen, N.]]></dc:creator>
<dc:date>2013-05-28T00:01:33-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303832</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303832</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Invasive measurement of coronary microvascular resistance in patients with acute myocardial infarction treated by primary PCI]]></dc:title>
<prism:publicationDate>2013-05-28</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304006v1?rss=1">
<title><![CDATA[Clinical parameters associated with collateral development in patients with chronic total coronary occlusion]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304006v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>Well-developed collaterals provide survival benefit in patients with obstructive coronary artery disease (CAD). Therefore, in this study we sought to determine which clinical variables are associated with arteriogenesis.</p></sec><sec><st>Design</st><p>Clinical and laboratory variables were collected before percutaneous coronary intervention. Multivariate analysis was performed to determine which variables are associated with the collateral flow index (CFI).</p></sec><sec><st>Patients</st><p>Data from 295 chronic total occlusion (CTO) patients (Bern, Switzerland, Amsterdam, the Netherlands and Jena, Germany) were pooled. In earlier studies, patients had varying degrees of stenosis. Therefore, different stages of development of the collaterals were used. In our study, a unique group of patients with CTO was analysed.</p></sec><sec><st>Interventions</st><p>Instead of angiography used earlier, we used a more accurate method to determine CFI using intracoronary pressure measurements. CFI was calculated from the occlusive pressure distal of the coronary lesion, the aortic pressure and central venous pressure.</p></sec><sec><st>Results</st><p>The mean CFI was 0.39&plusmn;0.14. After multivariate analysis, &beta; blockers, hypertension and angina pectoris duration were positively associated with CFI (B: correlation coefficient &beta;=0.07, SE=0.03, p=0.02, B=0.040, SE=0.02, p=0.042 and B=0.001, SE=0.000, p=0.02). Furthermore also after multivariate analysis, high serum leucocytes, prior myocardial infarction and high diastolic blood pressure were negatively associated with CFI (B=&ndash;0.01, SE=0.005, p=0.03, B=&ndash;0.04, SE=0.02, p=0.03 and B=&ndash;0.002, SE=0.001, p=0.011).</p></sec><sec><st>Conclusions</st><p>In this unique cohort, high serum leucocytes and high diastolic blood pressure are associated with poorly developed collaterals. Interestingly, the use of &beta; blockers is associated with well-developed collaterals, shedding new light on the potential action mode of this drug in patients with CAD.</p></sec>]]></description>
<dc:creator><![CDATA[van der Hoeven, N. W., Teunissen, P. F., Werner, G. S., Delewi, R., Schirmer, S. H., Traupe, T., van der Laan, A. M., Tijssen, J. G., Piek, J. J., Seiler, C., van Royen, N.]]></dc:creator>
<dc:date>2013-05-28T00:01:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304006</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304006</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Stable coronary heart disease, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Clinical parameters associated with collateral development in patients with chronic total coronary occlusion]]></dc:title>
<prism:publicationDate>2013-05-28</prism:publicationDate>
<prism:section>Coronary artery disease</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304085v1?rss=1">
<title><![CDATA[Cardiorespiratory fitness changes in patients receiving comprehensive outpatient cardiac rehabilitation in the UK: a multicentre study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304085v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p><b>The Authors' reply</b> We welcome the comments of Dr Ingle and Professor Carroll comparing our recent work<cross-ref type="bib" refid="R1">1</cross-ref> and their own important findings.<cross-ref type="bib" refid="R2">2</cross-ref> We agree with their suggestion that exercise test modality partially explains the relatively small gains in fitness reported for UK cardiac rehabilitation patients. The 1 metabolic equivalent (MET) gain reported by Carroll <I>et al</I><cross-ref type="bib" refid="R2">2</cross-ref> appears clinically important and such findings should serve to illustrate to commissioners that important health-related gains in fitness can be achieved in outpatient cardiac rehabilitation. The 1 MET fitness gain is broadly comparable with that reported for one of our<cross-ref type="bib" refid="R1">1</cross-ref> centres which used treadmill testing (0.76 METs (95% CI 0.4 to 1.12)). We<cross-ref type="bib" refid="R3">3</cross-ref> have previously illustrated that exercise testing modality mediates fitness gains by reporting substantially larger effect sizes (ES) for fitness gains in patients assessed using the Naughton (ES=2.4, 95% CI 1.08...]]></description>
<dc:creator><![CDATA[Sandercock, G., Cardoso, F., Almodhy, M.]]></dc:creator>
<dc:date>2013-05-28T00:01:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304085</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304085</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cardiorespiratory fitness changes in patients receiving comprehensive outpatient cardiac rehabilitation in the UK: a multicentre study]]></dc:title>
<prism:publicationDate>2013-05-28</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304083v1?rss=1">
<title><![CDATA[Is hepatic congestion a risk factor for cholangitis in heart failure patients with coexisting choledocholithiasis?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304083v1?rss=1</link>
<description><![CDATA[<sec><p><b>To the Editor</b> A corollary to the association of incident heart failure and an increase in serum gamma glutamyl transferase (GGT)<cross-ref type="bib" refid="R1">1</cross-ref> is that fluctuations in the severity of heart failure might also have the potential to trigger fluctuations in the blood levels of this parameter. Fluctuations in serum GGT levels (including restoration to the normal range) also occur during the course of the natural history of choledocholithiasis (CDL), even when calculi are still retained within the common bile duct (CBD).<cross-ref type="bib" refid="R2">2</cross-ref> The latter phenomenon is a confounding factor for identification of CDL when the latter coexists with congestive heart failure (CHF), as might well be the case in patients of mean age 56.5&nbsp;years.<cross-ref type="bib" refid="R3">3</cross-ref> In the latter study, 6.8% of 73&nbsp;064 patients with a discharge diagnosis of uncomplicated CDL were also documented as having coexisting CHF.<cross-ref type="bib" refid="R3">3</cross-ref> In the same study, there were 15&nbsp;121 patients...]]></description>
<dc:creator><![CDATA[Jolobe, O.]]></dc:creator>
<dc:date>2013-05-25T00:01:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304083</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304083</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Is hepatic congestion a risk factor for cholangitis in heart failure patients with coexisting choledocholithiasis?]]></dc:title>
<prism:publicationDate>2013-05-25</prism:publicationDate>
<prism:section>Postscript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304084v1?rss=1">
<title><![CDATA[Is hepatic congestion a risk factor for cholangitis in heart failure patients with coexisting choledocholithiasis: the response]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304084v1?rss=1</link>
<description><![CDATA[<p>We appreciate Jolobe for his comments on our results regarding serum gamma-glutamyltransferase (GGT) and the risk of heart failure.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> In our paper entitled &lsquo;Serum gamma-glutamyltransferase and the risk of heart failure in men and women in Finland&rsquo;, we demonstrated that moderate-to-high levels of serum GGT (more than 50th percentiles of serum GGT) were significantly associated with an increased risk of incident heart failure in Finnish men and women.<cross-ref type="bib" refid="R1">1</cross-ref> Fluctuation in serum GGT levels also associated with the occurrence of other diseases; for example, choledocholithiasis, a disease with which coexisting heart failure is prevalent. Therefore, the research question whether serum GGT is a risk factor for heart failure in patients with or without coexisting choledocholithiasis is of interest. In order to answer this question, we should stratify our sample by the participants&rsquo; choledocholithiasis status to investigate if we can observe the same trend of...]]></description>
<dc:creator><![CDATA[Wang, Y., Hu, G.]]></dc:creator>
<dc:date>2013-05-25T00:01:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304084</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304084</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Is hepatic congestion a risk factor for cholangitis in heart failure patients with coexisting choledocholithiasis: the response]]></dc:title>
<prism:publicationDate>2013-05-25</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304230v1?rss=1">
<title><![CDATA[Visualising the conduction tissues]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304230v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p><b>To the Editor</b> I was intrigued to read the editorial of Calum MacRae,<cross-ref type="bib" refid="R1">1</cross-ref> where he leads with the provocative statement that &lsquo;The sinoatrial node, atrioventricular (AV) node and proximal His-Purkinje system can each be seen with the naked eye in humans&rsquo;. I am sure that cardiac surgeons worldwide will be delighted at this news. It is, therefore, unfortunate that MacRae does not share with us the means of achieving the visualisation of these crucial structures. I have spent most of my career seeking to establish landmarks to help in determining their location, but never have I been fortunate enough, with certainty, to see them with &lsquo;the naked eye&rsquo;. It is the case that, with the eye of faith, it is possible to discern the likely site of the sinus node, but the AV node is buried within the floor of the triangle of Koch, while the proximal...]]></description>
<dc:creator><![CDATA[Anderson, R. H.]]></dc:creator>
<dc:date>2013-05-24T00:01:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304230</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304230</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Visualising the conduction tissues]]></dc:title>
<prism:publicationDate>2013-05-24</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303227v1?rss=1">
<title><![CDATA[Recent advances in hypertension in sub-Saharan Africa]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303227v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>Hypertension was once considered rare in sub-Saharan Africa (SSA), but currently it has become a widespread problem with immense socioeconomic importance. The purpose of this review is to summarise new information on hypertension in SSA that has been published since the last major review in 2008.</p></sec><sec><st>Methods and results</st><p>A literature search was performed in Pubmed, Embase, WHO Global Cardiovascular Infobase, African Journal On-Line, and African Index Medicus using the following search criteria: hypertension, high blood pressure, and Africa/SSA. Epidemiological surveys that used the WHO STEPS approach or similar methods were also included. The overall prevalence of hypertension in SSA was estimated at 16.2% (95% CI 14.2% to 20.3%) with an estimated number of hypertensive individuals to be 74.7 million. The prevalence of hypertension varies widely from country to country. It is projected that the number of affected individuals will increase by 68% (125.5 million) by 2025. Mass migration of rural Africans to urban areas and rapid changes in lifestyle and risk factors account for the rising prevalence of hypertension.</p></sec><sec><st>Conclusions</st><p>Proactive public health interventions at a population level need to be introduced to control the growing hypertension epidemic, and there needs to be a major improvement in access to hypertensive care for the individual. There is an important need for better epidemiological data and hypertension related outcome trials in SSA.</p></sec>]]></description>
<dc:creator><![CDATA[Ogah, O. S., Rayner, B. L.]]></dc:creator>
<dc:date>2013-05-24T00:01:07-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303227</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303227</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Recent advances in hypertension in sub-Saharan Africa]]></dc:title>
<prism:publicationDate>2013-05-24</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303843v1?rss=1">
<title><![CDATA[Cardiomyocyte specific adipose triglyceride lipase overexpression prevents doxorubicin induced cardiac dysfunction in female mice]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303843v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>Anthracyclines such as doxorubicin are an effective class of antineoplastic agents. Despite its efficacy in the treatment of a variety of cancers, the clinical use of doxorubicin is limited by cardiac side effects. While it has been suggested that doxorubicin alters myocardial fatty acid metabolism, it is poorly understood whether this is the case and whether variations in myocardial triacylglycerol (TAG) metabolism contribute to doxorubicin induced cardiotoxicity. Since TAG catabolism in the heart is controlled by adipose triglyceride lipase (ATGL), this study examined the influence of doxorubicin on cardiac energy metabolism and TAG values as well as the consequence of forced expression of ATGL in the setting of doxorubicin induced cardiotoxicity.</p></sec><sec><st>Design and setting</st><p>Wild type (WT) mice and mice with cardiomyocyte specific ATGL overexpression were divided into two groups per genotype that received a weekly intraperitoneal injection of saline or doxorubicin for 4&nbsp;weeks.</p></sec><sec><st>Results</st><p>Four weeks of doxorubicin administration significantly impaired in vivo systolic function (11% reduction in ejection fraction, p&lt;0.05), which was associated with increased lung wet to dry weight ratios. Furthermore, doxorubicin induced cardiac dysfunction was independent of changes in glucose and fatty acid oxidation in WT hearts. However, doxorubicin administration significantly reduced myocardial TAG content in WT mice (p&lt;0.05). Importantly, cardiomyocyte specific ATGL overexpression and the resulting decrease in cardiac TAG accumulation attenuated the decrease in ejection fraction (p&lt;0.05) and thus protected mice from doxorubicin induced cardiac dysfunction.</p></sec><sec><st>Conclusions</st><p>Taken together, our data suggest that chronic reduction in myocardial TAG content by cardiomyocyte specific ATGL overexpression is able to prevent doxorubicin induced cardiac dysfunction.</p></sec>]]></description>
<dc:creator><![CDATA[Nagendran, J., Kienesberger, P. C., Pulinilkunnil, T., Zordoky, B. N., Sung, M. M., Kim, T., Young, M. E., Dyck, J. R. B.]]></dc:creator>
<dc:date>2013-05-23T00:01:14-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303843</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303843</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cardiomyocyte specific adipose triglyceride lipase overexpression prevents doxorubicin induced cardiac dysfunction in female mice]]></dc:title>
<prism:publicationDate>2013-05-23</prism:publicationDate>
<prism:section>Basic research</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303349v1?rss=1">
<title><![CDATA[Suitability for subcutaneous defibrillator implantation: results based on data from routine clinical practice]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303349v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To assess the proportion of current implantable cardioverter defibrillator (ICD) recipients who would be suitable for a subcutaneous lead ICD (S-ICD).</p></sec><sec><st>Design</st><p>A retrospective cohort study.</p></sec><sec><st>Setting</st><p>Tertiary care facility in the Netherlands.</p></sec><sec><st>Patients</st><p>All patients who received a single- or dual-chamber ICD in the Leiden University Medical Center between 2002 and 2011. Patients with a pre-existent indication for cardiac pacing were excluded.</p></sec><sec><st>Main outcome measure</st><p>Suitability for an S-ICD defined as not reaching one of the following endpoints during follow-up: (1) an atrial and/or right ventricular pacing indication, (2) successful antitachycardia pacing without a subsequent shock or (3) an upgrade to a CRT-D device.</p></sec><sec><st>Results</st><p>During a median follow-up of 3.4&nbsp;years (IQR 1.7&ndash;5.7&nbsp;years), 463 patients (34% of the total population of 1345 patients) reached an endpoint. The cumulative incidence of ICD recipients suitable for an initial S-ICD implantation was 55.5% (95% CI 52.0% to 59.0%) after 5&nbsp;years. Significant predictors for the unsuitability of an S-ICD were: secondary prevention, severe heart failure and prolonged QRS duration.</p></sec><sec><st>Conclusions</st><p>After 5&nbsp;years of follow-up, approximately 55% of the patients would have been suitable for an S-ICD implantation. Several baseline clinical characteristics were demonstrated to be useful in the selection of patients suitable for an S-ICD implantation.</p></sec>]]></description>
<dc:creator><![CDATA[de Bie, M. K., Thijssen, J., van Rees, J. B., Putter, H., van der Velde, E. T., Schalij, M. J., van Erven, L.]]></dc:creator>
<dc:date>2013-05-23T00:01:15-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303349</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303349</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Suitability for subcutaneous defibrillator implantation: results based on data from routine clinical practice]]></dc:title>
<prism:publicationDate>2013-05-23</prism:publicationDate>
<prism:section>Heart rhythm disorders</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303983v1?rss=1">
<title><![CDATA[Duodenal cancer after cardiac transplantation?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303983v1?rss=1</link>
<description><![CDATA[<sec><p>A 42-year-old man was admitted to the hospital with epigastric discomfort, nausea and vomiting 3&nbsp;months after heart transplantation. Physical examination, chest and abdomen x-ray, electrocardiography and blood tests were unremarkable except for mild elevation of creatinine. Oesophagogastroduodenoscopy showed 30 mm-sized irregular shaped ulceroinfiltrative mass with nodular surface at duodenal second portion, proximal to ampulla of Vater, suspicious of duodenal cancer (<cross-ref type="fig" refid="HEARTJNL2013303983F1">figure 1</cross-ref>A). However, pathological examination revealed cytomegalovirus (CMV) infection with typical inclusions with no evidence of malignancy (<cross-ref type="fig" refid="HEARTJNL2013303983F1">figure 1</cross-ref>C,D). The patient recovered after 2&nbsp;weeks of ganciclovir treatment with marked reduction of CMV viraemia. Follow-up oesophagogastroduodenoscopy and biopsy revealed improved duodenitis (<cross-ref type="fig" refid="HEARTJNL2013303983F1">figure 1</cross-ref>B).</p><p><fig loc="float" id="HEARTJNL2013303983F1"><no>Figure&nbsp;1</no><caption><p>(A) Initial oesophagogastroduodenoscopy (OGD) finding (B) Follow-up OGD finding (C) Intranuclear inclusions with characteristic &lsquo;owl's eye&rsquo; feature (H&amp;E, <FONT FACE="arial,helvetica">x</FONT>400) (D) The immunohistochemical stain for cytomegalovirus (CMV) demonstrates strong nuclear reactivity.</p></caption><link locator="heartjnl2013303983f01"></fig></p><p>CMV causes major morbidity after cardiac transplantation and gastrointestinal involvement is...]]></description>
<dc:creator><![CDATA[Youn, J.-C., Nahm, J. H., Kang, S.-M.]]></dc:creator>
<dc:date>2013-05-22T00:02:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303983</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303983</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Duodenal cancer after cardiac transplantation?]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303871v1?rss=1">
<title><![CDATA[Intensive glucose control and hypoglycaemia: a new cardiovascular risk factor?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303871v1?rss=1</link>
<description><![CDATA[<p>Intensive glucose control is widely practiced in patients with diabetes mellitus and patients acutely admitted to hospitals with concomitant stress-induced hyperglycaemia. Such a strategy increases the risk of hypoglycaemia by several-fold. Hypoglycaemia leads to a surge in catecholamine levels with a profound haemodynamic response. In patients with a decreased cardiac reserve, such significant changes can culminate in serious or even fatal cardiovascular outcomes. This review is aimed at discussing in depth the evidence to date that links hypoglycaemia with cardiovascular mortality, reviewing the likely mechanisms underlying this association, as well as summarising these from a cardiologist's perspective.</p>]]></description>
<dc:creator><![CDATA[Rana, O. A., Byrne, C. D., Greaves, K.]]></dc:creator>
<dc:date>2013-05-22T00:02:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303871</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303871</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Intensive glucose control and hypoglycaemia: a new cardiovascular risk factor?]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304015v1?rss=1">
<title><![CDATA[Cardiac rehabilitation and exercise training]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304015v1?rss=1</link>
<description><![CDATA[<sec><p><b>To the Editor</b> We read with interest the recent multicentre UK study by Sandercock <I>et al</I><cross-ref type="bib" refid="R1">1</cross-ref> quantifying prescribed exercise volume and changes in cardiorespiratory fitness (CRF) involving 950 patients across four UK outpatient cardiac rehabilitation (CR) centres. Although CRF improvements varied, the overall improvement in CRF (0.52 METS) was only one-third the mean estimate reported in their earlier meta-analysis (1.55 METs).<cross-ref type="bib" refid="R2">2</cross-ref> The authors indicated that if representative of UK services, these low training volumes and small increases in CRF may partially explain the reported inefficacy of UK CR to reduce patient mortality and morbidity, as outlined by the RAMIT group.<cross-ref type="bib" refid="R3">3</cross-ref> We agree with the assertion that lower exercise training volumes may be partly responsible for the lower than expected CRF values reported in the UK centres evaluated. Indeed, the CRF improvements reported by Sandercock <I>et al</I><cross-ref type="bib" refid="R1">1</cross-ref> are not consistent with data observed...]]></description>
<dc:creator><![CDATA[Ingle, L., Carroll, S.]]></dc:creator>
<dc:date>2013-05-22T00:02:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304015</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304015</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cardiac rehabilitation and exercise training]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303960v1?rss=1">
<title><![CDATA[Tissue necrosis factor {alpha} and targeting its receptor in ischaemic heart disease]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303960v1?rss=1</link>
<description><![CDATA[<sec><p>The successful evolution of humans has included a highly complex and interwoven series of pathways that govern the balances of lipid storage and mobilisation, thrombosis and thrombolysis, and inflammation and immunity.<cross-ref type="bib" refid="R1">1</cross-ref> Atherosclerotic heart disease in many respects represents an &lsquo;abundance of success&rsquo; in storing fat, mounting an inflammatory response to oxidised lipids, and producing a prothrombotic response to inflammation and endothelial abnormalities. The culmination of ischaemic heart disease, an acute myocardial infarction (AMI), produces a much larger secondary inflammatory wave in response to tissue injury, and this wave can produce additional myocardial injury and mechanical dysfunction.<cross-ref type="bib" refid="R2">2</cross-ref> Separately, it is known that states of chronic inflammation, even those remote from the cardiovascular system such as rheumatologic disorders, result in an increased risk of atherosclerotic heart disease and myocardial infarction. It follows, therefore, that potent anti-inflammatory therapies may be of benefit in the setting of AMI.</p><p>Cytokines, the so-called...]]></description>
<dc:creator><![CDATA[Moliterno, D. J., Smyth, S. S.]]></dc:creator>
<dc:date>2013-05-22T00:02:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303960</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303960</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Acute coronary syndromes, Venous thromboembolism]]></dc:subject>
<dc:title><![CDATA[Tissue necrosis factor {alpha} and targeting its receptor in ischaemic heart disease]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303975v1?rss=1">
<title><![CDATA[Association of copeptin with myocardial infarct size and myocardial function after ST segment elevation myocardial infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303975v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To investigate the relationship between circulating plasma copeptin values and infarct size as well as myocardial function at baseline and 4&nbsp;months after mechanical reperfusion for ST segment elevation myocardial infarction (STEMI).</p></sec><sec><st>Design</st><p>Prospective observational cohort study.</p></sec><sec><st>Setting</st><p>University Hospital of Innsbruck.</p></sec><sec><st>Patients</st><p>54 patients with acute STEMI.</p></sec><sec><st>Main outcome measures</st><p>Correlation of plasma copeptin with infarct size as well as left ventricular ejection fraction (LVEF) and remodelling.</p></sec><sec><st>Methods</st><p>Participants underwent contrast enhanced cardiac MRI at baseline and 4&nbsp;months thereafter. Blood samples were drawn 2&nbsp;days after the onset of symptoms. Copeptin values were determined by an immunofluorescent assay.</p></sec><sec><st>Results</st><p>Copeptin concentrations (median 10.4&nbsp;pmol/l, IQR 6.0&ndash;14.4) were associated with early and chronic infarct size (r=0.388, p=0.004 at baseline; r=0.385, p=0.011 at follow-up) and inversely related to LVEF at both times (r=&ndash;0.484, p&lt;0.001 at baseline; r=&ndash;0.461, p&lt;0.001 at follow-up). Patients with adverse remodelling showed higher baseline copeptin values compared to patients without remodelling (p=0.02). Receiver operating characteristic analysis indicated a cut-off value of 16.7&nbsp;pmol/l for copeptin to best identify patients with future adverse remodelling.</p></sec><sec><st>Conclusions</st><p>Increased copeptin values 2&nbsp;days after STEMI are associated with larger acute and chronic infarct sizes. Moreover, elevated copeptin concentrations at baseline were associated with myocardial function and remodelling 4&nbsp;months post-STEMI. These findings strengthen the role of copeptin as a biomarker of adverse outcome after STEMI.</p></sec>]]></description>
<dc:creator><![CDATA[Reinstadler, S. J., Klug, G., Feistritzer, H.-J., Mayr, A., Harrasser, B., Mair, J., Bader, K., Streil, K., Hammerer-Lercher, A., Esterhammer, R., Metzler, B.]]></dc:creator>
<dc:date>2013-05-22T00:02:31-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303975</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303975</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Association of copeptin with myocardial infarct size and myocardial function after ST segment elevation myocardial infarction]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>Biomarkers and heart disease</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303255v1?rss=1">
<title><![CDATA[Monitoring of a paediatric cardiac tumour over 14 years]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303255v1?rss=1</link>
