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<title>Heart current issue</title>
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<prism:coverDisplayDate>Jun  1 2012 12:00:00:000AM</prism:coverDisplayDate>
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<title>Heart</title>
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<link>http://heart.bmj.com</link>
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<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/831?rss=1">
<title><![CDATA[Plasma asymmetric dimethylarginine in patients with acute decompensation of chronic heart failure]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/831?rss=1</link>
<description><![CDATA[ <p>The implications of abnormal endothelial function in the pathophysiology and prognosis in patients with chronic heart failure (CHF) has been extensively discussed.<cross-ref type="bib" refid="b1">1&ndash;3</cross-ref><cross-ref type="bib" refid="b2"></cross-ref><cross-ref type="bib" refid="b3"></cross-ref> Endothelial dysfunction may affect the cardiovascular system in different ways, such as impairment of peripheral perfusion, an adverse effect of vascular remodelling, reduced compliance of the failing left ventricle and consequently impaired left ventricular dysfunction.<cross-ref type="bib" refid="b4">4</cross-ref></p> <p>Endothelial dysfunction has been attributed to reduced production of endothelial nitric oxide (NO) production, and thus affects vasoreactivity and smooth muscle cell growth, platelet reactivity and leucocyte adhesion to the endothelium.</p> <p>Reduced production and bioavailability of NO can be caused by several mechanisms, one being increased production and/or accumulation of the amino acid asymmetric dimethylarginine (ADMA). ADMA is an endogenous competitive inhibitor of nitric oxide synthase (NOS),<cross-ref type="bib" refid="b5">5</cross-ref> and is synthesised by methylation of proteins containing <scp>l</scp>-arginine, which is the substrate of NOS....]]></description>
<dc:creator><![CDATA[Seljeflot, I.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301932</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301932</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Echocardiography, Acute coronary syndromes, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Plasma asymmetric dimethylarginine in patients with acute decompensation of chronic heart failure]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>831</prism:startingPage>
<prism:endingPage>832</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/833?rss=1">
<title><![CDATA[Identifying the patient who FADES away prior to appropriate ICD intervention]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/833?rss=1</link>
<description><![CDATA[ <p>Despite important progress, sudden cardiac death (SCD) continues to represent an important clinical challenge for contemporary cardiology. Randomised controlled trials performed in high risk patients, such as patients with ischaemic heart disease and left ventricular dysfunction, showed that an approach based on antiarrhythmic drugs is not only useless, but sometimes even potentially harmful.<cross-ref type="bib" refid="b1">1</cross-ref> Conversely, implantable cardioverter defibrillators (ICDs) have gained a specific role not only in patients with a previous ventricular tachyarrhythmia or cardiac arrest (secondary preventions of SCD) but also in the broader population of high-risk patients with ischaemic heart disease and left ventricular dysfunction, in whom use of ICDs for primary prevention of SCD may reduce overall mortality by 23%&ndash;54%.<cross-ref type="bib" refid="b1">1</cross-ref> The high upfront cost of ICDs, particularly when implementing cardiac resynchronisation therapy (CRT-D), has prompted both the search to improve patient targeting and the development of appropriate economic evaluations on the cost-effectiveness of...]]></description>
<dc:creator><![CDATA[Boriani, G., Diemberger, I.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301835</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301835</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Tachyarrhythmias, Drugs: cardiovascular system, Epidemiology, Diabetes, Metabolic disorders, Tobacco use]]></dc:subject>
<dc:title><![CDATA[Identifying the patient who FADES away prior to appropriate ICD intervention]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>833</prism:startingPage>
<prism:endingPage>834</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/835?rss=1">
<title><![CDATA[Pathogenesis and diagnosis of myocarditis]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/835?rss=1</link>
<description><![CDATA[
<p>Acute myocarditis is an inflammatory disease of the heart muscle that may progress to dilated cardiomyopathy and chronic heart failure. A number of factors including the sex hormone testosterone, components of innate immunity, and profibrotic cytokines have been identified in animal models as important pathogenic mechanisms that increase inflammation and susceptibility to chronic dilated cardiomyopathy. The clinical presentation of acute myocarditis is non-specific and mimics more common causes of heart failure and arrhythmias. Suspected myocarditis is currently confirmed using advanced non-invasive imaging and histopathologic examination of heart tissue. However, the diverse presentations of myocarditis and the lack of widely available, safe, and accurate non-invasive diagnostic tests remain major obstacles to early diagnosis and population based research. Recent advances in the understanding of disease pathogenesis described in this review should lead to more accurate diagnostic algorithms and non-invasive tests.</p>