<description><![CDATA[<sec><p>In 1996, a previously well 5&nbsp;month-old infant presented with ventricular tachycardia requiring cardioversion. Echocardiography revealed a 5&nbsp;cm myocardial tumour involving the ventricular septum and right ventriclular postero-inferior wall (<cross-ref type="fig" refid="HEARTJNL2012303255F1">figure 1</cross-ref>A). There was no obstruction to ventricular inflow or outflow, and the patient was managed conservatively (<cross-ref type="fig" refid="HEARTJNL2012303255F1">figure 1</cross-ref>B, see online supplementary&nbsp;video 1*).</p><p><fig loc="float" id="HEARTJNL2012303255F1"><no>Figure&nbsp;1</no><caption><p>Serial multimodality imaging of cardiac fibroma. An echocardiogram take at 1&nbsp;year of age demonstrates a large interventricular septal mass (A) which did not obstruct the left ventricular outflow tract (B). Three years later a CT scan of the chest demonstrated little change in size of the mass (C). A decade later, at age 14 years, cardiovascular magnetic resonance demonstrates little change in tumour size (D).</p></caption><link locator="heartjnl2012303255f01"></fig></p><p>Over a decade later, with the patient still clinically well, a CT scan demonstrated little change in tumour size and no local or regional spread (<cross-ref type="fig" refid="HEARTJNL2012303255F1">figure 1</cross-ref>C);...]]></description>
<dc:creator><![CDATA[Zaman, S., Zaman, S., Jabbour, A.]]></dc:creator>
<dc:date>2013-05-22T00:02:32-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303255</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303255</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Monitoring of a paediatric cardiac tumour over 14 years]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303032v1?rss=1">
<title><![CDATA[RE: Impact of transcatheter aortic valve implantation or surgical aortic valve replacement on right ventricular function]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303032v1?rss=1</link>
<description><![CDATA[<sec><p>We found the recent article looking at the impact of transcatheter aortic valve implantation (TAVI) and surgical aortic valve replacement (sAVR) on right ventricular (RV) function very interesting.<cross-ref type="bib" refid="R1">1</cross-ref> The authors used speckle tracking echocardiography to assess the impact of TAVI on RV function in two separate groups&mdash;one which had undergone TAVI, and the other which had undergone sAVR. They concluded that RV function deteriorated significantly in those who had undergone sAVR while there was no reduction in RV function following TAVI.</p><p>These results are in keeping with those of one of our studies, which assessed the effects different cardiothoracic operations had on postoperative RV function. We also noted a similar reduction in RV long axis function in patients post-surgery when assessed by tissue Doppler imaging. However, this was only seen in those patients where a traditional thoracotomy had been performed and the pericardium was fully opened; those patients who...]]></description>
<dc:creator><![CDATA[Unsworth, B., Francis, D. P., Mayet, J.]]></dc:creator>
<dc:date>2013-05-22T00:02:31-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303032</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303032</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[RE: Impact of transcatheter aortic valve implantation or surgical aortic valve replacement on right ventricular function]]></dc:title>
<prism:publicationDate>2013-05-22</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304130v1?rss=1">
<title><![CDATA[The 10 'Best Buys' to combat heart disease, diabetes and stroke in Africa]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304130v1?rss=1</link>
<description><![CDATA[<p><I>The Economist</I> has branded Africa as &lsquo;the world's fastest growing continent&rsquo;.<cross-ref type="bib" refid="R1">1</cross-ref> The economy in many African countries is growing at a rate that is higher than that of European countries. HIV infection is coming under control and life expectancy is increasing as a result of widespread use of antiretroviral therapy.<cross-ref type="bib" refid="R2">2</cross-ref> The rising economic prosperity and improving health status has been associated with what can be described as a renaissance in cardiovascular medicine that is characterised by the revival of pan-African professional organisations, such as the Pan African Society of Cardiology (PASCAR) and the creation of the <I>Cardiovascular Journal of Africa</I> as its mouthpiece.<cross-ref type="bib" refid="R3">3</cross-ref> Over the past decade, a number of African-led multinational research networks have been established to combat hypertension,<cross-ref type="bib" refid="R4">4</cross-ref> rheumatic heart disease,<cross-ref type="bib" refid="R5">5</cross-ref> pericardial disease<cross-ref type="bib" refid="R6">6</cross-ref> and heart failure.<cross-ref type="bib" refid="R7">7</cross-ref> Indeed, Africans have ushered in a new golden...]]></description>
<dc:creator><![CDATA[Mayosi, B. M.]]></dc:creator>
<dc:date>2013-05-16T01:54:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304130</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304130</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Acute coronary syndromes, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The 10 'Best Buys' to combat heart disease, diabetes and stroke in Africa]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303773v1?rss=1">
<title><![CDATA[New insights on diabetes mellitus and obesity in Africa-Part 2: prevention, screening and economic burden]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303773v1?rss=1</link>
<description><![CDATA[<p>Evidence has been accumulating on the importance of the rising burden of diabetes mellitus on the African continent at an increasingly higher pace. In the first paper of this series of two companion papers, recent evidence on the prevalence, pathogenesis and comorbidities of obesity and diabetes mellitus in Africa were summarised. In this second paper, we focus on recent developments pertaining to the prevention, screening and the economic burden of diabetes and obesity on the continent. There are indications that awareness on diabetes and chronic diseases at large has increased in Africa in recent times. However, the care for diabetes largely remains suboptimal in most countries, which are not adequately prepared to face the prevention and control of diabetes, as the costs of caring for the condition pose a tremendous challenge to most local economies. Moreover, translation strategies to prevent and control diabetes and obesity, on the continent, are still to be evaluated.</p>]]></description>
<dc:creator><![CDATA[Kengne, A. P., Sobngwi, E., Echouffo-Tcheugui, J.-B., Mbanya, J.-C.]]></dc:creator>
<dc:date>2013-05-16T01:44:28-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303773</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303773</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Epidemiology, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[New insights on diabetes mellitus and obesity in Africa-Part 2: prevention, screening and economic burden]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiovascular disease in Africa review series-Guest Editor Bongani Mayosi</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303592v1?rss=1">
<title><![CDATA[Recent advances in the epidemiology, pathogenesis and prognosis of acute heart failure and cardiomyopathy in Africa]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303592v1?rss=1</link>
<description><![CDATA[<p>This review addresses recent advances in the epidemiology, pathogenesis and prognosis of acute heart failure and cardiomyopathy based on research conducted in Africa. We searched Medline/PubMed for publications on acute decompensated heart failure and cardiomyopathy in Africa for the past 5&nbsp;years (ie, 1 January 2008 to 31 December 2012). This was supplemented with personal communications with colleagues from Africa working in the field. A large prospective registry has shown that acute decompensated heart failure is caused by hypertension, cardiomyopathy and rheumatic heart disease in 90% of cases, a pattern that is in contrast with the dominance of coronary artery disease in North America and Europe. Furthermore, acute heart failure is a disease of the young with a mean age of 52&nbsp;years, occurs equally in men and women, and is associated with high mortality at 6&nbsp;months (~18%), which is, however, similar to that observed in non-African heart failure registries, suggesting that heart failure has a dire prognosis globally, regardless of aetiology. The molecular genetics of dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy in Africans is consistent with observations elsewhere in the world; the unique founder effects in the Afrikaner provide an opportunity for the study of genotype&ndash;phenotype correlations in large numbers of individuals with cardiomyopathy due to the same mutation. Advances in the understanding of the molecular mechanisms of peripartum cardiomyopathy have led to promising clinical trials of bromocriptine in the treatment of peripartum heart failure. The key challenges of management of heart failure are the urgent need to increase the use of proven treatments by physicians, and the control of hypertension in primary care and at the population level.</p>]]></description>
<dc:creator><![CDATA[Sliwa, K., Mayosi, B. M.]]></dc:creator>
<dc:date>2013-05-16T01:24:43-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303592</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303592</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Congenital heart disease, Drugs: cardiovascular system, Heart failure, Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Recent advances in the epidemiology, pathogenesis and prognosis of acute heart failure and cardiomyopathy in Africa]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303896v1?rss=1">
<title><![CDATA[Congenital heart disease and rheumatic heart disease in Africa: recent advances and current priorities]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303896v1?rss=1</link>
<description><![CDATA[<p>Africa has one of the highest prevalence of heart diseases in children and young adults, including congenital heart disease (CHD) and rheumatic heart disease (RHD). We present here an extensive review of recent data from the African continent highlighting key studies and information regarding progress in CHD and RHD since 2005. Main findings include evidence that the CHD burden is underestimated mainly due to the poor outcome of African children with CHD. The interest in primary prevention for RHD has been recently re-emphasised, and new data are available regarding echocardiographic screening for subclinical RHD and initiation of secondary prevention. There is an urgent need for comprehensive service frameworks to improve access and level of care and services for patients, educational programmes to reinforce the importance of prevention and early diagnosis and a relevant research agenda focusing on the African context.</p>]]></description>
<dc:creator><![CDATA[Zuhlke, L., Mirabel, M., Marijon, E.]]></dc:creator>
<dc:date>2013-05-16T01:14:45-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303896</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303896</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Congenital heart disease, Drugs: cardiovascular system, Echocardiography, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Congenital heart disease and rheumatic heart disease in Africa: recent advances and current priorities]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303811v1?rss=1">
<title><![CDATA[Remote monitoring after recent hospital discharge in patients with heart failure: a systematic review and network meta-analysis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303811v1?rss=1</link>
<description><![CDATA[<sec><st>Context</st><p>Readmission to hospital for heart failure is common after recent discharge. Remote monitoring (RM) strategies have the potential to deliver specialised care and management and may be one way to meet the growing needs of the heart failure population.</p></sec><sec><st>Objective</st><p>To determine whether RM strategies improve outcomes for adults who have been recently discharged (&lt;28 days) following an unplanned admission due to heart failure.</p></sec><sec><st>Study design</st><p>Systematic review and network meta-analysis.</p></sec><sec><st>Data sources</st><p>Fourteen electronic databases (including MEDLINE, EMBASE and PsycINFO) were searched to January 2012, and supplemented by hand-searching relevant articles.</p></sec><sec><st>Study selection</st><p>All randomised-controlled trials (RCTs) or observational cohort studies with a contemporaneous control group were included. RM interventions included home telemonitoring (TM) (including implanted monitoring devices) with medical support provided during office hours or 24/7 and structured telephone support (STS) programmes delivered via human-to-human contact (HH) or human-to-machine interface (HM).</p></sec><sec><st>Data Extraction</st><p>Data were extracted and validity was assessed independently by two reviewers.</p></sec><sec><st>Results</st><p>Twenty-one RCTs that enrolled 6317 patients were identified (11 studies evaluated STS (10 of which were HH, while 1 was HM), 9 studies assessed TM, and 1 study assessed both STS and TM). No trial of implanted monitoring devices met the inclusion criteria. Compared with usual care, although not reaching statitistical significance, RM trended to reduce all-cause mortality for STS HH (HR: 0.77, 95% credible interval (CrI): 0.55, 1.08), TM during office hours (HR: 0.76, 95% CrI: 0.49, 1.18) and TM24/7 (HR: 0.49, 95% CrI: 0.20, 1.18). Exclusion of one trial that provided better-than-usual support to the control group rendered each of the above comparisons statistically significant. No beneficial effect on mortality was observed with STS HM. Reductions were also observed in all-cause hospitalisations for TM interventions but not for STS interventions. Care packages generally improved health-related quality-of-life and were acceptable to patients.</p></sec><sec><st>Conclusions</st><p>STS HH and TM with medical support provided during office hours showed beneficial trends, particularly in reducing all-cause mortality for recently discharged patients with heart failure. Where &lsquo;usual&rsquo; care is less good, the impact of RM is likely to be greater.</p></sec>]]></description>
<dc:creator><![CDATA[Pandor, A., Gomersall, T., Stevens, J. W., Wang, J., Al-Mohammad, A., Bakhai, A., Cleland, J. G. F., Cowie, M. R., Wong, R.]]></dc:creator>
<dc:date>2013-05-16T00:02:13-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303811</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303811</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Remote monitoring after recent hospital discharge in patients with heart failure: a systematic review and network meta-analysis]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Systematic review</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304003v1?rss=1">
<title><![CDATA[On the 50th anniversary of the first description of a multistage exercise treadmill test: re-visiting the birth of the 'Bruce protocol']]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304003v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Introduction</st><p>This calendar year, 2013, marks the 50th anniversary of the publication of an article which, unbeknown to the authors, was the first report of what would become one of the most widely used and researched tests in clinical cardiology throughout the world during the 20th century&mdash;the Bruce protocol exercise treadmill test (ETT).<cross-ref type="bib" refid="R1">1</cross-ref> This editorial describes the historical background to the introduction of the ETT, the rationale for a multistage protocol, the first account of the &lsquo;Bruce protocol&rsquo; and provides a brief discussion on the late Professor Robert Bruce himself.</p></sec><sec id="s2"><st>Historical background</st><p>Although it had long been known that evaluating a symptomatic patient during exertion might disclose evidence of coronary artery disease, before the advent of the Bruce treadmill test there was no safe, standardised and validated stress protocol that could be used to monitor cardiovascular haemodynamic changes in exercising patients. Master's two-step test,<cross-ref type="bib" refid="R2">2</cross-ref> a submaximal exercise...]]></description>
<dc:creator><![CDATA[Shah, B. N.]]></dc:creator>
<dc:date>2013-05-16T00:02:12-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304003</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304003</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system]]></dc:subject>
<dc:title><![CDATA[On the 50th anniversary of the first description of a multistage exercise treadmill test: re-visiting the birth of the 'Bruce protocol']]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304034v1?rss=1">
<title><![CDATA[Milk Alkali syndrome: an electrocardiographic masquerader for non-hypothermic Osborn phenomenon]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304034v1?rss=1</link>
<description><![CDATA[<p>A 46-year-old male with history of gastro-oesopahgeal reflux disease presented to the hospital with complaints of severe heartburn and epigastric pain. He reported to have ingested approximately 120 tablets of tums (calcium carbonate) within the last 24&nbsp;h, in order to alleviate his symptoms. He had normal vital signs; however, signs of mild dehydration were noted. Laboratory data were remarkable for severe hypercalcaemia (serum calcium: 16&nbsp;mg/dl) and acute renal failure (serum creatinine: 4.8&nbsp;mg/dl). ECG showed short QT and corrected QT (QTc) interval (385&nbsp;ms and 322&nbsp;ms, respectively) along with prominent Osborn waves (as marked) (<cross-ref type="fig" refid="HEARTJNL2013304034F1">figure 1</cross-ref>). Patient was rehydrated and a follow-up ECG after 2&nbsp;days showed complete normalisation when serum calcium was 9.8&nbsp;mg/dl (<cross-ref type="fig" refid="HEARTJNL2013304034F2">figure 2</cross-ref>).</p><p><fig loc="float" id="HEARTJNL2013304034F1"><no>Figure&nbsp;1</no><caption><p>ECG shows prominent Osborn waves and short QT/QTc interval in the presence of severe hypercalcaemia.</p></caption><link locator="heartjnl2013304034f01"></fig></p><p><fig loc="float" id="HEARTJNL2013304034F2"><no>Figure&nbsp;2</no><caption><p>ECG shows complete resolution of acute changes. Calcium levels were normal when this tracing was...]]></description>
<dc:creator><![CDATA[Chhabra, L., Spodick, D. H.]]></dc:creator>
<dc:date>2013-05-16T00:02:12-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304034</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304034</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Milk Alkali syndrome: an electrocardiographic masquerader for non-hypothermic Osborn phenomenon]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303987v1?rss=1">
<title><![CDATA[Pulsatile external compression of coronary arteries]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303987v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Descriptive text</st><p>A 54-year-old woman with hypertension presented with acute disabling chest pain for 2&nbsp;h and a blood pressure of 86/57mm&nbsp;Hg. The diagnosis of acute anterior wall ST segment elevation myocardial infarction (STEMI) was based on ECG (<cross-ref type="fig" refid="HEARTJNL2013303987F1">figure 1</cross-ref>) and bedside transthoracic echocardiography findings disclosing anterior wall hypokinesis with mild aortic regurgitation without pericardial effusion. Urgent coronary angiography revealed the striking pulsatile luminal collapse of all three coronary arteries mimicking severe coronary spasm (<cross-ref type="fig" refid="HEARTJNL2013303987F2">figure 2</cross-ref>A,B, white arrows and online supplementary video 1). Another intriguing finding was the distended lumen during the peak of dye injection, which turned into a cave-in at the end of the injection in the proximal segment of the artery. Intravascular ultrasound performed in the left main (<cross-ref type="fig" refid="HEARTJNL2013303987F2">figure 2</cross-ref>A,B, black arrow) and the left circumflex arteries (<cross-ref type="fig" refid="HEARTJNL2013303987F2">figure 2</cross-ref>A,B, arrow with a dashed line) indicated dynamic luminal narrowing caused by...]]></description>
<dc:creator><![CDATA[Yang, L.-T., Lee, C.-H.]]></dc:creator>
<dc:date>2013-05-16T00:02:12-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303987</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303987</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Pulsatile external compression of coronary arteries]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303769v1?rss=1">
<title><![CDATA[Huge left ventricular diverticulum simulating athlete's heart, a multimodality imaging study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303769v1?rss=1</link>
<description><![CDATA[<p>A 52-year-old man lost consciousness while running on a hot day. He had been a professional football player for 15&nbsp;years. ECG showed sinus rhythm, high R voltages with T inversion fulfilling the criteria for left ventricular (LV) hypertrophy (<cross-ref type="fig" refid="HEARTJNL2013303769F1">Figure&nbsp;1</cross-ref>A). This ECG LV hypertrophy pattern had been discovered at the age of 15 interpreted as &lsquo;athlete's heart&rsquo;. An echocardiographic exam showed normal ventricular volumes, wall thickness and contractility, but a defect in the apical interventricular septum was present (<cross-ref type="fig" refid="HEARTJNL2013303769F1">Figure&nbsp;1</cross-ref>B; online supplementary video S1). A cardiac MRI study revealed an &lsquo;outpouching&rsquo; of the apical segment of the interventricular septum protruding into the right ventricular apex and surrounded by trabeculations, diagnostic criteria for a muscular LV apical diverticulum (<cross-ref type="fig" refid="HEARTJNL2013303769F1">Figure&nbsp;1</cross-ref>C,D; online supplementary video S2). An ECG LV hypertrophy pattern with T waves inversion can be observed in half of LV diverticula; associated coronary arteries anomalies are described too.<cross-ref...]]></description>
<dc:creator><![CDATA[Cresti, A., Franci, L., Picotti, A.]]></dc:creator>
<dc:date>2013-05-16T00:02:12-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303769</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303769</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Huge left ventricular diverticulum simulating athlete's heart, a multimodality imaging study]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304039v1?rss=1">
<title><![CDATA[Pure arterial CABG using BIMA: the response]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304039v1?rss=1</link>
<description><![CDATA[<sec><p>The Authors&rsquo; reply</p><p>The question posed by Al-Attar <I>et al</I><cross-ref type="bib" refid="R1">1</cross-ref> in response to our analysis of bilateral internal mammary artery (BIMA) use in the USA using the Nationwide Inpatient Sample<cross-ref type="bib" refid="R2">2</cross-ref> cannot be answered by this or other national databases as, to the best of our knowledge, none currently contain data on the technique of conduit harvest, sternal closure or glycaemic control. Randomised multi-centre studies such as the Arterial Revascularization Trial<cross-ref type="bib" refid="R3">3</cross-ref> likely represent the best way to evaluate the optimal strategy for successful BIMA use. Irrespective, while the many barriers to BIMA revascularisation identified by John Puskas in his recent editorial &lsquo;Why did you not use both internal thoracic arteries?&rsquo; remain a factor in surgical decision making,<cross-ref type="bib" refid="R4">4</cross-ref> the rate of BIMA use in the USA is likely to remain close to the 3.9% we observed in our analysis. We agree wholeheartedly with Dr Puskas:...]]></description>
<dc:creator><![CDATA[Chikwe, J., Itagaki, S.]]></dc:creator>
<dc:date>2013-05-16T00:02:11-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304039</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304039</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Pure arterial CABG using BIMA: the response]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303193v1?rss=1">
<title><![CDATA[Recent advances in the epidemiology, diagnosis and treatment of endomyocardial fibrosis in Africa]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303193v1?rss=1</link>
<description><![CDATA[<p>Endomyocardial fibrosis (EMF) continues to be an important and disabling disease in many parts of Africa, although its prevalence has declined in some parts of the continent. Increased access to medical care in general and increased availability of echocardiography in some parts of the continent have led to recognition of the disease in areas in which the disease had not been previously reported, and this has given new insights into its natural history. However, the early manifestations of EMF continue to elude clinicians and researchers, and no progress has been made in defining its aetiology. Advances have, however, been made in establishing the epidemiology and improving clinical diagnosis and management, through modern medical therapy and improved surgical techniques. Research is still required to define clinical, biological and echocardiographic markers of early stages of EMF, so that advances in the knowledge of its pathogenesis and pathophysiology can be made. This will hopefully determine preventive measures and avoid the burden of this debilitating condition in this continent.</p>]]></description>
<dc:creator><![CDATA[Mocumbi, A. O. H., Falase, A. O.]]></dc:creator>
<dc:date>2013-05-16T03:49:49-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303193</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303193</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Echocardiography, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Recent advances in the epidemiology, diagnosis and treatment of endomyocardial fibrosis in Africa]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303316v1?rss=1">
<title><![CDATA[New insights on diabetes mellitus and obesity in Africa-Part 1: prevalence, pathogenesis and comorbidities]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303316v1?rss=1</link>
<description><![CDATA[<p>Evidence continues to accumulate on the rising burden of diabetes mellitus at a higher pace in Africa. In a series of two papers, we sought to summarise recent evidence on diabetes and obesity in Africa based on a systematic review of studies published between January 2002 and October 2012. This first paper on the prevalence, pathogenesis and comorbidities shows that the increase in diabetes prevalence has paralleled that of obesity in Africa. Recent surveys on diabetes and obesity have been largely suboptimal. Hence, the need for more representative and robust continent-wide prevalence figures, which may be somehow achieved through pooling of existing data. Prospective studies linking environmental risk factors to disease occurrence and outcomes remain scarce, and genetic factors for diabetes or obesity have not been extensively assessed. The health consequences of diabetes are manifold, and include a complex interaction with other conditions like HIV infection and sickle cell disease/trait.</p>]]></description>
<dc:creator><![CDATA[Kengne, A. P., Echouffo-Tcheugui, J.-B., Sobngwi, E., Mbanya, J.-C.]]></dc:creator>
<dc:date>2013-05-16T01:45:45-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303316</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303316</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[New insights on diabetes mellitus and obesity in Africa-Part 1: prevalence, pathogenesis and comorbidities]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303177v1?rss=1">
<title><![CDATA[Recent advances in HIV-associated cardiovascular diseases in Africa]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303177v1?rss=1</link>
<description><![CDATA[<p>The last decade has witnessed major advances in our understanding of the epidemiology and pathophysiology of HIV-related cardiovascular disease in sub-Saharan Africa. In this review, we summarise these and discuss clinically relevant advances in diagnosis and treatment. In the Heart of Soweto Study, 10% of patients with newly diagnosed cardiovascular disease were HIV positive, and the most common HIV-related presentations were cardiomyopathy (38%), pericardial disease (13%) and pulmonary arterial hypertension (8%). HIV-related cardiomyopathy is more common with increased immunosuppression and HIV viraemia. With adequate antiretroviral therapy, the prevalence is low. Contributing factors such as malnutrition and genetic predisposition are under investigation. In other settings, pericardial disease is the most common presentation of HIV-related cardiovascular disease (over 40%), and over 90% of pericardial effusions are due to <I>Mycobacterium tuberculosis</I> (TB) pericarditis. HIV-associated TB pericarditis is associated with a greater prevalence of myopericarditis, a lower rate of progression to constriction, and markedly increased mortality. The role of steroids is currently under investigation in the form of a randomised controlled trial. HIV-associated pulmonary hypertension is significantly more common in sub-Saharan Africa than in developed countries, possibly as a result of interactions between HIV and other infectious agents, with very limited treatment options. It has recently been recognised that patients with HIV are at increased risk of sudden death. Infection with HIV is independently associated with QT prolongation, which is more marked with hepatitis C co-infection and associated with a 4.5-fold higher than expected rate of sudden death. The contribution of coronary disease to the overall burden of HIV-associated cardiovascular disease is still low in sub-Saharan Africa.</p>]]></description>
<dc:creator><![CDATA[Syed, F. F., Sani, M. U.]]></dc:creator>
<dc:date>2013-05-16T01:32:12-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303177</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303177</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Recent advances in HIV-associated cardiovascular diseases in Africa]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303585v1?rss=1">
<title><![CDATA[Recent advances in the epidemiology, outcome, and prevention of myocardial infarction and stroke in sub-Saharan Africa]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303585v1?rss=1</link>
<description><![CDATA[<p>The early part of the new millennium witnessed reports of a growing burden of cardiovascular disease in Sub-Saharan Africa (SSA). However the contribution of ischemic heart disease and stroke to this increasing burden relative to that caused by hypertensive heart disease, cardiomyopathy and rheumatic heart disease was not clear. Over the last decade, data from the continent has begun to clarify this issue and suggests three main points. The burden of ischemic heart disease relative to other causes of heart disease remains low particularly in the black Africans majority. Stroke caused predominantly by hypertension is now a major cause of disability and premature death. Third, the burden of risk factors for atherosclerosis is increasing rapidly in most urban and some rural regions. A concerted effort to understand the primary drivers of this increase in cardiac risk factors is required to prevent a future epidemic of atherosclerosis and its sequelae.</p>]]></description>
<dc:creator><![CDATA[Ntsekhe, M., Damasceno, A.]]></dc:creator>
<dc:date>2013-05-16T01:29:31-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303585</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303585</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Acute coronary syndromes, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Recent advances in the epidemiology, outcome, and prevention of myocardial infarction and stroke in sub-Saharan Africa]]></dc:title>
<prism:publicationDate>2013-05-16</prism:publicationDate>
<prism:section>Cardiology in Africa review series</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303939v1?rss=1">
<title><![CDATA[A systematic review and meta-analysis of genotype-phenotype associations in patients with hypertrophic cardiomyopathy caused by sarcomeric protein mutations]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303939v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>The genetic basis of familial hypertrophic cardiomyopathy (HCM) is well described, but the relation between genotype and clinical phenotype is still poorly characterised.</p></sec><sec><st>Objective</st><p>To summarise and critically review the current literature on genotype&ndash;phenotype associations in patients with HCM and to perform a meta-analysis on selected clinical features.</p></sec><sec><st>Data sources</st><p>PubMed/Medline was searched up to January 2013. Retrieved articles were checked for additional publications.</p></sec><sec><st>Selection criteria</st><p>Observational, cross-sectional and prospectively designed English language human studies that analysed the relationship between the presence of mutations in sarcomeric protein genes and clinical parameters.</p></sec><sec><st>Data extraction and analysis</st><p>The pooled analysis was confined to studies reporting on cohorts of unrelated and consecutive patients in which at least two sarcomere genes were sequenced. A random effect meta-regression model was used to determine the overall prevalence of predefined clinical features: age at presentation, gender, family history of HCM, family history of sudden cardiac death (SCD), and maximum left ventricular wall thickness (MLVWT). The I<sup>2</sup> statistic was used to estimate the proportion of total variability in the prevalence data attributable to the heterogeneity between studies.</p></sec><sec><st>Results</st><p>Eighteen publications (corresponding to a total of 2459 patients) were selected for the pooled analysis. The presence of any sarcomere gene mutation was associated with a younger age at presentation (38.4 vs 46.0&nbsp;years, p&lt;0.0005), a family history of HCM (50.6% vs 23.1%, p&lt;0.0005), a family history of SCD (27.0% vs 14.9%, p&lt;0.0005) and greater MLVWT (21.0 vs 19.3&nbsp;mm, p=0.03). There were no differences when the two most frequently affected genes, <I>MYBPC3</I> and <I>MYH7</I>, were compared. A total of 53 family studies were also included in the review. These were characterised by pronounced variability and the majority of studies reporting on outcomes analysed small cross-sectional cohorts and were unsuitable for pooled analyses.</p></sec><sec><st>Conclusions</st><p>The presence of a mutation in any sarcomere gene is associated with a number of clinical features. The heterogeneous nature of the disease and the inconsistency of study design precludes the establishment of more precise genotype&ndash;phenotype relationships. Large scale studies examining the relation between genotype, disease severity, and prognosis are required.</p></sec>]]></description>
<dc:creator><![CDATA[Lopes, L. R., Rahman, M. S., Elliott, P. M.]]></dc:creator>
<dc:date>2013-05-14T00:01:12-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303939</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303939</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Hypertrophic cardiomyopathy, Drugs: cardiovascular system]]></dc:subject>
<dc:title><![CDATA[A systematic review and meta-analysis of genotype-phenotype associations in patients with hypertrophic cardiomyopathy caused by sarcomeric protein mutations]]></dc:title>
<prism:publicationDate>2013-05-14</prism:publicationDate>
<prism:section>Systematic review</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303794v1?rss=1">
<title><![CDATA[CT stress perfusion imaging for detection of haemodynamically relevant coronary stenosis as defined by FFR]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303794v1?rss=1</link>
<description><![CDATA[<sec><st>Objectives</st><p>To evaluate the diagnostic accuracy (DA) of CT-myocardial perfusion imaging (CT-MPI) and a combined approach with CT angiography (CTA) for the detection of haemodynamically relevant coronary stenoses in patients with both suspected and known coronary artery disease.</p></sec><sec><st>Design</st><p>Prospective, non-randomised, diagnostic study.</p></sec><sec><st>Setting</st><p>Academic hospital-based study.</p></sec><sec><st>Patients</st><p>65 patients (42 men age 70.4&plusmn;9) with typical or atypical chest pain.</p></sec><sec><st>Interventions</st><p>CTA and CT-MPI with adenosine stress using a fast dual-source CT system. At subsequent invasive angiography, FFR measurement was performed in coronary arteries to define haemodynamic relevance of stenosis.</p></sec><sec><st>Main outcome measures</st><p>We tried to correlate haemodynamically relevant stenosis (FFR &lt; 0.80) to a reduced myocardial blood flow (MBF) as assessed by CT-MPI and determined the DA of CT-MPI for the detection of haemodynamically relevant stenosis.</p></sec><sec><st>Results</st><p>Sensitivity and negative predictive value (NPV) of CTA alone were very high (100% respectively) for ruling out haemodynamically significant stenoses, specificity, Positive predictive value (PPV) and DA were low (43.8, 67.3 and 72%, respectively). CT-MPI showed a significant increase in specificity, PPV and DA for the detection of haemodynamically relevant stenoses (65.6, 74.4 and 81.5%, respectively) with persisting high sensitivity and NPV for ruling out haemodynamically relevant stenoses (97% and 95.5% respectively). The combination of CTA and CT-MPI showed no further increase in detection of haemodynamically significant stenosis compared with CT-MPI alone.</p></sec><sec><st>Conclusions</st><p>Our data suggest that CT-MPI permits the detection of haemodynamically relevant coronary artery stenoses with a moderate DA. CT may, therefore, allow the simultaneous assessment of both coronary morphology and function.</p></sec>]]></description>
<dc:creator><![CDATA[Greif, M., von Ziegler, F., Bamberg, F., Tittus, J., Schwarz, F., D'Anastasi, M., Marcus, R. P., Schenzle, J., Becker, C., Nikolaou, K., Becker, A.]]></dc:creator>
<dc:date>2013-05-14T00:01:11-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303794</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303794</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[CT stress perfusion imaging for detection of haemodynamically relevant coronary stenosis as defined by FFR]]></dc:title>
<prism:publicationDate>2013-05-14</prism:publicationDate>
<prism:section>Cardiovascular imaging</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303496v1?rss=1">
<title><![CDATA[Interaction between dietary marine-derived n-3 fatty acids intake and J-point elevation on the risk of cardiac death: a 24-year follow-up of Japanese men]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303496v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>Higher marine-derived n-3 fatty acids (MDn3FAs) intake reduces the risk of sudden cardiac death via antiarrhythmic effects. The article evaluates whether MDn3FAs intake attenuates the increased risk of cardiac death associated with J-point elevation (JPE), characterised by an elevation of QRS-ST junction (J-point) &ge;0.1&nbsp;mV on electrocardiography.</p></sec><sec><st>Design</st><p>A prospective population-based cohort study.</p></sec><sec><st>Setting</st><p>The National Survey on Circulatory Disorders and the National Nutrition Survey of Japan.</p></sec><sec><st>Participants</st><p>A total of 4348 community-dwelling men (mean age 49.3&nbsp;years), without cardiovascular diseases at baseline, from randomly selected areas across Japan.</p></sec><sec><st>Main outcome measures</st><p>Cardiac death (200 men) during the 24-year follow-up.</p></sec><sec><st>Results</st><p>Dietary MDn3FAs intake was assessed using a dietary method to estimate individual intake of household-based weighed food records for 3&nbsp;days. Cox models were used to calculate HRs and 95% CIs adjusted for possible confounding factors. JPE was present in 340 participants (7.8%). The median daily intake of MDn3FAs was 0.35%kcal (0.92&nbsp;g/day). The risk of cardiac death was significantly higher in participants with JPE than in those without JPE in the low intake group (&lt;0.35%kcal; adjusted HR 3.51; 95% CI 1.84 to 6.73; p&lt;0.001), but not in the high intake group (&ge;0.35%kcal; adjusted HR 1.09; 95% CI 0.56 to 2.16; p=0.795). The interaction between dietary MDn3FAs intake and JPE on the risk of cardiac death was statistically significant (p=0.006).</p></sec><sec><st>Conclusions</st><p>The increased risk of cardiac death associated with JPE may be attenuated by higher dietary MDn3FAs intake.</p></sec>]]></description>
<dc:creator><![CDATA[Hisamatsu, T., Miura, K., Ohkubo, T., Yamamoto, T., Fujiyoshi, A., Miyagawa, N., Kadota, A., Takashima, N., Okuda, N., Matsumura, Y., Yoshita, K., Kita, Y., Murakami, Y., Nakamura, Y., Okamura, T., Horie, M., Okayama, A., Ueshima, H., for the NIPPON DATA80 Research Group]]></dc:creator>
<dc:date>2013-05-10T00:00:54-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303496</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303496</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Pacing and electrophysiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Interaction between dietary marine-derived n-3 fatty acids intake and J-point elevation on the risk of cardiac death: a 24-year follow-up of Japanese men]]></dc:title>
<prism:publicationDate>2013-05-10</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304095v1?rss=1">
<title><![CDATA[Non-invasive decision making in stable angina-The response]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304095v1?rss=1</link>
<description><![CDATA[<p><b>The Authors&rsquo; reply</b>, We were intrigued by the comments from Meune <I>et al</I><cross-ref type="bib" refid="R1">1</cross-ref> on our article on treatment decisions based on hybrid single photon emission computed tomography (SPECT) and coronary computed tomography angiography (CCTA) for patients with stable anginal complaints.<cross-ref type="bib" refid="R2">2</cross-ref></p><p>Prognosis and relief of anginal complaints determine the treatment strategy for each individual patient with coronary artery disease (CAD).<cross-ref type="bib" refid="R3">3</cross-ref> In patients with high-risk CAD (two-vessel disease (VD) involving the left anterior descending, three-VD or left main disease), revascularisation is associated with better outcome compared with medical therapy.<cross-ref type="bib" refid="R4">4</cross-ref> Moreover, CABG is the standard of care for patients with three-VD or left main disease.<cross-ref type="bib" refid="R5">5</cross-ref> Overall, 51% of all included patients suffered significant CAD based on angiography. Of them, 37 (67%) had high-risk CAD. In all, 22% of patients with non-high-risk CAD were on dual antianginal medication. As such, despite similar baseline characteristics, the...]]></description>
<dc:creator><![CDATA[Schaap, J., de Groot, J. A. H., Nieman, K., Meijboom, W. B., Boekholdt, S. M., Post, M. C., Van der Heyden, J. A., de Kroon, T. L., Rensing, B. J. W. M., Moons, K. G., Verzijlbergen, J. F.]]></dc:creator>
<dc:date>2013-05-09T00:02:11-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304095</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304095</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Non-invasive decision making in stable angina-The response]]></dc:title>
<prism:publicationDate>2013-05-09</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304022v1?rss=1">
<title><![CDATA[Polyarteritis nodosa presenting as acute myocardial infarction in a young man: importance of invasive angiography]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304022v1?rss=1</link>
<description><![CDATA[<sec><p>A 31-year-old man, with a low risk-factor profile for coronary disease, presented with atypical left-sided chest pain. ECGs were normal, however, cardiac Troponin I was elevated at 4.57 (ref &lt;0.04). Invasive coronary angiography demonstrated an abnormality in the mid-left anterior descending artery (yellow arrow, <cross-ref type="fig" refid="HEARTJNL2013304022F1">figure 1</cross-ref>: right hand panel zoomed image) suggestive of microaneurysm formation. left ventricular (LV) angiography revealed an area of hypokinesis.</p><p><fig loc="float" id="HEARTJNL2013304022F1"><no>Figure&nbsp;1</no><caption><p>Coronary angiogram demonstrating microaneurysm in left anterior descending (LAD). Right hand panel is zoomed image.</p></caption><link locator="heartjnl2013304022f01"></fig></p><p>Magnetic resonance angiography showed a normal aorta, renal and major branch vessels. Subsequent invasive superior mesenteric angiography revealed multiple microaneurysms consistent with polyarteritis nodosa (<cross-ref type="fig" refid="HEARTJNL2013304022F2">figure 2</cross-ref>: yellow arrow, right hand panel zoomed image).</p><p><fig loc="float" id="HEARTJNL2013304022F2"><no>Figure&nbsp;2</no><caption><p>(A) Mesenteric artery angiogram showing multiple microaneurysms. (B) magnified image of outlined area in panel A with several representative microaneurysms outlined by arrows.</p></caption><link locator="heartjnl2013304022f02"></fig></p><p>Review of the history elicited postprandial abdominal pain, significant...]]></description>
<dc:creator><![CDATA[McWilliams, E. T., Khonizy, W., Jameel, A.]]></dc:creator>
<dc:date>2013-05-09T00:02:10-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304022</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304022</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Polyarteritis nodosa presenting as acute myocardial infarction in a young man: importance of invasive angiography]]></dc:title>
<prism:publicationDate>2013-05-09</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304035v1?rss=1">
<title><![CDATA[Pure arterial CABG using bilateral internal mammary artery]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304035v1?rss=1</link>
<description><![CDATA[<sec><p>To the Editor,</p><p>We read with interest the paper by Itagaki <I>et al</I> in <I>Heart</I>.<cross-ref type="bib" refid="R1">1</cross-ref> The authors investigate the impact of bilateral internal mammary artery (BIMA) use in 1&nbsp;526&nbsp;360 isolated coronary artery bypass operations on inhospital mortality and deep sternal wound infection (DSWI). While there is survival benefit with BIMA, it was associated with a higher incidence of DSWI but only in patients with chronic complications of diabetes mellitus. This finding correlates with those of the Arterial Revascularisation Trial in which half the patients requiring sternal reconstruction in the BIMA group had diabetes.<cross-ref type="bib" refid="R2">2</cross-ref> By harvesting the Internal Mammary Artery (IMA) in a skeletonised fashion,<cross-ref type="bib" refid="R3">3</cross-ref> longer conduits are obtained, and the risks of kinking are reduced. Moreover, a beneficial reduction in sternal wound infection has been observed with this effect being more evident in diabetic patients undergoing BIMA grafting.<cross-ref type="bib" refid="R4">4</cross-ref> Furthermore, since diabetic patients present...]]></description>
<dc:creator><![CDATA[Al-Attar, N., Morcos, K.]]></dc:creator>
<dc:date>2013-05-09T00:02:10-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304035</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304035</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Pure arterial CABG using bilateral internal mammary artery]]></dc:title>
<prism:publicationDate>2013-05-09</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302064v1?rss=1">
<title><![CDATA[Left ventricular twist dynamics: principles and applications]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302064v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Physiological fundamentals of left ventricular torsion</st><sec id="s1a"><st>Left ventricular anatomy</st><p>The normal left ventricular (LV) shape has been assimilated to a thick walled prolate ellipsoid with its long axis directed from apex to base.<cross-ref type="bib" refid="R1">1</cross-ref> <sup>w1</sup> The normal LV morphology is characterised by a high degree of regional heterogeneity. With the use of tagging magnetic resonance, a wide variation in circumferential and longitudinal radii of LV wall curvature has been shown, with a more oval shaped LV cavity in the short axis direction and more flattened LV wall towards the apex.<cross-ref type="bib" refid="R2">2</cross-ref> In addition, a gradual thinning of the LV wall was noted toward the apex, whereas around the LV circumference, the posterolateral wall was significantly thicker than the septum.<cross-ref type="bib" refid="R2">2</cross-ref> The law of Laplace and variations in the amount of longitudinally and circumferentially oriented fibres have been used to explain the wide variation in the thickness of...]]></description>
<dc:creator><![CDATA[Beladan, C. C., Calin, A., Rosca, M., Ginghina, C., Popescu, B. A.]]></dc:creator>
<dc:date>2013-05-09T00:02:10-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302064</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302064</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Education in Heart, Basic science, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Left ventricular twist dynamics: principles and applications]]></dc:title>
<prism:publicationDate>2013-05-09</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303339v1?rss=1">
<title><![CDATA[Alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy: low incidence of sudden cardiac death and reduced risk profile]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303339v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>The infarction induced by alcohol septal ablation (ASA) may predispose to arrhythmia and sudden cardiac death (SCD).</p></sec><sec><st>Objective</st><p>To assess survival, incidence of SCD after ASA and effects of ASA on the traditional risk factors (RFs) for SCD.</p></sec><sec><st>Design</st><p>An observational cohort-study (follow-up 8.4&plusmn;4&nbsp;years).</p></sec><sec><st>Setting</st><p>A dual-centre cohort.</p></sec><sec><st>Patients</st><p>470 consecutive patients (age 56&plusmn;14&nbsp;years) with obstructive hypertrophic cardiomyopathy (HCM) (1996&ndash;2010).</p></sec><sec><st>Interventions</st><p>Clinically applied echo-contrast-guided ASA treatments.</p></sec><sec><st>Main outcome measures</st><p>All-cause mortality, SCD and RFs for SCD before and after ASA.</p></sec><sec><st>Results</st><p>The 10-year survival was 88% (annual all-cause death rate 1.2%) after ASA compared with 84% (p=0.06) in a matched background population. The 10-year survival free of SCD was 95% (annual SCD rate 0.5%). ASA reduced the prevalence of abnormal blood pressure response (from 23% to 9%, p&lt;0.001), syncope (26% to 2%, p&lt;0.001), non-sustained ventricular tachycardia (NSVT) (23% to 17%, p&lt;0.05) and maximal wall thickness &ge;30&nbsp;mm (7% to 2%, p&lt;0.001). There was a family history of SCD in 19% of the patients. The proportion of patients at high risk&mdash;that is, two or more RFs (n=89), was reduced from 25% to 8% (p&lt;0.001). A RF score &ge;2 before ASA was not associated with SCD (n=361, p=0.31).</p></sec><sec><st>Conclusions</st><p>Survival in ASA-treated patients was similar to that in the background population. The number of RFs, including the prevalence of NSVT, was markedly reduced by ASA and the incidence of SCD was correspondingly low. Thus, clinically applied ASA was safe.</p></sec>]]></description>
<dc:creator><![CDATA[Jensen, M. K., Prinz, C., Horstkotte, D., van Buuren, F., Bitter, T., Faber, L., Bundgaard, H.]]></dc:creator>
<dc:date>2013-05-03T00:01:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303339</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303339</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Hypertrophic cardiomyopathy, Drugs: cardiovascular system, Hypertension, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy: low incidence of sudden cardiac death and reduced risk profile]]></dc:title>
<prism:publicationDate>2013-05-03</prism:publicationDate>
<prism:section>Cardiomyopathy</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303577v1?rss=1">
<title><![CDATA[Non-invasive decision making in stable angina]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303577v1?rss=1</link>
<description><![CDATA[<sec><p>To the Editor,</p><p>We read with great interest the study of Schaap <I>et al</I>.<cross-ref type="bib" refid="R1">1</cross-ref> During a 14-month period, they investigated patients with stable angina and compared a hybrid single-photon emission computed tomography (SPECT)/CT coronary angiography (CA) versus the combination of SPECT and CA on treatment decisions. Thus, they concluded that similar decisions can be reached using the non-invasive approach. While there is great potential of such a hybrid work-up, we would like to point out some aspects of their study that may mitigate their conclusion.</p><p>They included 107 patients, aged 62.8&nbsp;years, diabetes mellitus in 16.8%, with most of them having a class II angina. Although these characteristics are somewhat similar to the one of patients included in the COURAGE study,<cross-ref type="bib" refid="R2">2</cross-ref> they recommended revascularisation procedures in 54/107 of the cohort, a proportion higher than expected based on recent studies on stable angina.<cross-ref type="bib" refid="R2">2</cross-ref> <cross-ref type="bib" refid="R3">3</cross-ref> In addition,...]]></description>
<dc:creator><![CDATA[Meune, C., Aissou, L., Pop, N., Goudot, F.-X.]]></dc:creator>
<dc:date>2013-05-03T00:01:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303577</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303577</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Non-invasive decision making in stable angina]]></dc:title>
<prism:publicationDate>2013-05-03</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-3013-303863v1?rss=1">
<title><![CDATA[Dronedarone for the treatment of non-permanent atrial fibrillation: National Institute for Health and Clinical Excellence guidance]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-3013-303863v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>In September 2009, the European Union approved dronedarone &lsquo;in adult clinically stable patients with a history of, or current non-permanent atrial fibrillation (AF) to prevent recurrence of AF or to lower ventricular rate&rsquo;.<cross-ref type="bib" refid="R1">1</cross-ref> This was the first new oral anti-arrhythmic agent to be approved in more than 20&nbsp;years if dofetilide, which was never marketed in Europe, is discounted. The failure of multiple anti-arrhythmic drug development programmes for the prevention of ventricular arrhythmias led to a new but uncharted approach, the introduction of a drug specifically and only for the management of AF. This is an important therapeutic arena, which had not been directly addressed previously.<cross-ref type="bib" refid="R2">2</cross-ref> The marketing authorisation for dronedarone followed an extensive development programme involving six trials that enrolled over 7000 patients (<cross-ref type="tbl" refid="HEARTJNL3013303863TB1">table 1</cross-ref>).<cross-ref type="bib" refid="R3">3&ndash;9</cross-ref><cross-ref type="bib" refid="R4"></cross-ref><cross-ref type="bib" refid="R5"></cross-ref><cross-ref type="bib" refid="R6"></cross-ref><cross-ref type="bib" refid="R7"></cross-ref><cross-ref type="bib" refid="R8"></cross-ref><cross-ref type="bib" refid="R9"></cross-ref></p><p><tbl id="HEARTJNL3013303863TB1" loc="float"><no>Table&nbsp;1</no><caption><p>Clinical development programme...]]></description>
<dc:creator><![CDATA[Camm, A. J., Savelieva, I.]]></dc:creator>
<dc:date>2013-04-30T00:00:53-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-3013-303863</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-3013-303863</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Heart failure, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Dronedarone for the treatment of non-permanent atrial fibrillation: National Institute for Health and Clinical Excellence guidance]]></dc:title>
<prism:publicationDate>2013-04-30</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2011-301528v1?rss=1">
<title><![CDATA[Diagnostic approach and differential diagnosis in patients with hypertrophied left ventricles]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2011-301528v1?rss=1</link>
<description><![CDATA[<p>In daily clinical practice, cardiologists frequently encounter patients demonstrating left ventricular hypertrophy (LVH) of initially unknown origin. The exact diagnosis and differentiation of &lsquo;pathological&rsquo; LVH&mdash;which occurs in, for example, hypertensive heart disease (HHD), hypertrophic cardiomyopathy (HCM), myocardial storage/infiltrative disease, or systemic diseases such as mitochondrial myopathy&mdash;from &lsquo;physiological&rsquo; LVH (which occurs in athletes) is of paramount therapeutic and prognostic value. However, determination of the underlying aetiology of LVH&mdash;which is frequently defined by a left ventricular (LV) wall thickness of at least 13&nbsp;mm<sup>w1 w2</sup>&mdash;still constitutes a challenging and critical clinical problem. Hence, this article will focus on the current diagnosis of both common as well as rare (non-valvular) diseases that are associated with LVH.</p><sec id="s1"><st>Diagnostic approach to LVH</st><p>The diagnostic armamentarium for the work-up of LVH has increased greatly over the past years. Today, non-invasive imaging modalities such as cardiovascular magnetic resonance (CMR) allow a detailed and comprehensive work-up of hypertrophied hearts and...]]></description>
<dc:creator><![CDATA[Yilmaz, A., Sechtem, U.]]></dc:creator>