]]></description>
<dc:creator><![CDATA[Elamm, C., Fairweather, D., Cooper, L. T.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301686</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301686</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Pathogenesis and diagnosis of myocarditis]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Reviews</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>835</prism:startingPage>
<prism:endingPage>840</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/841?rss=1">
<title><![CDATA[Early repolarisation: controversies and clinical implications]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/841?rss=1</link>
<description><![CDATA[
<p>Early repolarisation was previously considered a benign variant but in recent years has emerged as a marker of risk for sudden death. In part, this appears to reflect a change in the definition. ECG territory, degree of J-point elevation and ST-segment morphology are associated with different degrees of risk for subsequent ventricular arrhythmia. At present the dataset is insufficient to allow risk stratification in asymptomatic individuals and further epidemiological and mechanistic research is required.</p>
]]></description>
<dc:creator><![CDATA[Bastiaenen, R., Behr, E. R.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301347</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301347</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Early repolarisation: controversies and clinical implications]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Reviews</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>841</prism:startingPage>
<prism:endingPage>847</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/848?rss=1">
<title><![CDATA[Newly diagnosed glucose intolerance and prognosis after acute myocardial infarction: comparison of post-challenge versus fasting glucose concentrations]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/848?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Recent studies have demonstrated that newly diagnosed glucose intolerance is common among patients with acute myocardial infarction (AMI). The purpose of this study was to assess the long-term clinical cardiovascular outcomes in participants with AMI with abnormal fasting glucose compared with normal fasting glucose and an abnormal oral glucose tolerance test (OGTT) compared with a normal OGTT.</p>
</sec>
<sec><st>Methods</st>
<p>A prospective study was performed in 275 consecutive patients with AMI, 85 of whom had pre-diagnosed diabetes mellitus (DM). Those without DM were divided into two groups based on the 75&nbsp;g OGTT at the time of discharge. Abnormal glucose tolerance (AGT) was defined as 2&nbsp;h glucose &ge;140&nbsp;mg/dl; 78 patients had normal glucose tolerance (NGT) and 112 had AGT. The same patients were also reclassified into the normal fasting glucose group (NFG; n=168) or the impaired fasting glucose group (IFG; n=22). The association between the glucometabolic status and long-term major adverse cardiovascular event rates was evaluated.</p>
</sec>
<sec><st>Results</st>
<p>Kaplan&ndash;Meier survival curves showed that the AGT group had a worse prognosis than the NGT group and an equivalent prognosis to the DM group (p&lt;0.0005). Cox proportional hazard model analysis showed that the HR of AGT to NGT for major adverse cardiovascular event rates was 2.65 (95% CI 1.37 to 5.15, p=0.004) while the HR of DM to NGT was 3.27 (1.68 to 6.38, p=0.0005). However, Cox HR of IFG to NFG for major adverse cardiovascular event rates was 1.83 (0.86 to 3.87), which was not significant.</p>
</sec>
<sec><st>Conclusion</st>
<p>In patients with AMI, an abnormal OGTT is a better risk factor for future adverse cardiovascular events than impaired fasting blood glucose.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Tamita, K., Katayama, M., Takagi, T., Yamamuro, A., Kaji, S., Yoshikawa, J., Furukawa, Y.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301629</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301629</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Unlocked, Editor's choice, Drugs: cardiovascular system, Acute coronary syndromes, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Newly diagnosed glucose intolerance and prognosis after acute myocardial infarction: comparison of post-challenge versus fasting glucose concentrations]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Acute coronary syndromes</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>848</prism:startingPage>
<prism:endingPage>854</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/855?rss=1">
<title><![CDATA[Adenosine plasma level and A2A adenosine receptor expression: correlation with laboratory tests in patients with neurally mediated syncope]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/855?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>The purpose of this study was to investigate the hypothesis that responses to the ATP test and head-up tilt test (HUT) may be correlated with different purinergic profiles.</p>
</sec>
<sec><st>Design and setting</st>
<p>The ATP and HUT identify distinct subsets of patients with neurally mediated syncope (NMS). Adenosine and its A<SUB>2A</SUB> receptors (A<SUB>2A</SUB>R) may be implicated in the pathophysiology of NMS in patients with positive HUT. Nothing is known about the purinergic profile of patients with positive ATP.</p>
</sec>
<sec><st>Patients and measures</st>