<dc:date>2013-04-30T00:00:26-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301528</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301528</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Myocardial disease, Education in Heart, Hypertrophic cardiomyopathy, Drugs: cardiovascular system, Echocardiography, Hypertension, Clinical diagnostic tests, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Diagnostic approach and differential diagnosis in patients with hypertrophied left ventricles]]></dc:title>
<prism:publicationDate>2013-04-30</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303654v1?rss=1">
<title><![CDATA[Family history, comorbidity and risk of thoracic aortic disease: a population-based case-control study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303654v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To examine the risk of thoracic aortic disease (TAD) when one or more first-degree relatives are affected, and to relate the risk of family history to the risk of other cardiopulmonary comorbidity.</p></sec><sec><st>Design</st><p>Population-based, matched, case-control study.</p></sec><sec><st>Setting</st><p>Registry-based investigation.</p></sec><sec><st>Patients</st><p>All cases, nationwide, of TAD diagnosed 2001&ndash;2005 in individuals born 1932 or later (n=2436) were identified, and a random control-group (n=12&nbsp;152) matched for age, sex and geography was generated. First-degree relatives were identified in the Multigeneration Registry. Family history of TAD was assessed by cross-linking nationwide health registries.</p></sec><sec><st>Interventions</st><p>None.</p></sec><sec><st>Results</st><p>Family history was present in 108 cases (4.4%), compared with 93 (0.77%) controls (p&lt;0.0001). The risk of TAD increased with number of affected relatives: OR 5.8 (95% CI 4.3 to 7.7) vs OR 20 (2.2 to 179) with one versus two or more affected relatives. The relative risk of TAD was highest in the youngest (&le;49&nbsp;years) age group and slightly more pronounced in women than in men (OR 7.2 (4.2 to 12) vs OR 5.5 (3.9 to 7.7)). Among cardiopulmonary comorbidities, heart failure conferred the highest relative risk, OR 6.3 (4.1 to 9.8).</p></sec><sec><st>Conclusions</st><p>Family history confers a significantly increased (sixfold to 20-fold) relative risk of TAD. The effect is more pronounced in women and in younger subjects, and is not conveyed by cardiopulmonary comorbidity. Knowledge of family history is important to counselling, treatment indications, surveillance and screening protocols.</p></sec>]]></description>
<dc:creator><![CDATA[Olsson, C., Granath, F., Stahle, E.]]></dc:creator>
<dc:date>2013-04-27T10:05:21-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303654</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303654</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Family history, comorbidity and risk of thoracic aortic disease: a population-based case-control study]]></dc:title>
<prism:publicationDate>2013-04-27</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303944v1?rss=1">
<title><![CDATA[Long-term efficacy of percutaneous mitral commissurotomy for restenosis after previous mitral commissurotomy]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303944v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>We analysed long-term results of percutaneous mitral commissurotomy (PMC) performed because of mitral restenosis after previous commissurotomy.</p></sec><sec><st>Design</st><p>Follow-up of a prospective cohort.</p></sec><sec><st>Setting</st><p>Tertiary university hospital.</p></sec><sec><st>Patients</st><p>We studied 163 consecutive patients who underwent PMC because of restenosis occurring 16&plusmn;8&nbsp;years after previous commissurotomy (closed-heart in 121, open-heart in 30 and PMC in 12). Mean age was 48&plusmn;14&nbsp;years; 62 patients (38%) had valve calcification. Restenosis was due to bicommissural fusion in all cases.</p></sec><sec><st>Intervention</st><p>PMC using a single or double balloon in 80 patients and the Inoue balloon in 83.</p></sec><sec><st>Results</st><p>Good immediate results (IR) (valve area &ge;1.5&nbsp;cm<sup>2</sup> with MR&le;2/4) were obtained in 135&nbsp;pts (83%). 20-year rates were 27.9&plusmn;4.7% for cardiovascular survival without mitral surgery and 14.8&plusmn;3.9% for good functional results (cardiovascular survival without reintervention on the mitral valve and in New York Heart Association (NYHA) class I or II). After good IR, 20-year rates were 33.2&plusmn;5.5% for cardiovascular survival without surgery and 17.9&plusmn;4.7% for good functional results. After good IR, multivariate predictive factors of poor late functional results were higher NYHA class (p=0.01), atrial fibrillation (p=0.0002) and higher mean mitral gradient after PMC (p=0.004).</p></sec><sec><st>Conclusions</st><p>In patients with restenosis after mitral commissurotomy, PMC provides good IR in most cases. After good IR, one patient out of three remains free from surgery and one out of five has good functional results at 20&nbsp;years. These findings support the use of PMC after previous commissurotomy, particularly in selected patients with few symptoms and in sinus rhythm.</p></sec>]]></description>
<dc:creator><![CDATA[Bouleti, C., Iung, B., Himbert, D., Brochet, E., Messika-Zeitoun, D., Detaint, D., Garbarz, E., Cormier, B., Vahanian, A.]]></dc:creator>
<dc:date>2013-04-27T10:05:21-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303944</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303944</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Long-term efficacy of percutaneous mitral commissurotomy for restenosis after previous mitral commissurotomy]]></dc:title>
<prism:publicationDate>2013-04-27</prism:publicationDate>
<prism:section>Valvular heart disease</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302976v1?rss=1">
<title><![CDATA[Clinical implications of the Third Universal Definition of Myocardial Infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302976v1?rss=1</link>
<description><![CDATA[<p>The definition of myocardial infarction (MI) continues to evolve as refined ECG criteria, more advanced imaging, and more sensitive and specific biomarkers are developed. The acceptance globally of a clinically practical standard definition for everyday practice would allow for better comparisons across clinical experiences and further facilitate research in this critical area. Because of the evolution of better diagnostic tools and more information about the value and limitations of previous definitions, there was a need to update the Universal Definition of MI published in 2007<cross-ref type="bib" refid="R1">1</cross-ref> and this has recently been accomplished.<cross-ref type="bib" refid="R2">2</cross-ref> Great efforts were made by the taskforce that developed these guidelines to establish clinical criteria which correspond to the contemporary management of patients suspected of having MI. Therefore, a combination of clinical symptoms, cardiac biomarkers, and ECG changes indicative of myocardial ischaemia are central to the 2012 Third Universal Definition of MI. It stresses the...]]></description>
<dc:creator><![CDATA[White, H. D., Thygesen, K., Alpert, J. S., Jaffe, A. S.]]></dc:creator>
<dc:date>2013-04-27T10:05:21-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302976</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302976</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Education in Heart, Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Venous thromboembolism, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Clinical implications of the Third Universal Definition of Myocardial Infarction]]></dc:title>
<prism:publicationDate>2013-04-27</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303884v1?rss=1">
<title><![CDATA[Cardiac MRI assessment of atrial fibrosis in atrial fibrillation: implications for diagnosis and therapy]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303884v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia in clinical practice, with a prevalence of 0.4&ndash;1% in the US population.<sup>w1</sup> AF is a potent risk factor, increasing the risk of stroke fivefold and accounting for approximately 15% of all strokes in the USA.<sup>w2</sup> AF also significantly increases the risk of mortality from heart failure.<sup>w3&ndash;7</sup> Many therapies, including pharmacological approaches and direct current cardioversion, have been tried to treat this malignant arrhythmia, but were not found to be that effective.<cross-ref type="bib" refid="R1">1</cross-ref> <sup>w8&ndash;w11</sup></p><p>Catheter ablation of AF has provided better outcomes compared with other treatments, especially by applying pulmonary vein (PV) isolation in patients with paroxysmal AF.<cross-ref type="bib" refid="R2">2</cross-ref> <sup>w12</sup></p><p>However, other procedures modifying the substrate of AF, such as complex fractionated atrial electrogram ablation<cross-ref type="bib" refid="R3">3</cross-ref> or posterior wall debulking,<cross-ref type="bib" refid="R4">4</cross-ref> are required to obtain satisfying results for persistent AF patients with massive left atrial structural remodelling (LASRM)...]]></description>
<dc:creator><![CDATA[Higuchi, K., Akkaya, M., Akoum, N., Marrouche, N. F.]]></dc:creator>
<dc:date>2013-04-25T00:01:44-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303884</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303884</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Tachyarrhythmias, Education in Heart, Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Drugs: cardiovascular system, Echocardiography, Heart failure, Acute coronary syndromes, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Cardiac MRI assessment of atrial fibrosis in atrial fibrillation: implications for diagnosis and therapy]]></dc:title>
<prism:publicationDate>2013-04-25</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303440v1?rss=1">
<title><![CDATA[Chronic exposure to biomass fuel is associated with increased carotid artery intima-media thickness and a higher prevalence of atherosclerotic plaque]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303440v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>Biomass fuels are used for cooking in the majority of rural households worldwide. While their use is associated with an increased risk of lung diseases and all-cause mortality, the effects on cardiovascular disease (CVD) are not well characterised. Exposure to biomass fuel smoke has been associated with lung-mediated inflammation and oxidative stress, which may increase the risk of atherosclerosis as evaluated by carotid intima-media thickness (CIMT), carotid atherosclerotic plaque prevalence and blood pressure.</p></sec><sec><st>Methods</st><p>A cross-sectional study was performed in 266 adults aged &ge;35&nbsp;years in Puno, Peru (3825&nbsp;m above sea level). We stratified participants by their long-term history of exposure to clean fuel (n=112) or biomass fuel (n=154) and measured 24&nbsp;h indoor particulate matter (PM<SUB>2.5</SUB>) in a random subset (n=84). Participants completed questionnaires and underwent a clinical assessment, laboratory analyses and carotid artery ultrasound. The main outcome measures were CIMT, carotid plaque and blood pressure.</p></sec><sec><st>Results</st><p>The groups were similar in age and gender. The biomass fuel group had greater unadjusted mean CIMT (0.66 vs 0.60&nbsp;mm; p&lt;0.001), carotid plaque prevalence (26% vs 14%; p=0.03), systolic blood pressure (118 vs 111 mm&nbsp;Hg; p&lt;0.001) and median household PM<SUB>2.5</SUB> (280 vs 14&nbsp;&micro;g/m<sup>3</sup>; p&lt;0.001). In multivariable regression, the biomass fuel group had greater mean CIMT (mean difference=0.03&nbsp;mm, 95% CI 0.01 to 0.06; p=0.02), a higher prevalence of carotid plaques (OR=2.6, 95% CI 1.1 to 6.0; p=0.03) and higher systolic blood pressure (mean difference=9.2 mm&nbsp;Hg, 95% CI 5.4 to 13.0; p&lt;0.001).</p></sec><sec><st>Conclusions</st><p>Chronic exposure to biomass fuel was associated with increased CIMT, increased prevalence of atherosclerotic plaques and higher blood pressure. These findings identify biomass fuel use as a risk factor for CVD, which may have important global health implications.</p></sec>]]></description>
<dc:creator><![CDATA[Painschab, M. S., Davila-Roman, V. G., Gilman, R. H., Vasquez-Villar, A. D., Pollard, S. L., Wise, R. A., Miranda, J. J., Checkley, W., CRONICAS Cohort Study Group, Bernabe-Ortiz, Casas, Smith, Ebrahim, Gamboa, Garcia, Malaga, Montori, Smeeth, Diette]]></dc:creator>
<dc:date>2013-04-25T00:01:44-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303440</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303440</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Chronic exposure to biomass fuel is associated with increased carotid artery intima-media thickness and a higher prevalence of atherosclerotic plaque]]></dc:title>
<prism:publicationDate>2013-04-25</prism:publicationDate>
<prism:section>Global burden of cardiovascular disease</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303202v1?rss=1">
<title><![CDATA[Analytically false or true positive elevations of high sensitivity cardiac troponin: a systematic approach]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303202v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Cardiac troponin (cTn) is a regulatory protein of the myofibrillar thin filament of striated muscle regulating excitation&ndash;contraction coupling in the heart.<sup>w1</sup> Among the three subunits (T, I, and C), only cardiac troponin T (cTnT) and I (cTnI) are expressed in cardiac muscle and released into blood following myocardial cell death. Several distinct pathobiological mechanisms leading to elevated troponin values have been suggested, not all of which involve myocyte necrosis.<sup>w2</sup></p><p>cTnT or cTnI are routinely used in emergency units as the preferred biomarkers for the diagnosis of acute myocardial infarction (MI). According to joint criteria for the diagnosis of acute MI by the European Society of Cardiology/American College of Cardiology/American Heart Association/World Heart Federation Task Force, an acute MI should be diagnosed in patients with symptoms of myocardial ischaemia and detection of a rise and/or fall of cardiac biomarkers (preferentially troponins) with at least one value above the 99th percentile of...]]></description>
<dc:creator><![CDATA[Vafaie, M., Biener, M., Mueller, M., Schnabel, P. A., Andre, F., Steen, H., Zorn, M., Schueler, M., Blankenberg, S., Katus, H. A., Giannitsis, E.]]></dc:creator>
<dc:date>2013-04-25T00:01:43-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303202</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303202</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Education in Heart, Hypertrophic cardiomyopathy, Drugs: cardiovascular system, Hypertension, Acute coronary syndromes, Venous thromboembolism, Epidemiology, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Analytically false or true positive elevations of high sensitivity cardiac troponin: a systematic approach]]></dc:title>
<prism:publicationDate>2013-04-25</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-304031v1?rss=1">
<title><![CDATA[Inappropriate defibrillator shocks and mortality]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-304031v1?rss=1</link>
<description><![CDATA[<p>Despite the established survival benefits of implantable cardioverter defibrillators (ICD) in patients with ischaemic cardiomyopathy and other forms of cardiomyopathies, a major limitation of this technology remains the delivery of inappropriate shocks for reasons other than life-threatening ventricular tachycardia or ventricular fibrillation. Inappropriate ICD shocks may occur as the result of atrial arrhythmias with rapid ventricular conduction, abnormal sensing (such as T-wave oversensing) or lead artefact/ICD malfunction. Such events have been estimated to occur in approximately 10&ndash;15% of patients with ICD, and result in significant morbidity and distress to the patient.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> An important objective for both physicians looking after patients with ICD and manufacturers of the technology is to decrease the burden of inappropriate ICD shocks and improve the quality of life of patients with ICD. When an ICD discharges a shock to the myocardium, whether for an appropriate or inappropriate reason, there is likely...]]></description>
<dc:creator><![CDATA[Liew, R.]]></dc:creator>
<dc:date>2013-04-20T00:01:10-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304031</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304031</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Inappropriate defibrillator shocks and mortality]]></dc:title>
<prism:publicationDate>2013-04-20</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302325v1?rss=1">
<title><![CDATA[Fractional flow reserve and beyond]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302325v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>In stable coronary artery disease, clinical decision making regarding percutaneous coronary intervention (PCI) of coronary artery stenoses is optimally based upon an evaluation of the functional severity of the coronary lesion.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> As such, intracoronary (IC) physiology has emerged as a standard diagnostic modality in the contemporary armamentarium of the interventional cardiologist during cardiac catheterisation.<cross-ref type="bib" refid="R3">3</cross-ref> Direct assessment of IC haemodynamics distal to a coronary lesion, by means of sensor equipped guide wires, provides a unique opportunity to determine the physiological impact of a coronary stenosis before coronary intervention.<cross-ref type="bib" refid="R4">4</cross-ref> Physiological assessment of coronary lesion severity is notably more accurate to evaluate the functional severity of a lesion compared with visual assessment on angiographic images.<cross-ref type="bib" refid="R5">5</cross-ref> <sup>w1&ndash;w3</sup> Consequently, physiologically guided PCI improves patient outcomes with respect to relief of anginal complaints and the necessity for (repeat) revascularisation.<cross-ref type="bib" refid="R2">2</cross-ref> <cross-ref type="bib" refid="R6">6</cross-ref>...]]></description>
<dc:creator><![CDATA[van de Hoef, T. P., Meuwissen, M., Piek, J. J.]]></dc:creator>
<dc:date>2013-04-20T00:00:23-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302325</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302325</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Education in Heart, Interventional cardiology, Drugs: cardiovascular system, Hypertension, Interventional cardiology, Percutaneous intervention, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Fractional flow reserve and beyond]]></dc:title>
<prism:publicationDate>2013-04-20</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302034v1?rss=1">
<title><![CDATA[Timing of angiography in non-ST elevation myocardial infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302034v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Acute coronary syndromes</st><p>Acute chest pain remains one of the most difficult challenges for the clinician. Nowadays, chest pain and its related complaints account for up to 10% of the adult emergency admissions and around 25% of all hospital admissions.<sup>w1</sup> Notably, the number of patients presenting with complaints of chest pain is rising.<sup>w2</sup> In a typical population of patients presented for the evaluation of acute chest pain in emergency departments, about 20% will have an acute coronary syndrome (ACS).<sup>w3 w4</sup> The principal pathophysiological mechanism of an ACS is one of myocardial underperfusion resulting from either atherosclerotic plaque rupture or from erosion with different degrees of superimposed thrombus.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> A minority of patients, estimated to be around 10% of those who presented with chest pain, will not have an ACS but another life threatening problem such as a pulmonary embolism or an acute aortic dissection.<sup>w1</sup> Most patients...]]></description>
<dc:creator><![CDATA[Riezebos, R. K., Verheugt, F. W. A.]]></dc:creator>
<dc:date>2013-04-20T00:00:23-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302034</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302034</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Acute coronary syndromes, Education in Heart, Drugs: cardiovascular system, Echocardiography, Acute coronary syndromes, Stable coronary heart disease, Venous thromboembolism, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Timing of angiography in non-ST elevation myocardial infarction]]></dc:title>
<prism:publicationDate>2013-04-20</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303643v1?rss=1">
<title><![CDATA[Normal presenting levels of high-sensitivity troponin and myocardial infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303643v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To analyse whether levels of high-sensitivity cardiac troponin (hs-cTn) below their respective 99th percentile can be used as a single parameter to rule out acute myocardial infarction (AMI) at presentation.</p></sec><sec><st>Design</st><p>Prospective, multicentre study.</p></sec><sec><st>Main outcome measures</st><p>We measured hs-cTn using four different methods (hs-cTnT Roche, hs-cTnI Siemens, hs-cTnI Beckman Coulter and hs-cTnI Abbott) in consecutive patients presenting to the emergency department with acute chest pain. Two independent cardiologists adjudicated the final diagnosis. Patients were followed for death or AMI during a mean period of 24&nbsp;months.</p></sec><sec><st>Results</st><p>Among 2072 consecutive patients with hs-cTnT measurements available, 21.4% had an adjudicated diagnosis of AMI (sensitivity 89.6%, 95% CI 86.4% to 92.3%, negative predictive value (NPV): 96.5%, 95% CI 95.4% to 97.4%). Among 1180 consecutive patients with hs-cTnI Siemens measurements available, 20.0% had AMI (sensitivity 94.1%, 95% CI 90.3% to 96.7%, NPV: 98.0%, 95% CI: 96.6% to 98.9%). Among 1151 consecutive patients with hs-cTnI Beckman Coulter measurements available, 19.7% had AMI (sensitivity 92.1%, 95% CI 87.8% to 95.2%, NPV: 97.5%, 95% CI 96.0% to 98.5%). Among 1567 consecutive patients with hs-cTnI Abbott measurements available, 20.0% had AMI (sensitivity 77.2%, 95% CI 72.1% to 81.7%, NPV: 94.3%, 95% CI 92.8% to 95.5%).</p></sec><sec><st>Conclusions</st><p>Normal hs-cTn levels at presentation should not be used as a single parameter to rule out AMI as 6%&ndash;23% of adjudicated AMI cases had normal levels of hs-cTn levels at presentation. Our data highlight the lack of standardisation among hs-cTnI assays resulting in substantial differences in sensitivity and NPV at the 99th percentile.</p></sec>]]></description>
<dc:creator><![CDATA[Hoeller, R., Rubini Gimenez, M., Reichlin, T., Twerenbold, R., Zellweger, C., Moehring, B., Wildi, K., Freese, M., Stelzig, C., Hartmann, B., Stoll, M., Mosimann, T., Reiter, M., Haaf, P., Mueller, M., Meller, B., Hochgruber, T., Balmelli, C., Sou, S. M., Murray, K., Freidank, H., Steuer, S., Minners, J., Osswald, S., Mueller, C.]]></dc:creator>
<dc:date>2013-04-19T00:00:43-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303643</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303643</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Acute coronary syndromes, Drugs: cardiovascular system, Acute coronary syndromes]]></dc:subject>
<dc:title><![CDATA[Normal presenting levels of high-sensitivity troponin and myocardial infarction]]></dc:title>
<prism:publicationDate>2013-04-19</prism:publicationDate>
<prism:section>Acute coronary syndromes</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303905v1?rss=1">
<title><![CDATA[Hypoxia exacerbated by mechanical ventilation: when the trap door opens in severe right ventricular failure]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303905v1?rss=1</link>
<description><![CDATA[<p>A 49-year-old man with non-ischaemic cardiomyopathy presented with acute hypoxia. Weeks earlier, his right ventricle was found to be severely impaired in function, with signs suggestive of extensive myocardial fibrosis (<cross-ref type="fig" refid="HEARTJNL2013303905F1">figure 1</cross-ref>), while his left ventricle had an ejection fraction of 33% and patchy tissue abnormalities. Despite comprehensive testing then, including biopsies from both ventricles, the cause of his cardiomyopathy remained unclear.</p><p><fig loc="float" id="HEARTJNL2013303905F1"><no>Figure&nbsp;1</no><caption><p>Cardiac magnetic resonance image (short axis view at the level of the papillary muscles). There is dilatation and extensive late gadolinium enhancement of the right ventricle (RV), which extends into the endocardial aspect of the right interventricular septum. Contrast retention is also observed in parts of the left ventricle (LV), particularly in its inferior and anterior walls.</p></caption><link locator="heartjnl2013303905f01"></fig></p><p>Following admission, oxygen delivery failed to improve his hypoxia. Instead, the latter worsened significantly when invasive positive-pressure ventilation (PPV) was applied. Transoesophageal echocardiography demonstrated a large right-to-left shunt,...]]></description>
<dc:creator><![CDATA[Margulescu, A. D., Wheeler, R., Leong, F. T.]]></dc:creator>
<dc:date>2013-04-18T00:02:14-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303905</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303905</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Hypoxia exacerbated by mechanical ventilation: when the trap door opens in severe right ventricular failure]]></dc:title>
<prism:publicationDate>2013-04-18</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303763v1?rss=1">
<title><![CDATA[Impact of prior coronary artery bypass graft surgery on chronic total occlusion revascularisation: insights from a multicentre US registry]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303763v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To investigate the impact of prior coronary artery bypass graft (CABG) surgery on the outcomes of percutaneous coronary intervention (PCI) for chronic total occlusions (CTO).</p></sec><sec><st>Design</st><p>Observational retrospective study.</p></sec><sec><st>Setting</st><p>Three tertiary hospitals in the USA.</p></sec><sec><st>Participants</st><p>1363 consecutive patients who underwent CTO PCI between 2006 and 2011.</p></sec><sec><st>Main outcome measures</st><p>Procedural success and inhospital complications, which were compared between patients with and without prior CABG.</p></sec><sec><st>Results</st><p>Compared to patients without prior CABG, those with prior CABG were older, had more comorbidities, were treated more frequently with the retrograde approach (46.7% vs 27.1%, p&lt;0.001) and had lower technical success rates (79.7% vs 88.3%, p=0.015). Of the 24 (1.8%) major inhospital complications, 11 occurred in patients with prior CABG and 13 in patients without prior CABG (2.1% vs 1.5%, p=0.392). In multivariable analysis prior CABG was independently associated with lower technical success rate (OR 0.49, 95% CIs 0.35 to 0.70, p&lt;0.001).</p></sec><sec><st>Conclusions</st><p>In a large multicentre registry, CTO PCI was frequently performed among patients with prior CABG, with higher use of the retrograde approach and similar complications but lower technical success rates compared to patients without prior CABG.</p></sec>]]></description>
<dc:creator><![CDATA[Michael, T. T., Karmpaliotis, D., Brilakis, E. S., Abdullah, S. M., Kirkland, B. L., Mishoe, K. L., Lembo, N., Kalynych, A., Carlson, H., Banerjee, S., Lombardi, W., Kandzari, D. E.]]></dc:creator>
<dc:date>2013-04-18T00:02:14-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303763</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303763</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Percutaneous intervention]]></dc:subject>
<dc:title><![CDATA[Impact of prior coronary artery bypass graft surgery on chronic total occlusion revascularisation: insights from a multicentre US registry]]></dc:title>
<prism:publicationDate>2013-04-18</prism:publicationDate>
<prism:section>Coronary revascularisation</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303863v1?rss=1">
<title><![CDATA[Exercise heart rate recovery: analysis of methods and call for standards]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303863v1?rss=1</link>
<description><![CDATA[<p>In the last several years, measures of exercise heart rate recovery (HRR) have been increasingly utilised to help assess risk and functional autonomic status in both healthy individuals and those with a wide variety of diseases. However, currently there are no national or international standards for obtaining and reporting HRR. Lack of uniformity in how HRR is obtained, analysed and reported makes comparisons between studies difficult, and hinders interpretation of results for individual subjects. This paper will review HRR methodology and promote establishing uniform standards for exercise laboratories performing the study.</p><sec id="s1"><st>Exercise protocol</st><p>In order to assess current practice measuring HRR, we surveyed 74 studies that used a variety of exercise types, protocols and methods of analysis. A tally of these studies indicates that graded treadmill exercise was the preferred exercise protocol, having been used in approximately 72% of the studies, followed by cycle ergometry in 25% and other methods in...]]></description>
<dc:creator><![CDATA[Adabag, S., Pierpont, G. L.]]></dc:creator>
<dc:date>2013-04-16T00:01:05-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303863</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303863</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Echocardiography, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Exercise heart rate recovery: analysis of methods and call for standards]]></dc:title>
<prism:publicationDate>2013-04-16</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303733v1?rss=1">
<title><![CDATA[Periprocedural type IVa myocardial infarction and the importance of platelet inhibition]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303733v1?rss=1</link>
<description><![CDATA[<p>More than two million percutaneous coronary intervention (PCI) procedures are performed worldwide each year.<cross-ref type="bib" refid="R1">1</cross-ref> Periprocedural myocardial infarction is one of the most common complications with evidence of myonecrosis in almost half of all PCI procedures.<cross-ref type="bib" refid="R2">2</cross-ref> Defining periprocedural myocardial infarction is, however, not straightforward. The latest expert consensus on the Universal Definition of Myocardial Infarction defines PCI-related myocardial infarction (type IVa) as either an increase in cardiac troponin 5-fold greater than the 99th percentile upper reference limit (URL) in patients with normal baseline values (&le;99th percentile URL), or a more than 20% increase in patients with already elevated but stable or falling baseline troponin concentrations.<cross-ref type="bib" refid="R3">3</cross-ref> In addition to this, the definition further stipulates that clinical evidence of myocardial ischaemia, angiographic loss of patency of a major or minor coronary artery patency or imaging evidence of new loss of viable myocardium or new regional wall motion...]]></description>
<dc:creator><![CDATA[Shah, A. S. V., Mills, N. L., Newby, D. E.]]></dc:creator>
<dc:date>2013-04-16T00:01:05-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303733</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303733</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Venous thromboembolism, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Periprocedural type IVa myocardial infarction and the importance of platelet inhibition]]></dc:title>
<prism:publicationDate>2013-04-16</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303667v1?rss=1">
<title><![CDATA[Biomarkers and ST-elevation myocardial infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303667v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>In the recent <I>Heart</I> paper, Cuculi <I>et al</I><cross-ref type="bib" refid="R1">1</cross-ref> from Oxford University challenge two conventional wisdoms in clinical cardiology: first, biomarkers do not have a role in the management of patients presenting with suspected ST-elevation myocardial infarction (STEMI); and second, in the absence of cardiogenic shock, there is no remaining unmet clinical need in STEMI as contemporary coronary reperfusion strategies yield excellent patient outcomes.</p><p>In their investigation, the authors report the course of plasma neuropeptide Y levels in patients undergoing successful percutaneous coronary intervention (PCI) and relate these to non-invasive and invasive measures of the success of myocardial reperfusion and the coronary microcirculation.<cross-ref type="bib" refid="R1">1</cross-ref> In the vast majority of patients with STEMI, a complete thrombotic occlusion in the epicardial segment of one of the coronary arteries results in ischaemia and cell death of a large amount of cardiomyocytes supplied by that artery. To salvage cardiomyocytes at risk, therapy...]]></description>
<dc:creator><![CDATA[Mueller, C.]]></dc:creator>
<dc:date>2013-04-10T00:00:26-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303667</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303667</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Biomarkers and ST-elevation myocardial infarction]]></dc:title>
<prism:publicationDate>2013-04-10</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303964v1?rss=1">
<title><![CDATA[Valvular heart disease: a call for global collaborative research initiatives]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303964v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Introduction</st><p>The burden of valvular heart disease (VHD) is rising rapidly as life expectancy increases. The prevalence in the USA alone is 13% in those aged over 75 years,<cross-ref type="bib" refid="R1">1</cross-ref> while the global prevalence of rheumatic heart disease is estimated at 15.6&ndash;19.6 million.<cross-ref type="bib" refid="R2">2</cross-ref> Despite this, the treatment of VHD still lacks an adequate research base. None of the 64 recommendations in the 2012 European Society of Cardiology (ESC) VHD guidelines<cross-ref type="bib" refid="R3">3</cross-ref> had Level A evidence and only 14% had Level B evidence. This compares with 28% at Level A and 42% at Level B among the 270 recommendations in the 2010 ESC myocardial revascularisation guidelines.<cross-ref type="bib" refid="R4">4</cross-ref> Therefore, there is an urgent need to stimulate the investigation. In this article, we identify deficits in our knowledge which may be amenable to research and make a call for national and international collaborative efforts to address this evidence...]]></description>
<dc:creator><![CDATA[Chambers, J. B., Shah, B. N., Prendergast, B., Lawford, P. V., McCann, G. P., Newby, D. E., Ray, S., Briffa, N., Shanson, D., Lloyd, G., Hall, R., on behalf of the British Heart Valve Society]]></dc:creator>
<dc:date>2013-04-10T00:00:25-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303964</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303964</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Echocardiography, Interventional cardiology, Aortic valve disease, Mitral valve disease, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Valvular heart disease: a call for global collaborative research initiatives]]></dc:title>
<prism:publicationDate>2013-04-10</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303648v1?rss=1">
<title><![CDATA[Cardiovascular effects of tumour necrosis factor {alpha} antagonism in patients with acute myocardial infarction: a first in human study]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303648v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>The inflammatory cytokine, tumour necrosis factor &alpha; (TNF-&alpha;), exerts deleterious cardiovascular effects. We wished to determine the effects of TNF-&alpha; antagonism on endothelial function and platelet activation in patients with acute myocardial infarction.</p></sec><sec><st>Design and setting and patients</st><p>A double-blind, parallel group, randomised controlled trial performed in a tertiary referral cardiac centre. 26 patients presenting with acute myocardial infarction randomised to receive an intravenous infusion of etanercept (10&nbsp;mg) or saline placebo.</p></sec><sec><st>Main outcome measures</st><p>Leucocyte count, plasma cytokine concentrations, flow cytometric measures of platelet activation and peripheral vasomotor and fibrinolytic function were determined before and 24&nbsp;h after study intervention.</p></sec><sec><st>Results</st><p>Consistent with effective conjugation of circulating TNF-&alpha;, plasma TNF-&alpha; concentrations increased in all patients following etanercept (254&plusmn;15 vs 0.12&plusmn;0.02 pg/ml; p&lt;0.0001), but not saline infusion. Etanercept treatment reduced neutrophil (7.4&plusmn;0.6 vs 8.8&plusmn;0.6<FONT FACE="arial,helvetica">x</FONT>10<sup>9</sup> cells/l; p=0.03) and plasma interleukin-6 concentrations (5.8&plusmn;2.0 vs 10.6&plusmn;4.0&nbsp;pg/ml; p=0.012) at 24&nbsp;h but increased platelet&ndash;monocyte aggregation (30&plusmn;5 vs 20&plusmn;3%; p=0.02). Vasodilatation in response to substance P, acetylcholine and sodium nitroprusside, and acute tissue plasminogen activator release were unaffected by either treatment (p&gt;0.1 for all).</p></sec><sec><st>Conclusions</st><p>Following acute myocardial infarction, etanercept reduces systemic inflammation but increases platelet activation without affecting peripheral vasomotor or fibrinolytic function. We conclude that TNF-&alpha; antagonism is unlikely to be a beneficial therapeutic strategy in patients with acute myocardial infarction.</p></sec>]]></description>
<dc:creator><![CDATA[Padfield, G. J., Din, J. N., Koushiappi, E., Mills, N. L., Robinson, S. D., Cruden, N. L. M., Lucking, A. J., Chia, S., Harding, S. A., Newby, D. E.]]></dc:creator>
<dc:date>2013-04-10T00:00:25-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303648</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303648</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Acute coronary syndromes, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Cardiovascular effects of tumour necrosis factor {alpha} antagonism in patients with acute myocardial infarction: a first in human study]]></dc:title>
<prism:publicationDate>2013-04-10</prism:publicationDate>
<prism:section>Cardiovascular physiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-301996v1?rss=1">
<title><![CDATA[Prevention of sudden cardiac death in hypertrophic cardiomyopathy]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-301996v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Hypertrophic cardiomyopathy (HCM) is a genetic disorder of cardiac muscle with a prevalence of 1 in 500 of the general population.<sup>w1</sup> In most adults, HCM is inherited as an autosomal dominant trait caused by mutations in genes encoding cardiac sarcomere proteins.<cross-ref type="bib" refid="R1">1</cross-ref> The disease is clinically defined by left ventricular hypertrophy (LVH) unexplained by abnormal loading conditions,<cross-ref type="bib" refid="R2">2</cross-ref> and is often associated with left ventricular outflow tract obstruction (LVOTO) caused by the systolic anterior movement of the mitral valve.<sup>w2</sup> Histologically, HCM is characterised by cardiomyocyte hypertrophy and disarray, myocardial fibrosis, and small vessel disease.<cross-ref type="bib" refid="R1">1</cross-ref> <sup>w3</sup></p><p>Sudden cardiac death (SCD), heart failure, and thromboembolism are the main causes of death.<cross-ref type="bib" refid="R3">3</cross-ref> Early studies of small HCM cohorts from tertiary referral centres reported cardiovascular mortality rates of ~6%/year, but later less selected studies demonstrated a more favourable clinical course with an overall cardiovascular mortality of ~2%/year.<cross-ref type="bib"...]]></description>
<dc:creator><![CDATA[O'Mahony, C., Elliott, P. M.]]></dc:creator>
<dc:date>2013-04-10T00:00:25-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301996</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301996</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Bradyarrhythmias and heart block, Myocardial disease, Education in Heart, Hypertrophic cardiomyopathy, Drugs: cardiovascular system, Pacing and electrophysiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Prevention of sudden cardiac death in hypertrophic cardiomyopathy]]></dc:title>
<prism:publicationDate>2013-04-10</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2011-300919v1?rss=1">
<title><![CDATA[The evolving role of multimodality imaging in valvular heart disease]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2011-300919v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>The public health burden of valvular heart disease (VHD) is projected to grow over the ensuing years owing to the persistent spectre of rheumatic heart disease in developing countries,<sup>w1</sup> and the increasing rate of degenerative VHD among the ageing population in developed countries.<cross-ref type="bib" refid="R1">1</cross-ref> Morbidity and mortality associated with these conditions and their treatment are high.<sup>w2</sup> Thus optimal evaluation of VHD is of clear importance.</p><p>There are many approaches to the assessment of VHD.<cross-ref type="bib" refid="R2">2</cross-ref> The aim of this article is first to provide a brief overview of the pathophysiology of the four most common valvular lesions: mitral regurgitation, mitral stenosis, aortic stenosis, and aortic regurgitation. The evolving role of cardiac imaging in the evaluation of these conditions will then be examined. The focus of this article is on multimodality imaging, and the complementary information these techniques provide on the most common valvular lesions (<cross-ref type="tbl" refid="HEARTJNL2011300919TB1">table 1</cross-ref>)....]]></description>
<dc:creator><![CDATA[Leong, D. P., Joseph, M. X., Selvanayagam, J. B.]]></dc:creator>
<dc:date>2013-04-10T00:00:50-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-300919</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-300919</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Valvular heart disease, Education in Heart, Drugs: cardiovascular system, Echocardiography, Aortic valve disease, Mitral valve disease, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The evolving role of multimodality imaging in valvular heart disease]]></dc:title>
<prism:publicationDate>2013-04-10</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303852v1?rss=1">
<title><![CDATA[Tuberculous brain abscess in an adolescent with complex congenital cyanotic heart disease]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303852v1?rss=1</link>
<description><![CDATA[<p>A 15-year-old boy presented with low-grade fever, frontal headache and projectile vomiting. Physical examination revealed clubbing, central cyanosis and systolic murmur at the base of heart. Electrocardiogram revealed rightward P wave axis, prominent anterior precordial forces with an R/S ratio in V1 that approaches 1 and reverse precordial progression, suggestive of dextrocardia (<cross-ref type="fig" refid="HEARTJNL2013303852F1">figure 1</cross-ref>), which was confirmed by chest roentgenogram (<cross-ref type="fig" refid="HEARTJNL2013303852F2">figure 2</cross-ref>). CT scan of the brain demonstrated multiple abscesses in the left parietooccipital region (<cross-ref type="fig" refid="HEARTJNL2013303852F3">figure 3</cross-ref>). PCR tested positive for <I>Mycobacterium tuberculae</I> from the abscess drainage, with growth on cultures. Four-drug antitubercular therapy with steroids was initiated. Echocardiography revealed dextrocardia, double outlet right ventricle, common atrioventricular canal Rastelli type C and pulmonary stenosis. Diagnostic cardiac catheterisation was deferred until the infection was under control. Ultrasound of the abdomen revealed absence of spleen. MRI at 3&nbsp;months showed a significant reduction in the size of...]]></description>
<dc:creator><![CDATA[Desai, N., Gable, B., Ortman, M.]]></dc:creator>
<dc:date>2013-04-05T00:01:01-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303852</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303852</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Tuberculous brain abscess in an adolescent with complex congenital cyanotic heart disease]]></dc:title>
<prism:publicationDate>2013-04-05</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303671v1?rss=1">
<title><![CDATA[Real time monitoring of risk-adjusted paediatric cardiac surgery outcomes using variable life-adjusted display: implementation in three UK centres]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303671v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To implement routine in-house monitoring of risk-adjusted 30-day mortality following paediatric cardiac surgery.</p></sec><sec><st>Design</st><p>Collaborative monitoring software development and implementation in three specialist centres.</p></sec><sec><st>Patients and methods</st><p>Analyses incorporated 2&nbsp;years of data routinely audited by the National Institute of Cardiac Outcomes Research (NICOR). Exclusion criteria were patients over 16 or undergoing non-cardiac or only catheter procedures. We applied the partial risk adjustment in surgery (PRAiS) risk model for death within 30&nbsp;days following surgery and generated variable life-adjusted display (VLAD) charts for each centre. These were shared with each clinical team and feedback was sought.</p></sec><sec><st>Results</st><p>Participating centres were Great Ormond Street Hospital, Evelina Children's Hospital and The Royal Hospital for Sick Children in Glasgow. Data captured all procedures performed between 1 January 2010 and 31 December 2011. This incorporated 2490 30-day episodes of care, 66 of which were associated with a death within 30&nbsp;days.The VLAD charts generated for each centre displayed trends in outcomes benchmarked to recent national outcomes. All centres ended the 2-year period within four deaths from what would be expected. The VLAD charts were shared in multidisciplinary meetings and clinical teams reported that they were a useful addition to existing quality assurance initiatives. Each centre is continuing to use the prototype software to monitor their in-house surgical outcomes.</p></sec><sec><st>Conclusions</st><p>Timely and routine monitoring of risk-adjusted mortality following paediatric cardiac surgery is feasible. Close liaison with hospital data managers as well as clinicians was crucial to the success of the project.</p></sec>]]></description>
<dc:creator><![CDATA[Pagel, C., Utley, M., Crowe, S., Witter, T., Anderson, D., Samson, R., McLean, A., Banks, V., Tsang, V., Brown, K.]]></dc:creator>
<dc:date>2013-04-05T00:01:01-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303671</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303671</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Real time monitoring of risk-adjusted paediatric cardiac surgery outcomes using variable life-adjusted display: implementation in three UK centres]]></dc:title>
<prism:publicationDate>2013-04-05</prism:publicationDate>
<prism:section>Cardiovascular surgery</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2011-301321v1?rss=1">
<title><![CDATA[Diagnosis of heart failure with preserved ejection fraction: role of clinical Doppler echocardiography]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2011-301321v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>In developed countries, at least 38&ndash;54% of patients with heart failure show preserved left ventricular (LV) ejection fraction.<cross-ref type="bib" refid="R1">1</cross-ref><sup>&ndash;</sup><cross-ref type="bib" refid="R3">3</cross-ref> The prevalence of heart failure with preserved ejection fraction (HFPEF) is steadily increasing and its prognosis is poor.<cross-ref type="bib" refid="R1">1</cross-ref><sup>&ndash;</sup><cross-ref type="bib" refid="R3">3</cross-ref> LV diastolic dysfunction, either alone or in combination with other factors (<cross-ref type="fig" refid="HEARTJNL2011301321F1">figure 1</cross-ref>), is the major underlying mechanism of HFPEF.<cross-ref type="bib" refid="R3">3</cross-ref><sup>&ndash;</sup><cross-ref type="bib" refid="R5">5</cross-ref> In the general population, the presence of even mild clinical diastolic dysfunction has been associated with pronounced increases in all cause mortality.<cross-ref type="bib" refid="R6">6</cross-ref> Hence, the diagnosis of clinical (prognostic) diastolic dysfunction leading to HFPEF is of critical importance.</p><p><fig loc="float" id="HEARTJNL2011301321F1"><no>Figure&nbsp;1</no><caption><p>Causes of heart failure with preserved ejection fraction (HFPEF). Diastolic dysfunction is present in the majority of patients with HFPEF and thus it can be viewed as a marker of HFPEF. Diastolic dysfunction is a sensitive rather than a...]]></description>
<dc:creator><![CDATA[Penicka, M., Vanderheyden, M., Bartunek, J.]]></dc:creator>
<dc:date>2013-03-30T00:00:50-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301321</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301321</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Heart failure, Education in Heart, Hypertrophic cardiomyopathy, Restrictive cardiomyopathy, Drugs: cardiovascular system, Echocardiography, Hypertension, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Diagnosis of heart failure with preserved ejection fraction: role of clinical Doppler echocardiography]]></dc:title>
<prism:publicationDate>2013-03-30</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303642v1?rss=1">
<title><![CDATA[State of the evidence: mechanical ventilation with PEEP in patients with cardiogenic shock]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303642v1?rss=1</link>
<description><![CDATA[<p>The need to provide invasive mechanical ventilatory support to patients with myocardial infarction and acute left heart failure is common. Despite the large number of patients requiring mechanical ventilation in this setting, there are remarkably few data addressing the ideal mode of respiratory support in such patients. Although there is near universal acceptance regarding the use of non-invasive positive pressure ventilation in patients with acute pulmonary oedema, there is more concern with invasive positive pressure ventilation owing to its more significant haemodynamic impact. Positive end-expiratory pressure (PEEP) is almost universally applied in mechanically ventilated patients due to benefits in gas exchange, recruitment of alveolar units, counterbalance of hydrostatic forces leading to pulmonary oedema and maintenance of airway patency. The limited available clinical data suggest that a moderate level of PEEP is safe to use in severe left ventricular (LV) dysfunction and cardiogenic shock, and may provide haemodynamic benefits as well in LV failure which exhibits afterload-sensitive physiology.</p>]]></description>
<dc:creator><![CDATA[Wiesen, J., Ornstein, M., Tonelli, A. R., Menon, V., Ashton, R. W.]]></dc:creator>
<dc:date>2013-03-28T00:00:26-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303642</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303642</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[State of the evidence: mechanical ventilation with PEEP in patients with cardiogenic shock]]></dc:title>
<prism:publicationDate>2013-03-28</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302482v1?rss=1">
<title><![CDATA[The SYNTAX score and its clinical implications]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302482v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) are both treatment options for coronary revascularisation in selected patients with stable coronary artery disease and ischaemia. Current European and US revascularisation guidelines indicate that the treatment selection depends on patient preferences, comorbidity, and complexity of coronary artery disease (CAD).<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> Less complex single- or double-vessel coronary artery disease is preferably treated with PCI, where the level of acceptance is higher for PCI compared to CABG, whereas complex three-vessel disease is best treated with CABG, where the level of acceptance is higher for CABG.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref></p><p>The number of diseased coronary vessels is not the only marker for CAD severity. The location of the lesions and their impact on blood flow,<sup>w1</sup> the degree of vessel stenosis, lesion classifications, and the diameter and calcification of the vessel are also important factors that affect the...]]></description>
<dc:creator><![CDATA[Head, S. J., Farooq, V., Serruys, P. W., Kappetein, A. P.]]></dc:creator>
<dc:date>2013-03-28T00:00:46-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302482</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302482</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Education in Heart, Interventional cardiology, Drugs: cardiovascular system, Interventional cardiology, Percutaneous intervention, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[The SYNTAX score and its clinical implications]]></dc:title>
<prism:publicationDate>2013-03-28</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303237v1?rss=1">
<title><![CDATA[Miscarriage and future maternal cardiovascular disease: a systematic review and meta-analysis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303237v1?rss=1</link>
<description><![CDATA[<sec><st>Context</st><p>The 2011 American Heart Association guidelines identified pregnancy complications as a risk factor for cardiovascular disease in women. However, miscarriage was not mentioned within the guidelines, and there is no consensus on the association between miscarriage and future risk of cardiovascular disease.</p></sec><sec><st>Objective</st><p>To confirm or refute the association, a meta-analysis of published papers was conducted.</p></sec><sec><st>Data sources</st><p>PubMed, Web of Knowledge and Scopus were systematically searched to identify appropriate articles. Reference lists were then hand searched for additional relevant titles.</p></sec><sec><st>Study Selection</st><p>To be included, articles had to assess the association between miscarriage and subsequent cardiovascular disease in otherwise healthy women. Only women who had miscarriages were considered exposed. Pooled association measures, using random effects meta-analysis, were calculated for coronary heart disease and cerebrovascular disease. Publication bias and between-study heterogeneity were evaluated.</p></sec><sec><st>Data Extraction</st><p>Two authors individually reviewed all studies and extracted data on patient and study characteristics along with cardiovascular outcomes.</p></sec><sec><st>Results</st><p>10 studies were identified, with 517 504 individuals included in the coronary heart disease meta-analysis and 134 461 individuals in the cerebrovascular disease analysis. A history of miscarriage was associated with a greater odds of developing coronary heart disease, OR (95% CI) =1.45 (1.18 to 1.78), but not with cerebrovascular disease, OR=1.11 (0.72 to 1.69). There was a strong association between recurrent miscarriage and coronary heart disease OR=1.99 (1.13 to 3.50). Evidence was found for moderate between-study heterogeneity and publication bias in the coronary heart disease analysis.</p></sec><sec><st>Conclusions</st><p>The meta-analysis indicates that a history of miscarriage or recurrent miscarriage is associated with a greater risk of subsequent coronary heart disease.</p></sec>]]></description>
<dc:creator><![CDATA[Oliver-Williams, C. T., Heydon, E. E., Smith, G. C. S., Wood, A. M.]]></dc:creator>
<dc:date>2013-03-28T00:00:26-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303237</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303237</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Hypertension]]></dc:subject>
<dc:title><![CDATA[Miscarriage and future maternal cardiovascular disease: a systematic review and meta-analysis]]></dc:title>
<prism:publicationDate>2013-03-28</prism:publicationDate>
<prism:section>Systematic review</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303754v1?rss=1">
<title><![CDATA[Specialist valve clinics: recommendations from the British Heart Valve Society working group on improving quality in the delivery of care for patients with heart valve disease]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303754v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Introduction</st><p>The population prevalence of moderate or severe valve disease in industrialised countries is as high as 13% in those aged 75&nbsp;years or older.<cross-ref type="bib" refid="R1">1</cross-ref> Undetected valve disease leads to premature death<cross-ref type="bib" refid="R1">1</cross-ref> but valve surgery, when indicated, can prolong life.<cross-ref type="bib" refid="R2">2</cross-ref> Access to medical care in industrialised countries is usually good, but limitations exist<cross-ref type="bib" refid="R3">3</cross-ref> and better ways of organising care are needed.<cross-ref type="bib" refid="R4">4</cross-ref></p><p>A working group was therefore convened by the British Heart Valve Society with representatives of all interested national bodies and a panel of invited international commentators. The aim was to produce recommendations to improve the detection, conservative management and interventional treatment of valve disease. This paper focusses on conservative management and proposes recommendations for overcoming limitations in care by means of a specialist valve clinic.</p></sec><sec id="s2"><st>Limitations in current services</st><p>The initial management of patients with valve disease is usually conservative and meticulous...]]></description>
<dc:creator><![CDATA[Chambers, J. B., Ray, S., Prendergast, B., Taggart, D., Westaby, S., Grothier, L., Arden, C., Wilson, J., Campbell, B., Sandoe, J., Gohlke-Barwolf, C., Mestres, C.-A., Rosenhek, R., Otto, C.]]></dc:creator>
<dc:date>2013-03-26T00:00:33-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303754</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303754</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Echocardiography, Aortic valve disease, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Specialist valve clinics: recommendations from the British Heart Valve Society working group on improving quality in the delivery of care for patients with heart valve disease]]></dc:title>
<prism:publicationDate>2013-03-26</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303591v1?rss=1">
<title><![CDATA[Life-threatening iliac artery rupture during transcatheter aortic valve implantation (TAVI): diagnosis and management]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303591v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>A 76-year-old man had severe aortic stenosis and underwent elective transcatheter aortic valve implantation (TAVI). Aortic annulus sizing by transthoracic echocardiography (TTE) was 25&nbsp;mm. Multislice CT showed adequate iliofemoral arteries calibre with no severe calcifications. The procedure took place by right transfemoral access using a percutaneous closure device (ProStar XL Percutaneous Vascular Surgical System; Abbott Vascular, Redwood City, California, USA). A 26&nbsp;mm balloon-expandable Edwards&ndash;Sapien XT valve (Edwards Lifesciences, Irvine, California, USA) was successfully advanced, however, with some resistance at the level of the iliac artery. After the deployment of the stented valve (<cross-ref type="fig" refid="HEARTJNL2013303591F1">figure 1</cross-ref>A), and the retrieval of the delivery system, acute haemodynamic deterioration occurred. Supra-aortic angiography confirmed the patency of the coronaries with a well-seated valve with no significant intravalvular or paravalvular aortic leak. TTE showed no pericardial effusion. Abdominal aortic angiography identified massive contrast media extravasation at the level of the right external iliac artery...]]></description>
<dc:creator><![CDATA[Dahdouh, Z., Roule, V., Grollier, G.]]></dc:creator>
<dc:date>2013-03-22T00:00:34-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303591</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303591</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Life-threatening iliac artery rupture during transcatheter aortic valve implantation (TAVI): diagnosis and management]]></dc:title>
<prism:publicationDate>2013-03-22</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303308v1?rss=1">
<title><![CDATA[Current outlook of cardiac stem cell therapy towards a clinical application]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303308v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Cardiovascular diseases are the major cause of death worldwide and currently affect 36.3% of the US population.<sup>w1</sup> The majority of this population comprises patients with acute myocardial infarction (AMI) and chronic ischaemic heart failure. Despite the considerable contribution of percutaneous coronary revascularisation and coronary artery bypass grafting (CABG) in coronary artery disease (CAD) patients, the long term benefits remain unsatisfactory. Moreover, heart transplantation, as a last resort, is available for a very limited patient population.</p><p>Cell transplantation emerged initially as a potential therapy to treat heart failure. Cardiomyocytes are generally considered to be post-mitotic, and do not regenerate upon loss or damage. However, recently Bergmann and co-workers were able to demonstrate that 50% of adult cardiomyocytes are exchanged during a normal lifespan,<cross-ref type="bib" refid="R1">1</cross-ref> which has propelled investigations into the potential use of cardiovascular regenerative therapy. Moreover, recent improvements in preparation techniques of stem cells, the creation of stable stem...]]></description>
<dc:creator><![CDATA[Takashima, S.-i., Tempel, D., Duckers, H. J.]]></dc:creator>
<dc:date>2013-03-22T00:00:18-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303308</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303308</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Cardiovascular disease prevention, Education in Heart, Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Current outlook of cardiac stem cell therapy towards a clinical application]]></dc:title>
<prism:publicationDate>2013-03-22</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303656v1?rss=1">
<title><![CDATA[Stroke prevention for patients with atrial fibrillation: improving but not perfect yet]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303656v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Atrial fibrillation (AF) is the most common cardiac rhythm disorder<cross-ref type="bib" refid="R1">1</cross-ref> and one of the most important risk factors for stroke, particularly in the elderly. Stroke-related AF is associated with significant morbidity, mortality and healthcare costs.<cross-ref type="bib" refid="R2">2</cross-ref> Although we have abundant evidence from randomised trials that anticoagulation, and to a lesser extent antiplatelet therapy, is highly efficacious in preventing stroke in patients with AF, these therapies remain underused, especially in older patients. With an ageing population and an AF prevalence that is rapidly rising,<cross-ref type="bib" refid="R1">1</cross-ref> a better understanding of the stroke prevention practices in real-world settings is critically important to implement preventive strategies that will improve the outcomes and reduce healthcare costs.</p><p>Cowan <I>et al</I><cross-ref type="bib" refid="R3">3</cross-ref> report the results of their investigation on the use of stroke prevention therapy for management of AF among 1857 primary-care practices across England from July 2009 to March 2012. Using...]]></description>
<dc:creator><![CDATA[Sandhu, R. K., McAlister, F. A.]]></dc:creator>
<dc:date>2013-03-21T00:00:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303656</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303656</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Health policy, Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Stroke prevention for patients with atrial fibrillation: improving but not perfect yet]]></dc:title>
<prism:publicationDate>2013-03-21</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302048v1?rss=1">
<title><![CDATA[Non-compaction cardiomyopathy]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302048v1?rss=1</link>
<description><![CDATA[<p>Non-compaction cardiomyopathy (NCM) is a myocardial disorder, which is thought to occur due to the failure of left ventricle (LV) compaction during embryogenesis, leading to distinct morphological characteristics in the ventricular chamber.<cross-ref type="bib" refid="R1">1</cross-ref> It was first described about 80&nbsp;years ago, in association with complex congenital heart diseases. More recently, Chin <I>et al</I><cross-ref type="bib" refid="R2">2</cross-ref> reported the isolated form of non-compaction LV, and since then many other reports have been published. The involvement of the right ventricle in the non-compaction process has been increasingly identified and the condition is now included among the cardiomyopathies. The nomenclature of this entity has been variable, being known as &lsquo;spongy myocardium&rsquo; or &lsquo;persistent embryonic myocardium&rsquo;, but more frequently known as &lsquo;LV non-compaction&rsquo; or NCM. Therefore, the latter term will be the one used in this article.</p><p>The characteristic features of NCM have been described as including a two-layered ventricular wall, comprising a thinner compact epicardial...]]></description>
<dc:creator><![CDATA[Almeida, A. G., Pinto, F. J.]]></dc:creator>
<dc:date>2013-03-16T00:00:25-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302048</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302048</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Myocardial disease, Education in Heart, Hypertrophic cardiomyopathy, Congenital heart disease, Drugs: cardiovascular system, Echocardiography, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Non-compaction cardiomyopathy]]></dc:title>
<prism:publicationDate>2013-03-16</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303790v1?rss=1">
<title><![CDATA[Reflections on 40 years of the British Society for Cardiovascular Research (BSCR)]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303790v1?rss=1</link>
<description><![CDATA[<p>This editorial celebrates 40&nbsp;years of the British Society for Cardiovascular Research (BSCR). The Society originated, as many things do, in a small informal gathering. David Hearse (working in London with Professor Sir Ernst Chain in the Department of Biochemistry at the Imperial College of Science and Technology) and Keith Gibson (working with Peter Harris at the Cardiothoracic Institute in Beaumont Street) were lamenting the lack of a forum in which to discuss current issues in basic cardiovascular research. To improve the situation, they assembled a committee with John Muir, Winifred Nayler, Mark Noble, Desmond Fitzgerald and Peter Harris, who was elected as the first Chair of the nascent Society (<cross-ref type="tbl" refid="HEARTJNL2013303790TB1">table 1</cross-ref>), named at that time the Cardiac Muscle Research Group (CMRG). Encouragingly, attendance at their inaugural meeting on 12 December 1973 far exceeded expectations of &lsquo;perhaps as many as nineteen&rsquo;. Indeed, over 60 delegates enjoyed two sessions; one...]]></description>
<dc:creator><![CDATA[Davidson, S. M., Hearse, D.]]></dc:creator>
<dc:date>2013-03-12T00:00:35-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303790</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303790</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology]]></dc:subject>
<dc:title><![CDATA[Reflections on 40 years of the British Society for Cardiovascular Research (BSCR)]]></dc:title>
<prism:publicationDate>2013-03-12</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302337v3?rss=1">
<title><![CDATA[Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302337v3?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Notice of retraction</st><p>This paper was published on-line in <I>Heart</I> on 21 August 2012. It reports a meta-analysis of six earlier papers.<cross-ref type="bib" refid="R1">1&ndash;6</cross-ref><cross-ref type="bib" refid="R2"></cross-ref><cross-ref type="bib" refid="R3"></cross-ref><cross-ref type="bib" refid="R4"></cross-ref><cross-ref type="bib" refid="R5"></cross-ref><cross-ref type="bib" refid="R6"></cross-ref> It has come to our attention that two of these papers contain duplicate data in tables reporting baseline data and treatment effects.<cross-ref type="bib" refid="R3">3</cross-ref> <cross-ref type="bib" refid="R4">4</cross-ref></p><p>The matter was considered by <I>BMJ</I> Publishing Ethics Committee. The Committee considered that without sight of the raw data on which the two papers containing the duplicate data were based, their reliability could not be substantiated. Following inquiries, it turns out that the raw data are no longer available having been lost as a result of computer failure.</p><p>Under the circumstances, it was the Committee's recommendation that the <I>Heart</I> meta-analysis should be retracted on the ground that the reliability of the data on which it is based cannot be substantiated.</p></sec>]]></description>
<dc:creator><![CDATA[DiNicolantonio, J. J., Pasquale, P. D., Taylor, R. S., Hackam, D. G.]]></dc:creator>
<dc:date>2013-03-12T02:42:41-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302337</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302337</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis]]></dc:title>
<prism:publicationDate>2013-03-12</prism:publicationDate>
<prism:section>Retraction notice</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303465v1?rss=1">
<title><![CDATA[Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete's heart]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303465v1?rss=1</link>
<description><![CDATA[<sec><st>Context</st><p>The athlete's heart (AH) remains a popular topic of study. Controversy related to training-specific cardiac adaptation in male athletes, and continuing developments in imaging technology and scaling prompted this systematic review and meta-analysis.</p></sec><sec><st>Objective</st><p>To provide new insight in relation to: 1) cardiac adaptation to divergent training patterns in male athletes, 2) a developing research database using cardiac magnetic resonance (CMR) in athletes; 3) functional data derived from tissue-Doppler analysis as well as right ventricular (RV) and left atrial (LA) measurements in athletes; and 4) an awareness of the impact of body size on cardiac dimensions.</p></sec><sec><st>Study design</st><p>Systematic review and meta-analysis of prospective trials. Data extraction performed by two researchers.</p></sec><sec><st>Data sources</st><p>Pub Med, Medline, Scopus and ISI Web of knowledge scholarly data base.</p></sec><sec><st>Study selection</st><p>Prospective studies were included if they were echocardiographic or CMR trials of elite young male athletes, with clear indication of type of sports and passed a quality criteria checklist.</p></sec><sec><st>Results</st><p>All left ventricular (LV) structural parameters were higher in athletes than in controls. Only LV end-diastolic diameter and volume were higher in endurance athletes than in resistance athletes: 54.8 mm (95% CI 54.1 to 55.6) vs 52.4 mm (95% CI 51.2 to 53.6); p&lt;0.001 and 171 ml (95% CI 157 to 185) vs 131 ml (95% CI 120 to 142); p&lt;0.001, respectively. RV end-diastolic volume, mass and LA diameter were higher in endurance athletes than controls. LV end-diastolic volume was larger when CMR was used rather than echocardiography: 178 ml (95% CI Q7 162 to 194) vs 135 ml (95% CI 128 to 142); p&lt;0.001. Meta-analysis regression models demonstrated positive and significant associations between body surface area (BSA) and LV mass, RV mass and LA diameter.</p></sec><sec><st>Conclusions</st><p>Morphological features of the male AH were noted in both athlete groups. A training-specific pattern of concentric hypertrophy was not discerned in resistance athletes. Both imaging mode and BSA can have a significant impact on the interpretation of AH data.</p></sec>]]></description>
<dc:creator><![CDATA[Utomi, V., Oxborough, D., Whyte, G. P., Somauroo, J., Sharma, S., Shave, R., Atkinson, G., George, K.]]></dc:creator>
<dc:date>2013-03-09T00:00:35-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303465</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303465</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Echocardiography, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Systematic review and meta-analysis of training mode, imaging modality and body size influences on the morphology and function of the male athlete's heart]]></dc:title>
<prism:publicationDate>2013-03-09</prism:publicationDate>
<prism:section>Systematic review</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303820v1?rss=1">
<title><![CDATA[Multivessel coronary artery disease revascularisation strategies in patients with diabetes mellitus]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303820v1?rss=1</link>
<description><![CDATA[<p>Patients with diabetes mellitus have increased rates of coronary artery disease (CAD), myocardial infarction (MI), heart failure and death. Importantly, approximately 25% of patients undergoing coronary artery revascularisation have diabetes.<cross-ref type="bib" refid="R1">1</cross-ref> Recently, the Future Revascularisation Evaluation in Patients with Diabetes Mellitus: Optimal Management of Multivessel Disease trial found coronary artery bypass graft (CABG) surgery superior to percutaneous coronary intervention (PCI) in significantly reducing rates of death and MI.<cross-ref type="bib" refid="R2">2</cross-ref> It has been suggested that this study settles the controversy over the comparative effectiveness of CABG versus PCI for patients with diabetes and stable multivessel CAD.<cross-ref type="bib" refid="R3">3</cross-ref> <cross-ref type="bib" refid="R4">4</cross-ref> However, the optimal revascularisation strategy in this patient subgroup has been debated for years because of conflicting reports.</p><sec id="s1"><st>Subgroup analyses</st><p>Early results comparing CABG with PCI in patients with diabetes came from randomised clinical trial subgroup analyses.<cross-ref type="bib" refid="R5">5</cross-ref> Only one reported a significant survival advantage for CABG,<cross-ref type="bib"...]]></description>
<dc:creator><![CDATA[Bates, E. R.]]></dc:creator>
<dc:date>2013-03-08T00:02:08-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303820</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303820</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Clinical diagnostic tests, Epidemiology, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Multivessel coronary artery disease revascularisation strategies in patients with diabetes mellitus]]></dc:title>
<prism:publicationDate>2013-03-08</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302883v1?rss=1">
<title><![CDATA[Genetic discoveries in hypertension: steps on the road to therapeutic translation]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302883v1?rss=1</link>
<description><![CDATA[<p>Genes and environmental factors contribute to an individual's risk of hypertension. Recent advances in DNA sequencing technology have enabled the discovery of new causative genes in inherited forms of hypertension, identifying novel pathways for blood pressure control. Meta-analyses of genome-wide association studies have also identified regions of the genome that are significantly associated with blood pressure control, and these regions may be involved in an individual's response to antihypertensive medication. This article reviews the latest gene discoveries in inherited forms of hypertension, recent meta-analyses of genome-wide association studies, genetic determinants of antihypertensive therapy response, and development of genetic risk scores.</p>]]></description>
<dc:creator><![CDATA[Lind, J. M., Chiu, C. L.]]></dc:creator>
<dc:date>2013-03-08T00:02:09-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302883</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302883</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension]]></dc:subject>
<dc:title><![CDATA[Genetic discoveries in hypertension: steps on the road to therapeutic translation]]></dc:title>
<prism:publicationDate>2013-03-08</prism:publicationDate>
<prism:section>Translational medicine</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303346v1?rss=1">
<title><![CDATA[Bioabsorbable scaffolds for the treatment of obstructive coronary artery disease: the next revolution in coronary intervention?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303346v1?rss=1</link>
<description><![CDATA[<p>Conventional drug eluting stents allow predictable long-term relief from coronary obstruction in most cases. However, rigid permanent metallic stents alter flow dynamics, abolish vascular reactivity, limit the potential for maximal vasodilation and promote ongoing inflammation and abnormalities of endothelial function. It is hypothesised that they may contribute to mal-apposition of stent struts, accelerated atheroma within the stented segment and perhaps very late stent thrombosis. Dramatic advances in bioabsorbable materials and technology have delivered the potential for a fully absorbable scaffold, which is able to mechanically support the coronary artery, and elute a drug, for a predetermined time period and is then fully absorbed in to the vascular wall. This could permit the &lsquo;normalisation&rsquo; of vascular function, with a number of potential advantages including true normalisation of vasomotor function, restoration of physiological responses to stress/exercise and completion of the vascular response to stenting, without the long-term consequences related to inflammation, accelerated atherosclerosis and thrombosis. Currently, over 16 different scaffolds are at varying stages of development. This review summarises the rationale for the development of absorbable scaffolds and the principal clinical research data.</p>]]></description>
<dc:creator><![CDATA[Patel, N., Banning, A. P.]]></dc:creator>
<dc:date>2013-03-08T00:02:08-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303346</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303346</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Bioabsorbable scaffolds for the treatment of obstructive coronary artery disease: the next revolution in coronary intervention?]]></dc:title>
<prism:publicationDate>2013-03-08</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2013-303792v1?rss=1">
<title><![CDATA[Percutaneous mitral valve repair using the MitraClip system: time to move forward]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2013-303792v1?rss=1</link>
<description><![CDATA[<p>The MitraClip therapy is a percutaneous edge-to-edge procedure (the only one currently available) derived from a surgical technique developed by Professor Alfieri in the early 1990s. This surgical technique, which consists of the suture of the free edges of the leaflets with the creation of a double valve orifice, has been reported as safe, effective and durable in experience hands.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> Despite not exactly reproducing the surgical technique&mdash;no concomitant annuloplasty is performed, whereas it has been shown that it improves early and long-term results&mdash;the MitraClip has emerged as a promising option for the treatment of both organic mitral regurgitation (OMR) and functional mitral regurgitation (FMR).</p><p>After the EVEREST I trial and registry had shown the safety, feasibility and efficacy of the MitraClip<cross-ref type="bib" refid="R3">3</cross-ref> with immediate and significant haemodynamic improvement,<cross-ref type="bib" refid="R4">4</cross-ref> the EVEREST II trial was conducted. The EVEREST II trial is a multicentre, randomised controlled...]]></description>
<dc:creator><![CDATA[Messika-Zeitoun, D.]]></dc:creator>
<dc:date>2013-03-07T00:01:07-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303792</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303792</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Mitral valve disease]]></dc:subject>
<dc:title><![CDATA[Percutaneous mitral valve repair using the MitraClip system: time to move forward]]></dc:title>
<prism:publicationDate>2013-03-07</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-301995v1?rss=1">
<title><![CDATA[New approaches to the clinical diagnosis of inherited heart muscle disease]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-301995v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Cardiomyopathies are defined as disorders of heart muscle unexplained by coronary artery disease, hypertension, valvular disease or congenital heart disease.<cross-ref type="bib" refid="R1">1</cross-ref> They are classified by morphological and functional phenotype into hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), and arrhythmogenic right ventricular cardiomyopathy (ARVC) subtypes.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="tbl" refid="HEARTJNL2012301995TB1">Table&nbsp;1</cross-ref> shows the European Society of Cardiology working group classification of cardiomyopathies.</p><p><tbl id="HEARTJNL2012301995TB1" loc="float"><no>Table&nbsp;1</no><caption><p>European Society of Cardiology classification of cardiomyopathies</p></caption><tblbdy top-stubs="1"><r><c cspan="1" rspan="1"></c><c cspan="1" rspan="1">HCM</c><c cspan="1" rspan="1">DCM</c><c cspan="1" rspan="1">ARVC</c><c cspan="1" rspan="1">RCM</c><c cspan="1" rspan="1">Unclassified</c></r><r><c cspan="1" rspan="1">Familial</c><c cspan="1" rspan="1"><l type="tab"><li><p> Familial, unknown gene</p></li><li><p> Sarcomeric protein mutations</p></li><li><p> GSD (eg, Pompe's, <I>PRKAG2</I>, Forbes&rsquo;, Danon's)</p></li><li><p> Lysosomal storage diseases (eg, Anderson&ndash;Fabry, Hurler's)</p></li><li><p> Disorders of fatty acid metabolism</p></li><li><p> Carnitine deficiency</p></li><li><p> Phosphorylase B kinase deficiency</p></li><li><p> Mitochondrial cytopathies</p></li><li><p> Syndromic HCM (eg, Noonan's syndrome, LEOPARD syndrome)</p></li><li><p> Familial amyloid</p></li></l></c><c cspan="1" rspan="1"><l type="tab"><li><p> Familial, unknown gene</p></li><li><p> Sarcomeric protein</p></li><li><p> Z-band</p></li><li><p> Cytoskeletal protein</p></li><li><p> Nuclear membrane protein</p></li><li><p> Intercalated disc proteins (desmosomes)</p></li><li><p> Mitochondrial cytopathy</p></li></l></c><c...]]></description>
<dc:creator><![CDATA[Lopes, L. R., Elliott, P. M.]]></dc:creator>
<dc:date>2013-03-06T00:01:06-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301995</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301995</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Myocardial disease, Education in Heart, Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Restrictive cardiomyopathy, Congenital heart disease, Drugs: cardiovascular system, Heart failure, Hypertension, Interventional cardiology, Clinical diagnostic tests, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[New approaches to the clinical diagnosis of inherited heart muscle disease]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302028v1?rss=1">
<title><![CDATA[Management of cardiogenic shock complicating acute coronary syndromes]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302028v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Cardiogenic shock (CS) remains the leading cause of mortality in patients hospitalised with acute myocardial infarction (AMI).<cross-ref type="bib" refid="R1">1</cross-ref> Recent guidelines supporting a strategy of early revascularisation (ERV) have led to some improvements in the outcomes of this patient subset.<cross-ref type="bib" refid="R2">2</cross-ref> <cross-ref type="bib" refid="R3">3</cross-ref> However, despite significant improvements in treatment, the mortality rate associated with CS in the context of AMI remains high, especially in those patients who present to hospital late or have delayed coronary reperfusion. This article aims to review the available data relating to this important condition, and provide guidelines for current best practice in the management of CS.</p><sec id="s1a"><st>Definition</st><p>CS is a condition characterised by inadequate tissue perfusion, usually in the setting of AMI. There have been many definitions applied to the diagnosis of CS, but the most uniformly accepted clinical definition of CS is decreased cardiac output and evidence of tissue hypoxia in the...]]></description>
<dc:creator><![CDATA[Tharmaratnam, D., Nolan, J., Jain, A.]]></dc:creator>
<dc:date>2013-03-06T00:01:05-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302028</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302028</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Acute coronary syndromes, Education in Heart, Drugs: cardiovascular system, Hypertension, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Management of cardiogenic shock complicating acute coronary syndromes]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302160v2?rss=1">
<title><![CDATA[Pros and cons of screening for sudden cardiac death in sports]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302160v2?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Sudden cardiac death (SCD) in the athlete, though uncommon, is the most devastating sport related event. It is widely publicised by the news media with the implication that such a fatality is preventable. The previous year of 2012 was notorious for SCD during sports. Several tragic events occurred in top level athletes&mdash;including a 25-year-old Italian soccer player, a 26-year-old Norwegian swimmer, a 24-year-old Serbian rower, and a 32-year-old runner in the London marathon. In addition, the 23-year-old soccer player Fabrice Muamba experienced an on-pitch aborted SCD during an English FA Cup match. These events have revived the debate regarding the need for a preparticipation cardiovascular evaluation of athletes and the inclusion of a 12 lead ECG in the screening protocol.</p><p>This article aims to review the field of SCD in the athlete, to highlight the areas of controversy on preparticipation screening, to address the opposing points of view in a...]]></description>
<dc:creator><![CDATA[Corrado, D., Basso, C., Thiene, G.]]></dc:creator>
<dc:date>2013-03-06T00:00:46-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302160</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302160</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Sudden cardiac death & resuscitation, Health policy, Education in Heart, Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Pros and cons of screening for sudden cardiac death in sports]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302042v2?rss=1">
<title><![CDATA[Patterns of coronary vasomotor responses to intracoronary acetylcholine provocation]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302042v2?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Since the inaugural description in 1959 by Prinzmetal,<cross-ref type="bib" refid="R1">1</cross-ref> coronary artery spasm and abnormal coronary artery vasomotion have been extensively studied both clinically and scientifically. There is no doubt that abnormal epicardial and microvascular coronary vasomotion play an important role in ischaemic heart disease. However, after the introduction of percutaneous coronary intervention, the number of articles and the clinical interest in abnormal coronary vasomotion have declined considerably, at least in the USA and Europe. As a consequence, the functional aspects of coronary artery disease have received less and less attention. There has been a revival of the topic recently, mainly because abnormal coronary vasomotion of the microcirculation has come into focus,<cross-ref type="bib" refid="R2">2</cross-ref> but also because the clinical presentation of chest pain with unobstructed coronary arteries continues to represent a diagnostic challenge for the clinician.<cross-ref type="bib" refid="R3">3</cross-ref></p><p>In this article we describe common patterns of coronary vasomotor responses to...]]></description>
<dc:creator><![CDATA[Ong, P., Athanasiadis, A., Sechtem, U.]]></dc:creator>
<dc:date>2013-03-06T00:00:45-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302042</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302042</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Ischaemic heart disease, Education in Heart, Drugs: cardiovascular system, Interventional cardiology, Percutaneous intervention, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Patterns of coronary vasomotor responses to intracoronary acetylcholine provocation]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-301751v2?rss=1">
<title><![CDATA[Role of tomographic imaging in preoperative planning and postoperative assessment in cardiovascular surgery]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-301751v2?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Cardiovascular surgeries have become progressively more sophisticated and complicated, due to factors such as the increasingly advanced age of patients, significant comorbidities, and increasing surgical complexity&mdash;minimally invasive procedures, reoperations and simultaneous procedures such as combined valve surgery and revascularisation, multiple valve replacements, combined valve and vascular surgery, as well as complicated aneurysm surgeries. Traditionally imaging studies with echocardiography and conventional angiography are increasingly complemented by tomographic techniques such as multidetector CT and MRI. In this context, echocardiography and angiography have significant shortcomings due to limited field of view focused on the examined cardiovascular structures, without significant insight into their spatial relationship vis-&agrave;-vis surrounding structures. The strength of CT and MRI is in the assessment of the spatial relationship of cardiovascular and extracardiac structures. In addition, the broadening of the scope of practice of both imaging and interventional cardiologists has made it more imperative to understand the various aspects of...]]></description>
<dc:creator><![CDATA[To, A. C. Y., Schoenhagen, P., Desai, M. Y.]]></dc:creator>
<dc:date>2013-03-06T00:00:44-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301751</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301751</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Non-invasive imaging, Education in Heart, Echocardiography, Hypertension, Interventional cardiology, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Role of tomographic imaging in preoperative planning and postoperative assessment in cardiovascular surgery]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-301725v2?rss=1">
<title><![CDATA[Percutaneous renal denervation: new treatment option for resistant hypertension and more?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-301725v2?rss=1</link>
<description><![CDATA[<p>Hypertension is highly prevalent and one of the most frequent chronic diseases worldwide.<cross-ref type="bib" refid="R1">1</cross-ref> Prognoses for the next decades suggest that up to 50% of the adult population will be diagnosed as hypertensives using the standard guideline definitions of hypertension.<cross-ref type="bib" refid="R1">1</cross-ref> Approximately 5&ndash;20% of all patients with high blood pressure are resistant to drug treatment,<cross-ref type="bib" refid="R2">2</cross-ref> defined as blood pressure uncontrolled (&gt;140/90&nbsp;mm&nbsp;Hg; &gt;130&ndash;139/80&ndash;85&nbsp;mm&nbsp;Hg in patients with diabetes mellitus; &gt;130/80&nbsp;mm&nbsp;Hg in chronic kidney disease), despite the use of at least three antihypertensive agents of different classes, including a diuretic, at maximum or highest tolerated doses.<cross-ref type="bib" refid="R3">3</cross-ref> Attention should be paid to differentiate between true resistance and pseudo-resistance, which is probably related to poor medication adherence, situational evoked blood pressure elevation (white coat hypertension), or suboptimal drug combination.<cross-ref type="bib" refid="R4">4</cross-ref> In approximately 20% of all patients suffering from resistant hypertension, a secondary, potentially reversible cause can be found,...]]></description>
<dc:creator><![CDATA[Ewen, S., Ukena, C., Bohm, M., Mahfoud, F.]]></dc:creator>
<dc:date>2013-03-06T00:00:43-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301725</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301725</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Hypertension, Education in Heart, Drugs: cardiovascular system, Hypertension, Interventional cardiology, Epidemiology, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Percutaneous renal denervation: new treatment option for resistant hypertension and more?]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302527v2?rss=1">
<title><![CDATA[Role of real-time three dimensional transoesophageal echocardiography as guidance imaging modality during catheter based edge-to-edge mitral valve repair]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302527v2?rss=1</link>
<description><![CDATA[<p>Percutaneous catheter based edge-to-edge mitral valve (MV) repair with a mitral clip (MitraClip, Abbott Vascular, Abbott Park, Illinois, USA) mimics Alfieri's surgical technique, bringing the anterior and posterior leaflets together from beneath the valve with a metallic stitch (clip). The procedure creates a &lsquo;double orifice&rsquo; repair, re-establishing leaflet coaptation and thereby reducing mitral regurgitation (MR).</p><p>In 2005, Feldman <I>et al</I> published their initial feasibility data (EVEREST (Endovascular Valve Edge-to-Edge&nbsp;Repair) phase 1 clinical trial) of a cohort of 27 patients with moderate-to-severe MR who were symptomatic or asymptomatic with compromised left ventricular (LV) function.<cross-ref type="bib" refid="R1">1</cross-ref> Patients were selected on the basis of specific valve morphology for which the procedure was thought to be particularly suited. In the case of degenerative MV regurgitation (ie, flail leaflet), anatomical inclusion criteria were a regurgitant jet originating from the A2/P2 segment with a flail gap of &lt;10&nbsp;mm and a flail width of &lt;15&nbsp;mm. In the...]]></description>
<dc:creator><![CDATA[Faletra, F. F., Pedrazzini, G., Pasotti, E., Petrova, I., Drasutiene, A., Dequarti, M. C., Muzzarelli, S., Moccetti, T.]]></dc:creator>
<dc:date>2013-03-06T00:00:42-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302527</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302527</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Non-invasive imaging, Education in Heart, Drugs: cardiovascular system, Echocardiography, Interventional cardiology, Mitral valve disease, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Role of real-time three dimensional transoesophageal echocardiography as guidance imaging modality during catheter based edge-to-edge mitral valve repair]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303407v1?rss=1">
<title><![CDATA[Prognostic impact of inappropriate defibrillator shocks in a population cohort]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303407v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>There is a relative paucity of data linking inappropriate implantable cardioverter-defibrillator (ICD) shocks to adverse clinical outcomes.</p></sec><sec><st>Objective</st><p>To examine the association between inappropriate ICD shocks and mortality or heart transplantation in a large population cohort.</p></sec><sec><st>Design, setting, patients</st><p>A cohort study which included all subjects who underwent ICD implantation between 1998 and 2008 and were followed up at our institution.</p></sec><sec><st>Main outcome measures</st><p>Multivariable Cox regression analyses were conducted to investigate the effect of inappropriate shocks on the risk of death and heart transplantation. Appropriate and inappropriate ICD therapies were modelled as time-dependent covariates.</p></sec><sec><st>Results</st><p>A total of 1698 patients were included. During a median follow-up of 30&nbsp;months, there were 246 (14.5%) deaths and 42 (2.5%) heart transplants. The incidence of inappropriate shocks was 10% at 1&nbsp;year and 14% at 2&nbsp;years. In the adjusted model, inappropriate shocks were not associated with death or transplantation (HR=0.97, 95% CI 0.70 to 1.36, p value=0.873). In contrast, appropriate shocks were associated with adverse outcomes (HR=3.11, 95% CI 2.41 to 4.02, p value&lt;0.001). The lack of association between inappropriate shocks and outcomes persisted for those with severely impaired &nbsp;left ventricular function (ejection fraction &lt;30%) and for those receiving multiple inappropriate treatments.</p></sec><sec><st>Conclusions</st><p>In this study, we observed no association between inappropriate ICD shocks and increased mortality or heart transplantation, even among those with severely impaired cardiac function. These findings question whether inappropriate ICD shocks lead to adverse outcomes.</p></sec>]]></description>
<dc:creator><![CDATA[Deyell, M. W., Qi, A., Chakrabarti, S., Yeung-Lai-Wah, J. A.-F., Tung, S., Khoo, C., Bennett, M. T., Qian, H., Kerr, C. R.]]></dc:creator>
<dc:date>2013-03-06T00:00:27-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303407</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303407</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Prognostic impact of inappropriate defibrillator shocks in a population cohort]]></dc:title>
<prism:publicationDate>2013-03-06</prism:publicationDate>
<prism:section>Heart rhythm disorders</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303103v1?rss=1">
<title><![CDATA[A novel approach to systematically implement the universal definition of myocardial infarction: insights from the CHAMPION PLATFORM trial]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303103v1?rss=1</link>
<description><![CDATA[<sec><st>Objective</st><p>To reassess the efficacy of cangrelor efficacy using the universal definition of myocardial infarction (MI).</p></sec><sec><st>Design</st><p>We adopted a novel approach to systematically implement the universal definition of MI. Two physicians blinded to treatment allocation reviewed plots of CK-MB and troponin values in relation to time of randomisation and percutaneous coronary intervention (PCI) to identify patients with stable or falling biomarkers pre-PCI (ie, primary cohort), and those with post-PCI CK-MB elevations.</p></sec><sec><st>Setting</st><p>The CHAMPION PLATFORM trial.</p></sec><sec><st>Patients</st><p>Non-ST-elevation acute coronary syndromes (95%) and stable angina patients (5%).</p></sec><sec><st>Interventions</st><p>Cangrelor versus placebo.</p></sec><sec><st>Main outcome measures</st><p>The efficacy of cangrelor compared with placebo using the reclassified events (type 4a MI) and the original clinical events committee-adjudicated (CEC PCI-MI) results was investigated.</p></sec><sec><st>Results</st><p>Of 5295 patients, 3406 (64.4%) were in the primary cohort. Type 4a MI occurred in 4.3% (226 events/5295 patients) while original CEC PCI-MI occurred in 6.5% (344 events/5295 patients), a significant difference (p&lt;0.0001). Using the reclassified MI events, the primary composite endpoint of death, MI, or ischaemia-driven revascularisation through 48&nbsp;h occurred in 5.4% of patients (4.9% cangrelor, 6.0% placebo; OR 0.80; 95% CI 0.63 to 1.02) as opposed to 7.5% of the primary analyses (7.0% cangrelor, 8.0% placebo; OR 0.87; 95% CI 0.71 to 1.07).</p></sec><sec><st>Conclusions</st><p>Systematic, strict implementation of the universal MI definition with emphasis on baseline assessment may enhance discrimination in detecting PCI-MI and may allow for more rigorous assessment of interventions in patients undergoing early PCI.</p></sec>]]></description>
<dc:creator><![CDATA[Leonardi, S., Truffa, A. A. M., Neely, M. L., Tricoci, P., White, H. D., Gibson, C. M., Wilson, M., Stone, G. W., Harrington, R. A., Bhatt, D. L., Mahaffey, K. W.]]></dc:creator>
<dc:date>2013-02-23T00:00:52-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303103</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303103</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention]]></dc:subject>
<dc:title><![CDATA[A novel approach to systematically implement the universal definition of myocardial infarction: insights from the CHAMPION PLATFORM trial]]></dc:title>
<prism:publicationDate>2013-02-23</prism:publicationDate>
<prism:section>Cardiovascular pharmacology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302888v1?rss=1">
<title><![CDATA[Coronary heart disease: what hope for the developing world?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302888v1?rss=1</link>
<description><![CDATA[<p>Coronary heart disease (CHD) is the leading cause of death worldwide with the greatest absolute contribution of deaths coming from low-income and middle-income populations.<cross-ref type="bib" refid="R1">1</cross-ref> At the outset of the global epidemic, early in the 20th century and continuing for a few decades, CHD rates steeply increased stemming from the prosperity and societal-level changes that industrialisation and urbanisation brought to populations.<cross-ref type="bib" refid="R2">2</cross-ref> These same populations experienced a near universal regression of rates in the latter portion of the century due to a combination of population approaches for prevention as well as advances in medical care. Notably, these countries and populations are typically categorised as high income in the present day. The current concern in high-income countries is whether the decreased rates of CHD have plateaued, especially in the light of major risk factors including obesity, hypertension and type 2 diabetes being on the rise in younger populations.<cross-ref type="bib"...]]></description>
<dc:creator><![CDATA[Odegaard, A. O.]]></dc:creator>
<dc:date>2013-02-22T00:01:15-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302888</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302888</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Epidemiology, Diabetes, Metabolic disorders, Tobacco use]]></dc:subject>
<dc:title><![CDATA[Coronary heart disease: what hope for the developing world?]]></dc:title>
<prism:publicationDate>2013-02-22</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303443v1?rss=1">
<title><![CDATA[Relationship of plasma Neuropeptide Y with angiographic, electrocardiographic and coronary physiology indices of reperfusion during ST elevation myocardial infarction]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303443v1?rss=1</link>
<description><![CDATA[<sec><st>Objectives</st><p>The co-transmitter neuropeptide Y (NPY) is released during high levels of sympathetic stimulation and is a potent vasoconstrictor. We defined the release profile of plasma NPY during acute ST elevation myocardial infarction, and tested the hypothesis that levels correlate with reperfusion measures after treatment with primary percutaneous coronary intervention (PPCI).</p></sec><sec><st>Design</st><p>Prospective observational study.</p></sec><sec><st>Setting</st><p>University hospital heart centre.</p></sec><sec><st>Patients</st><p>64 patients (62.6&plusmn;11.7&nbsp;years-old, 73% male) presenting throughout the 24-h cycle of clinical activity with ST elevation myocardial infarction.</p></sec><sec><st>Interventions</st><p>PPCI.</p></sec><sec><st>Main outcome measures</st><p>NPY was measured (ELISA) in peripheral blood taken before and immediately after PPCI and at 6, 24 and 48&nbsp;h post-PPCI. Reperfusion was assessed by angiographic criteria, ST segment resolution, invasive measurement of coronary flow reserve and the index of microcirculatory resistance.</p></sec><sec><st>Results</st><p>Plasma NPY levels were highest before PPCI (17.4 (8.8&ndash;42.2) pg/ml, median (IQR)) and dropped significantly post-PPCI (12.4 (6.5&ndash;26.7) pg/ml, p&lt;0.0001) and after 6&nbsp;h (9.0 (2.6&ndash;21.5) pg/ml, p=0.008). Patients with admission NPY levels above the median were significantly more hypertensive and tachycardic and were more likely to have diabetes mellitus. Patients with angiographic no-reflow (less than thrombolysis in myocardial infarction 3 flow and myocardial blush grade &gt;2, n=16) or no electrocardiographic ST resolution (&lt;70%, n=30) following PPCI had significantly higher plasma NPY levels. Patients with a coronary flow reserve &lt;1.5 or index of microcirculatory resistance &gt;33 also had significantly higher plasma NPY levels pre-PPCI and post-PPCI.</p></sec><sec><st>Conclusions</st><p>Plasma NPY levels correlate with indices of reperfusion and coronary microvascular resistance.</p></sec>]]></description>
<dc:creator><![CDATA[Cuculi, F., Herring, N., De Caterina, A. R., Banning, A. P., Prendergast, B. D., Forfar, J. C., Choudhury, R. P., Channon, K. M., Kharbanda, R. K.]]></dc:creator>
<dc:date>2013-02-12T00:01:22-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303443</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303443</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Pacing and electrophysiology, Clinical diagnostic tests, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Relationship of plasma Neuropeptide Y with angiographic, electrocardiographic and coronary physiology indices of reperfusion during ST elevation myocardial infarction]]></dc:title>
<prism:publicationDate>2013-02-12</prism:publicationDate>
<prism:section>Interventional cardiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303460v1?rss=1">
<title><![CDATA[BACPR scientific statement: British standards and core components for cardiovascular disease prevention and rehabilitation]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303460v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Aims of the British Association for Cardiovascular Prevention and Rehabilitation standards and core components</st><p>This second edition of the <I>Standards and Core Components (SCC) for Cardiovascular Disease Prevention and Rehabilitation</I> from the British Association for Cardiovascular Prevention and Rehabilitation (BACPR) define cardiac rehabilitation (CR), operationally, through seven standards and seven core components for assuring a quality service of care using a multidisciplinary biopsychosocial approach.<cross-ref type="bib" refid="R1">1</cross-ref> The seven standards aim to ensure that service commissioners, providers and health professionals are aware of the requirements for providing a multidisciplinary CR team that is competent and thus clinically effective, cost-effective and ultimately cost-saving as a result of preventing hospital readmissions. The seven core components (<cross-ref type="fig" refid="HEARTJNL2012303460F1">figure 1</cross-ref>), delivered as a coordinated sum of activities aim to best influence uptake, adherence, quality of life and long-term healthier living.<cross-ref type="bib" refid="R2">2</cross-ref> Details of the full version and related evidence base of the BACPR...]]></description>
<dc:creator><![CDATA[Buckley, J. P., Furze, G., Doherty, P., Speck, L., Connolly, S., Hinton, S., Jones, J. L., on behalf of BACPR]]></dc:creator>
<dc:date>2013-02-12T00:01:21-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303460</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303460</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[BACPR scientific statement: British standards and core components for cardiovascular disease prevention and rehabilitation]]></dc:title>
<prism:publicationDate>2013-02-12</prism:publicationDate>
<prism:section>Editorial - standalone</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303472v1?rss=1">
<title><![CDATA[The use of anticoagulants in the management of atrial fibrillation among general practices in England]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303472v1?rss=1</link>
<description><![CDATA[<sec><st>Objectives</st><p>To investigate the use of oral anticoagulants (AC) and antiplatelet agents (AP) in the management of atrial fibrillation (AF) among patients in primary care in England.</p></sec><sec><st>Design</st><p>Epidemiological study.</p></sec><sec><st>Setting</st><p>1857 general practices in England representing a practice population of 13.1 million registered patients.</p></sec><sec><st>Patients</st><p>231&nbsp;833 patients with a history of AF.</p></sec><sec><st>Main outcome measures</st><p>The primary outcome was AC and AP use by CHADS<SUB>2</SUB> score and age groups &lt;30&nbsp;years, 30&ndash;49&nbsp;years, 50&ndash;64&nbsp;years, 65&ndash;79&nbsp;years and &gt;79&nbsp;years.</p></sec><sec><st>Results</st><p>231&nbsp;833 patients with a history of AF were identified, giving a prevalence among uploading practices of 1.76%. Prevalence of AF varied markedly between practices, related to differing practice age profiles. The total number of patients with AF in a practice was strongly predicted by the number of patients aged 65 years and over in the practice. 57.0% of the AF population had a CHADS<SUB>2</SUB> score &ge;2 and 83.7%&ge;1. 114&nbsp;212 (49.3%) patients received AC therapy. AC uptake increased with increasing CHADS<SUB>2</SUB> score up to a score of 3, but thereafter reached a plateau. Among 132&nbsp;099 patients with a CHADS<SUB>2</SUB> score &ge;2, 72&nbsp;211 (54.7%) received an AC, 14&nbsp;987(11.3%) were recorded as having a contraindication or having declined AC therapy, leaving 44&nbsp;901 (34.0%) not on AC therapy and without a recorded contraindication or recorded refusal. Among patients not prescribed an AC, 79.9% were prescribed an AP. The use of AC declined in the elderly (for CHADS<SUB>2</SUB>&ge;2, 47.4% of patients &ge;80 years, compared with 64.5% for patients aged &lt;80 years, p&lt;0.001). By contrast, AP uptake was more prevalent among elderly patients.</p></sec><sec><st>Conclusions</st><p>Over one-third of patients with AF and known risk factors who are eligible for AC do not receive them. There is a high use of AP among patients not receiving AC. Uptake of AC is particularly poor among patients aged 80 years and over.</p></sec>]]></description>
<dc:creator><![CDATA[Cowan, C., Healicon, R., Robson, I., Long, W. R., Barrett, J., Fay, M., Tyndall, K., Gale, C. P.]]></dc:creator>
<dc:date>2013-02-07T00:11:33-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303472</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303472</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The use of anticoagulants in the management of atrial fibrillation among general practices in England]]></dc:title>
<prism:publicationDate>2013-02-07</prism:publicationDate>
<prism:section>Heart rhythm disorders</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303307v1?rss=1">
<title><![CDATA[Incidental finding of a giant coronary artery aneurysm of the left anterior descending artery]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303307v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>An asymptomatic 84-year-old man was referred for cardiology assessment in view of incidental radiology findings. He had coronary artery bypass grafting in 1982 with vein grafts to the right coronary artery and left anterior descending artery (LAD). Angiography in 2000 for recurrent angina demonstrated severe native disease, patent LAD graft and occluded right coronary artery graft. He underwent uncomplicated PCI to the native right and circumflex arteries with drug eluting stents. He had rate-controlled atrial fibrillation and hypertension.</p><p>Echocardiography showed normal ventricular function, the only abnormalities were biatrial dilatation and mild aortic regurgitation. A chest roentgenogram showed ectasia of the thoracic aorta and a 7.7&nbsp;cm left hilar mass (<cross-ref type="fig" refid="HEARTJNL2012303307F1">figure 1</cross-ref>). Subsequent CT revealed a giant aneurysm (7.5<FONT FACE="arial,helvetica">x</FONT>6.8&nbsp;cm) arising from native LAD containing mural thrombus (<cross-ref type="fig" refid="HEARTJNL2012303307F2">figure 2</cross-ref>). Following multidisciplinary team discussion the patient was managed conservatively, including oral anticoagulation (INR 2.0&ndash;3.0).</p><p><fig loc="float" id="HEARTJNL2012303307F1"><no>Figure&nbsp;1</no><caption><p>AP chest roentgenogram.</p></caption><link locator="heartjnl2012303307f01"></fig></p><p><fig loc="float"...]]></description>
<dc:creator><![CDATA[Whittaker, A., Wilkinson, J. R.]]></dc:creator>
<dc:date>2013-02-07T00:11:33-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303307</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303307</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Incidental finding of a giant coronary artery aneurysm of the left anterior descending artery]]></dc:title>
<prism:publicationDate>2013-02-07</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303433v1?rss=1">
<title><![CDATA[Methods used for the assessment of LV systolic function: common currency or tower of Babel?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303433v1?rss=1</link>
<description><![CDATA[<p>The last decade has produced a proliferation of techniques for the assessment of left ventricular systolic function, and there now seems to be more choice than seems rational for the questions that we need answers to. In some instances, simple estimation is all that is required&mdash;the risk stratification process is inexact, as emphasised by the variety of modalities used to characterise ejection fraction (EF) in studies that validated the efficacy of treatments selected on the basis of EF. Nonetheless, while technical advances often cause disruption and confusion, it would be wrong to dismiss them as lacking benefit. The purpose of this review is to try to provide rational grounds for selecting both test modality and physiological parameter in various specific clinical situations.</p>]]></description>
<dc:creator><![CDATA[Marwick, T. H.]]></dc:creator>
<dc:date>2013-02-02T08:38:53-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303433</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303433</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Methods used for the assessment of LV systolic function: common currency or tower of Babel?]]></dc:title>
<prism:publicationDate>2013-02-02</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302970v1?rss=1">
<title><![CDATA[Molecular targets of current and prospective heart failure therapies]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302970v1?rss=1</link>
<description><![CDATA[<p>Heart failure (HF) is a vicious circle in which an original insult leading to mechanical cardiac dysfunction initiates multiple morphological, biochemical and molecular pathological alterations referred to as cardiac remodelling. Remodelling leads to further deterioration of cardiac function and functional reserve. Interrupting or reversing cardiac remodelling is a major therapeutic goal of HF therapies. The role of molecules and molecular pathways in cardiac remodelling and HF has been extensively studied. Multiple approaches are now used or investigated in HF therapy, including pharmacological therapy, device therapy, gene therapy, cell therapy and biological therapy targeting cytokines and growth factors. This review explores the molecular targets and molecular bases of current and prospective therapies in HF.</p>]]></description>
<dc:creator><![CDATA[Chemaly, E. R., Hajjar, R. J., Lipskaia, L.]]></dc:creator>
<dc:date>2013-01-24T00:01:00-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302970</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302970</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Molecular targets of current and prospective heart failure therapies]]></dc:title>
<prism:publicationDate>2013-01-24</prism:publicationDate>
<prism:section>Reviews</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303421v1?rss=1">
<title><![CDATA[Plaques with high lipid burden: keeping the fat out of the fire]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303421v1?rss=1</link>
<description><![CDATA[<p>Two recent papers published in <I>Heart</I> have evaluated the utility of advanced imaging modalities for the morphological detection and evaluation of high-risk atherosclerotic plaques.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> While these studies employed differing methodologies (CT angiography (CTA), optical coherence tomography (OCT) and optic angioscopy), the results are broadly concordant and of major potential clinical significance. Notably, when subjected to percutaneous coronary intervention (PCI), such high-risk plaques may embolise and release a slurry of lipid-rich necrotic debris to the distal circulation, with consequent myocardial damage. In addition, it has been proposed that PCI of lipid-rich plaques (LRP) with thin fibrous caps (&lt;65&nbsp;&mu;m; thin-cap fibroatheroma (TCFA)) may be associated with lipid embolisation. However, since stable angina patients do not require urgent intervention, detailed assessment of target lesions may be feasible for the recognition and assessment of LRP before elective PCI.</p><p>Radiofrequency intravascular ultrasound (RF-IVUS) analysis is useful in defining the distribution, severity...]]></description>
<dc:creator><![CDATA[Roleder, T., Suh, W., Sharma, R., Hecht, H., Kovacic, J. C., Narula, J., Kini, A. S.]]></dc:creator>
<dc:date>2013-01-24T00:00:59-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303421</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303421</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Plaques with high lipid burden: keeping the fat out of the fire]]></dc:title>
<prism:publicationDate>2013-01-24</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303105v1?rss=1">
<title><![CDATA[Predictors for efficacy of percutaneous mitral valve repair using the MitraClip system: the results of the MitraSwiss registry]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303105v1?rss=1</link>
<description><![CDATA[<sec><st>Background</st><p>Percutaneous mitral valve repair (MVR) using the MitraClip system has become a valid alternative for patients with severe mitral regurgitation (MR) and high operative risk.</p></sec><sec><st>Objective</st><p>To identify clinical and periprocedural factors that may have an impact on clinical outcome.</p></sec><sec><st>Design</st><p>Multi-centre longitudinal cohort study.</p></sec><sec><st>Setting</st><p>Tertiary referral centres.</p></sec><sec><st>Patients</st><p>Here we report on the first 100 consecutive patients treated with percutaneous MVR in Switzerland between March 2009 and April 2011. All of them had moderate&ndash;severe (3+) or severe (4+) MR, and 62% had functional MR. 82% of the patients were in New York Heart Association (NYHA) class III/IV, mean left ventricular ejection fraction was 48% and the median European System for Cardiac Operative Risk Evaluation was 16.9%.</p></sec><sec><st>Interventions</st><p>MitraClip implantation performed under echocardiographic and fluoroscopic guidance in general anaesthesia.</p></sec><sec><st>Main outcome measures</st><p>Clinical, echocardiographic and procedural data were prospectively collected.</p></sec><sec><st>Results</st><p>Acute procedural success (APS, defined as successful clip implantation with residual MR grade &le;2+) was achieved in 85% of patients. Overall survival at 6 and 12&nbsp;months was 89.9% (95% CI 81.8 to 94.6) and 84.6% (95% CI 74.7 to 91.0), respectively. Univariate Cox regression analysis identified APS (p=0.0069) and discharge MR grade (p=0.03) as significant predictors of survival.</p></sec><sec><st>Conclusions</st><p>In our consecutive cohort of patients, APS was achieved in 85%. APS and residual discharge MR grade are important predictors of mid-term survival after percutaneous MVR.</p></sec>]]></description>
<dc:creator><![CDATA[Surder, D., Pedrazzini, G., Gaemperli, O., Biaggi, P., Felix, C., Rufibach, K., Maur, C. a. d., Jeger, R., Buser, P., Kaufmann, B. A., Moccetti, M., Hurlimann, D., Buhler, I., Bettex, D., Scherman, J., Pasotti, E., Faletra, F. F., Zuber, M., Moccetti, T., Luscher, T. F., Erne, P., Grunenfelder, J., Corti, R.]]></dc:creator>
<dc:date>2013-01-23T00:02:59-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303105</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303105</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Echocardiography, Interventional cardiology, Mitral valve disease, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Predictors for efficacy of percutaneous mitral valve repair using the MitraClip system: the results of the MitraSwiss registry]]></dc:title>
<prism:publicationDate>2013-01-23</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303483v1?rss=1">
<title><![CDATA[Identifying excellence in contemporary cardiology practice: transparency, professionalism and the role of the professional society]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303483v1?rss=1</link>
<description><![CDATA[<sec><p>A recent article in the <I>British Medical Journal</I> raised important questions about professional transparency, the collection and use of outcome data and the respective roles of professional societies, commissioners of care, regulators and politicians.<cross-ref type="bib" refid="R1">1</cross-ref> Professional societies have traditionally been viewed both internally and externally as existing largely for the benefit of their members in providing a forum for education and scientific exchange as well as focus for interaction with other professional organisations and with various regulatory bodies.<cross-ref type="bib" refid="R2">2</cross-ref> This perception has evolved with the increasing involvement of large international societies in the development of guidelines for the delivery of cardiology care. The mission statement of the European Society of Cardiology is to reduce the burden of cardiovascular disease in Europe, that of the American College of Cardiology to transform cardiovascular care and improve heart health and that of the British Cardiovascular Society to promote excellence in cardiovascular...]]></description>
<dc:creator><![CDATA[Ray, S., Jeremy, R., Nishimura, R., Simpson, I. A.]]></dc:creator>
<dc:date>2013-01-23T00:02:58-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303483</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303483</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology]]></dc:subject>
<dc:title><![CDATA[Identifying excellence in contemporary cardiology practice: transparency, professionalism and the role of the professional society]]></dc:title>
<prism:publicationDate>2013-01-23</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303456v1?rss=1">
<title><![CDATA[The Society of Thoracic Surgeons National Database]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303456v1?rss=1</link>
<description><![CDATA[<sec><st>Aims</st><p>The Society of Thoracic Surgeons (STS) National Database collects detailed clinical information on patients undergoing adult cardiac, paediatric and congenital cardiac, and general thoracic surgical operations. These data are used to support risk-adjusted, nationally benchmarked performance assessment and feedback; voluntary public reporting; quality improvement initiatives; guideline development; appropriateness determination; shared decision making; research using cross-sectional and longitudinal registry linkages; comparative effectiveness studies; government collaborations including postmarket surveillance; regulatory compliance and reimbursement strategies.</p></sec><sec><st>Interventions</st><p>All database participants receive feedback reports which they may voluntarily share with their hospitals or payers, or publicly report. STS analyses are regularly used as the basis for local, regional and national quality improvement efforts.</p></sec><sec><st>Population</st><p>More than 90% of adult cardiac programmes in the USA participate, as do the majority of paediatric cardiac programmes, and general thoracic participation continues to increase. Since the inception of the Database in 1989, more than 5 million patient records have been submitted.</p></sec><sec><st>Baseline data</st><p>Each of the three subspecialty databases includes several hundred variables that characterise patient demographics, diagnosis, medical history, clinical risk factors and urgency of presentation, operative details and postoperative course including adverse outcomes.</p></sec><sec><st>Data capture</st><p>Data are entered by trained data abstractors and by the care team, using detailed data specifications for each element.</p></sec><sec><st>Data quality</st><p>Quality and consistency checks assure accurate and complete data, missing data are rare, and audits are performed annually of selected participant sites.</p></sec><sec><st>Endpoints</st><p>All major outcomes are reported including complications, status at discharge and mortality.</p></sec><sec><st>Data access</st><p>Applications for STS Database participants to use aggregate national data for research are available at <A HREF="http://www.sts.org/quality-research-patient-safety/research/publications-and-research/access-data-sts-national-database">http://www.sts.org/quality-research-patient-safety/research/publications-and-research/access-data-sts-national-database</A>.</p></sec>]]></description>
<dc:creator><![CDATA[Shahian, D. M., Jacobs, J. P., Edwards, F. H., Brennan, J. M., Dokholyan, R. S., Prager, R. L., Wright, C. D., Peterson, E. D., McDonald, D. E., Grover, F. L.]]></dc:creator>
<dc:date>2013-01-18T00:01:30-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303456</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303456</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Epidemiology]]></dc:subject>
<dc:title><![CDATA[The Society of Thoracic Surgeons National Database]]></dc:title>
<prism:publicationDate>2013-01-18</prism:publicationDate>
<prism:section>Registry</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303369v1?rss=1">
<title><![CDATA[The diagnosis of apical hypertrophic cardiomyopathy with myocardial perfusion imaging]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303369v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Case description</st><p>A 67-year-old male with a history of hypertension, dyslipidaemia, diabetes mellitus type 2, obstructive sleep apnoea and obesity was referred for evaluation of an abnormal ECG. At presentation, the patient was asymptomatic and denied prior cardiac symptoms. Resting 12-lead ECG demonstrated marked ST and T-wave abnormalities consistent with anterolateral ischaemia (<cross-ref type="fig" refid="HEARTJNL2012303369F1">Figure&nbsp;1</cross-ref>A). On single-photon emission CT myocardial perfusion (SPECT) wall motion images, the left ventricular chamber was noted to have a peculiar &lsquo;spade-shaped&rsquo; contour (<cross-ref type="fig" refid="HEARTJNL2012303369F1">Figure&nbsp;1</cross-ref>B,C, online supplementary media clip 1). On this basis, a transthoracic echocardiogram was performed, confirming the suspected diagnosis of apical variant hypertrophic cardiomyopathy with a small apical pouch (<cross-ref type="fig" refid="HEARTJNL2012303369F2">Figure&nbsp;2</cross-ref>A; online supplementary media clips 2&ndash;5). MRI confirmed presence of the small apical pouch (<cross-ref type="fig" refid="HEARTJNL2012303369F2">Figure&nbsp;2</cross-ref>B, online supplementary media clip 6).</p><p><fig loc="float" id="HEARTJNL2012303369F1"><no>Figure&nbsp;1</no><caption><p>Presenting 12-lead ECG and exercise single-photon emission CT (SPECT). (A) ECG demonstrates sinus bradycardia with marked ST-segment and...]]></description>
<dc:creator><![CDATA[Jouni, H., Geske, J. B., Miller, T. D.]]></dc:creator>
<dc:date>2013-01-12T00:02:32-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303369</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303369</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[The diagnosis of apical hypertrophic cardiomyopathy with myocardial perfusion imaging]]></dc:title>
<prism:publicationDate>2013-01-12</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/2012-303403v1?rss=1">
<title><![CDATA[Transient loss of consciousness: summary of NICE guidance]]></title>
<link>http://heart.bmj.com/cgi/content/short/2012-303403v1?rss=1</link>
<description><![CDATA[<sec id="s1"><st>Introduction</st><p>The National Institute of Clinical Excellence (NICE), in August 2010, published the Transient Loss of Consciousness guideline<cross-ref type="bib" refid="R1">1</cross-ref> which dealt with the assessment, diagnosis and specialist referral of adults and young people (aged 16 and older), who had experienced transient loss of consciousness (TLoC), also commonly described in the UK as a &lsquo;blackout&rsquo;. The guideline defines TLoC as spontaneous loss of consciousness with complete recovery, implying full recovery of consciousness without any residual neurological deficit. This first ever to be published guideline in the UK dealt with a very common condition which has a lifetime incidence of up to 50%.<cross-ref type="bib" refid="R2">2</cross-ref> Transient loss of consciousness is a symptom with several causes, with cardiovascular causes (syncope) being the most common. Other common causes of TLoC include neurological conditions, principally epilepsy and psychogenic attacks. Syncope, in turn, has many causes, ranging from those with a benign prognosis, for example,...]]></description>
<dc:creator><![CDATA[Petkar, S., Bullock, I., Davis, S., Cooper, P.]]></dc:creator>
<dc:date>2013-01-10T00:00:53-08:00</dc:date>
<dc:identifier>info:doi/10.1136/2012-303403</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;2012-303403</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Hypertension, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Transient loss of consciousness: summary of NICE guidance]]></dc:title>
<prism:publicationDate>2013-01-10</prism:publicationDate>
<prism:section>Editorial-standalone</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303147v1?rss=1">
<title><![CDATA[The Authors' reply]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303147v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>We thank Dr Marijan Bosevski for his comments<cross-ref type="bib" refid="R1">1</cross-ref> and appreciate his interest in our recent publication.<cross-ref type="bib" refid="R2">2</cross-ref> In this letter, Dr Bosevski addresses an important issue concerning the potential prognostic implication of carotid plaque thermal heterogeneity or/and plaque neoangiogenesis, when added in current risk stratification models to improve the overall predictive ability for cardiovascular events. Although our study was not oriented towards prognosis, this is certainly an issue worthy of further discussion.</p><p>Since the last few years, there has been a particular interest in identifying novel atherosclerotic plaque features that may have additive predictive value in current risk stratification models. Among other plaque features, inflammation and neoangiogenesis seem to play a central role in plaque destabilisation.<cross-ref type="bib" refid="R3">3</cross-ref> The aforementioned plaque features have not been assessed as potential prognostic factors and their role in risk stratification of vulnerable patients has not been elucidated because only recently have...]]></description>
<dc:creator><![CDATA[Toutouzas, K., Drakopoulou, M., Aggeli, C., Nikolaou, C., Felekos, I., Grassos, H., Synetos, A., Stathogiannis, K., Karanasos, A., Tsiamis, E., Siores, E., Stefanadis, C.]]></dc:creator>
<dc:date>2012-12-22T00:01:48-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303147</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303147</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[The Authors' reply]]></dc:title>
<prism:publicationDate>2012-12-22</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-303287v1?rss=1">
<title><![CDATA[Statement on matching language to the type of evidence used in describing outcomes data]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-303287v1?rss=1</link>
<description><![CDATA[<sec id="s1"><p>Editors of the HEART Group Journals</p><p>There are many different types of studies that can be conducted to provide evidence for clinical and outcomes research, including but not limited to retrospective observational analyses, case-control studies and randomised controlled trials. Each of these analyses has strengths and limitations, but most importantly, they all result in different types of conclusions about an intervention.</p><p>As illustrated in a series of examples provided in a separate review,<cross-ref type="bib" refid="R1">1</cross-ref> inappropriate word choice to describe results can lead to scientific inaccuracy. Therefore, the editors of the HEART Group (representing the world's cardiovascular journals) recommend that all investigators and editors carefully select language to &lsquo;match&rsquo; the type of study conducted, without overstating findings or drawing erroneous conclusions about causality when they cannot be established.</p><p>As an illustrative example, when reporting results from an observational study that shows fewer deaths in one arm than in another, one should use...]]></description>
<dc:creator><![CDATA[Editors, H. G.]]></dc:creator>
<dc:date>2012-11-22T00:02:40-08:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303287</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303287</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Epidemiology]]></dc:subject>
<dc:title><![CDATA[Statement on matching language to the type of evidence used in describing outcomes data]]></dc:title>
<prism:publicationDate>2012-11-22</prism:publicationDate>
<prism:section>Editorials</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-302710v1?rss=1">
<title><![CDATA[Clapping atrio-ventricular valves]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-302710v1?rss=1</link>
<description><![CDATA[<p>We describe a 30-year-old male who presented with progressively increasing effort intolerance since his adolescence. On examination, he was cyanosed with a pulse rate of 50 /min. He was found to have a localised, grade 2/6 systolic murmur at the base of the heart. He was diagnosed to have atrioventricular discordance with ventricular- arterial discordance (congenitally corrected transposition of the great arteries) along with large subpulmonic ventricular septal defect and severe pulmonary artery hypertension (<cross-ref type="fig" refid="fig1">figure 1</cross-ref>). His estimated mean pulmonary artery pressure was 70&nbsp;mm&nbsp;Hg. ECG showed atrial flutter with an atrial rate of 300/min, and ventricular rate of 50/min. 2D Transthoracic echocardiography (TTE) revealed an interesting finding of mitral valve movements (online video 1). TTE with single ECG lead recording confirms that every atrial flutter wave makes the AV valves to open in a rhythmic fashion. It gives the appearance of clapping AV valves and dancing interatrial septum.</p><p><fig...]]></description>
<dc:creator><![CDATA[Senguttuvan, N. B., Goswami, K. C.]]></dc:creator>
<dc:date>2012-08-15T02:01:54-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302710</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302710</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Clapping atrio-ventricular valves]]></dc:title>
<prism:publicationDate>2012-08-15</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2011-301101v2?rss=1">
<title><![CDATA[Clinical impact of intracoronary abciximab in patients undergoing primary percutaneous coronary intervention: an individual patient data pooled analysis of randomised studies]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2011-301101v2?rss=1</link>
<description><![CDATA[<sec><st>Objectives</st><p>The aim of this study was to perform an individual patient-level pooled analysis of randomised trials, comparing intracoronary versus intravenous abciximab bolus use in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).</p></sec><sec><st>Background</st><p>Abciximab represents a cornerstone in the treatment of STEMI patients undergoing primary PCI. Intracoronary abciximab bolus administration has been proposed as an alternative strategy to the standard intravenous route. However, whether intracoronary abciximab effectively improves clinical outcomes compared with standard route remains unknown.</p></sec><sec><st>Methods</st><p>Individual data of 1198 patients enrolled in five trials were entered into the pooled analysis. The primary endpoint of the study was the occurrence of all-cause death and reinfarction at 30-day follow-up. Secondary endpoints were all-cause death, reinfarction and target-vessel revascularisation (TVR).</p></sec><sec><st>Results</st><p>No significant heterogeneity was found across trials. Compared with the intravenous route, intracoronary abciximab administration significantly reduced the risk of the composite of death and reinfarction (HR 0.52, 95% CI 0.29 to 0.94; p=0.03), death (HR 0.44, 95% CI 0.20 to 0.95; p=0.04) and TVR (HR 0.53, 95% CI 0.29 to 0.99; p=0.045), without a significant impact on the risk of reinfarction (HR 0.54, 95% CI 0.24 to 1.21; p=0.13). However, after correction for baseline differences, only the composite of death/reinfarction and death remained significant.</p></sec><sec><st>Conclusions</st><p>In STEMI patients undergoing primary PCI, intracoronary abciximab administration, when compared with the intravenous standard route, can improve short-term clinical outcomes mainly by reducing the risk of death.</p></sec>]]></description>
<dc:creator><![CDATA[Piccolo, R., Gu, Y. L., Iversen, A. Z., Dominguez-Rodriguez, A., de Smet, B. J. G. L., Mahmoud, K. D., Eitel, I., Abreu-Gonzalez, P., Thiele, H., Piscione, F.]]></dc:creator>
<dc:date>2012-05-24T02:01:13-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301101</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301101</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Percutaneous intervention]]></dc:subject>
<dc:title><![CDATA[Clinical impact of intracoronary abciximab in patients undergoing primary percutaneous coronary intervention: an individual patient data pooled analysis of randomised studies]]></dc:title>
<prism:publicationDate>2012-05-24</prism:publicationDate>
<prism:section>Interventional cardiology</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2012-301983v1?rss=1">
<title><![CDATA[Is RAMIT reflecting the real world?]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2012-301983v1?rss=1</link>
<description><![CDATA[<p><b>To the Editor</b> Rehabilitation after myocardial infarction trial (RAMIT) explored the effect of a phase II outpatient-based cardiac rehabilitation (CR) concept. The authors reported no effect on mortality, cardiac or psychological morbidity, risk factors, health-related quality of life or physical activity of a comprehensive CR programme after myocardial infarction. However, in our opinion these findings cannot be generalised and merit an in-depth critical analysis. In many European countries a residential CR programme starts within weeks after myocardial infarction. After 3&ndash;4&nbsp;weeks of intense residential CR (physical training 3&ndash;4&nbsp;h/week) patients are offered participation in an outpatient CR programme for an additional 8&ndash;12&nbsp;weeks. The intensity of the physical activity is essential for the success of a CR programme. In the RAMIT trial the minimum CR duration was 10&nbsp;h, which included exercise as well as education and counselling. In fact, the mean CR duration was 20&nbsp;h within 6&ndash;8&nbsp;weeks. This comprised approximately 10&nbsp;h of exercise...]]></description>
<dc:creator><![CDATA[Berger, T., Brenneis, C., Alber, H.]]></dc:creator>
<dc:date>2012-05-23T02:01:58-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301983</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301983</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Is RAMIT reflecting the real world?]]></dc:title>
<prism:publicationDate>2012-05-23</prism:publicationDate>
<prism:section>PostScript</prism:section>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/heartjnl-2011-300740v1?rss=1">
<title><![CDATA[Assessment of vascular phenotype using a novel very high resolution ultrasound technique in adolescents after aortic coarctation repair and/or stent implantation: relationship to central haemodynamics and left ventricular mass]]></title>
<link>http://heart.bmj.com/cgi/content/short/heartjnl-2011-300740v1?rss=1</link>
<description><![CDATA[<sec><st>Objectives</st><p>The objective was to determine the severity of residual cardiovascular abnormalities in youths after coarctation of the aorta (CoA) repair and their relation to regional blood pressure (BP).</p></sec><sec><st>Design</st><p>Prospective cross-sectional study in tertiary health care setting.</p></sec><sec><st>Methods</st><p>Thirty-six CoAs (age 16&plusmn;1 years; neonatal surgery only: n=16; surgery and/or stent implantation: n=20) and 37 age-matched controls were examined by very-high resolution ultrasound, echocardiography and applanation tonometry.</p></sec><sec><st>Results</st><p>CoA was associated with increased right arm systolic BP (p&lt;0.001), intima-media thickness (IMT) in the common carotid (p&lt;0.001), right brachial (p&lt;0.05) and radial (p&lt;0.05) arteries and ascending aortic stiffness (p&lt;0.05). Carotid IMT correlated positively with age at first intervention (r=0.36, p&lt;0.05). With left subclavian flap type repair, left arm systolic BP (p&lt;0.001) and left brachial (p&lt;0.001), radial (p&lt;0.001) and ulnar (p&lt;0.05) arterial IMTs were all reduced. When adjusted for BP, body mass index, age and gender, only carotid IMT (p&lt;0.001) and LV-mass (p=0.013) of stented patients, as well as left arm arterial IMTs (p&lt;0.01) in subclavian flap type repair patients remained different from controls. The significant associations of stented patients disappeared after adjustment for later patient age at intervention (median 8.7 vs 0.03 years, p&lt;0.001). Residual arm-leg BP gradients correlated positively with carotid and brachial IMT.</p></sec><sec><st>Conclusion</st><p>CoA repair in early childhood is associated with increased preductal arterial IMT, LV mass and ascending aortic stiffness in adolescents. The more pronounced cardiovascular abnormalities after CoA stent implantation are likely related to the older patient age at the time of intervention.</p></sec>]]></description>
<dc:creator><![CDATA[Sarkola, T., Redington, A. N., Slorach, C., Hui, W., Bradley, T., Jaeggi, E.]]></dc:creator>
<dc:date>2011-09-13T14:28:57-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-300740</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-300740</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Congenital heart disease, Echocardiography, Hypertension, Interventional cardiology, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Assessment of vascular phenotype using a novel very high resolution ultrasound technique in adolescents after aortic coarctation repair and/or stent implantation: relationship to central haemodynamics and left ventricular mass]]></dc:title>
<prism:publicationDate>2011-09-13</prism:publicationDate>
<prism:section>Original article</prism:section>
</item>
</rdf:RDF>