<p>This prospective study includes a consecutive series of patients with suspected NMS. All patients underwent both HUT and ATP. Before testing, samples were collected for measurement of baseline adenosine plasma level (APL) and expression.</p>
</sec>
<sec><st>Results</st>
<p>A total of 46 patients (25 men and 21 women) with a mean age of 57&plusmn;18&nbsp;years were enrolled. The HUT test was positive in 27 patients and the ATP test in 20. Both tests were positive in 9 and negative in 8. High APL was associated with high probability of positive HUT while low APL was associated with high probability of positive ATP. Expression of A<SUB>2A</SUB>R was lower in patients with positive ATP than in those with positive HUT.</p>
</sec>
<sec><st>Conclusion</st>
<p>These findings indicate that patients with NMS present different purinergic profiles and that responses to HUT and ATP are correlated with these profiles.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Deharo, J.-C., Mechulan, A., Giorgi, R., Franceschi, F., Prevot, S., Peyrouse, E., Condo, J., By, Y., Ruf, J., Brignole, M., Guieu, R.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301411</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301411</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Adenosine plasma level and A2A adenosine receptor expression: correlation with laboratory tests in patients with neurally mediated syncope]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Cardiac syncopey</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>855</prism:startingPage>
<prism:endingPage>859</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/860?rss=1">
<title><![CDATA[Plasma asymmetric dimethylarginine and mortality in patients with acute decompensation of chronic heart failure]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/860?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To investigate the prognostic value of circulating levels of asymmetric dimethylarginine (ADMA) in patients with acute decompensation of (New York Heart Association (NYHA) class III/IV) chronic heart failure and reduced left ventricular ejection fraction.</p>
</sec>
<sec><st>Design</st>
<p>Single-centre prospective observational study.</p>
</sec>
<sec><st>Setting</st>
<p>Tertiary referral centre.</p>
</sec>
<sec><st>Patients</st>
<p>A total of 651 consecutive and eligible hospitalised patients were studied. Patients were divided into four groups according to the quartiles of circulating levels of ADMA upon presentation.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Incidence of in-hospital (or 7-day in the case of prolonged hospitalisation), 31-day and 1-year cardiac mortality were the pre-specified study end points.</p>
</sec>
<sec><st>Results</st>
<p>Cumulative rates of in-hospital, 31-day and 1-year cardiac mortality were 10.6%, 18.7% and 36.4%, respectively. There was a gradual increased risk of in-hospital (p<SUB>for trend</SUB>=0.011), 31-day (p<SUB>for trend</SUB>=0.044) and 1-year (p<SUB>for trend</SUB>&lt;0.001) mortality with increasing ADMA quartiles. After adjustment for possible confounders, patients at the highest ADMA quartile were at significantly higher risk for in-hospital (p=0.042), 31-day (p=0.032) and 1-year (p&lt;0.001) mortality than those in the lowest quartile.</p>
</sec>
<sec><st>Conclusions</st>
<p>According to the present results, an elevated circulating level of ADMA is a strong independent predictor of short-term and long-term mortality in patients with acute decompensation of NYHA class III/IV chronic heart failure and reduced left ventricular ejection fraction. ADMA levels upon presentation may confer enhanced risk stratification in this setting.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Zairis, M. N., Patsourakos, N. G., Tsiaousis, G. Z., Theodossis Georgilas, A., Melidonis, A., Makrygiannis, S. S., Velissaris, D., Batika, P. C., Argyrakis, K. S., Tzerefos, S. P., Prekates, A. A., Foussas, S. G.]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301372</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301372</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Plasma asymmetric dimethylarginine and mortality in patients with acute decompensation of chronic heart failure]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Heart failure</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>860</prism:startingPage>
<prism:endingPage>864</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/865?rss=1">
<title><![CDATA[ASPIRE-2-PREVENT: a survey of lifestyle, risk factor management and cardioprotective medication in patients with coronary heart disease and people at high risk of developing cardiovascular disease in the UK]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/865?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To determine in patients with coronary heart disease (CHD) and people at high risk of developing cardiovascular disease (CVD) whether the Joint British Societies' guidelines on CVD prevention (JBS2) are followed in everyday clinical practice.</p>
</sec>
<sec><st>Design</st>
<p>A cross-sectional survey was undertaken of medical records and patient interviews and examinations at least 6&nbsp;months after the recruiting event or diagnosis using standardised instruments and a central laboratory for measurement of lipids and glucose.</p>
</sec>
<sec><st>Settings</st>
<p>The ASPIRE-2-PREVENT survey was undertaken in 19 randomly selected hospitals and 19 randomly selected general practices in 12 geographical regions in England, Northern Ireland, Wales and Scotland.</p>
</sec>
<sec><st>Patients</st>
<p>In hospitals, 1474 consecutive patients with CHD were identified and 676 (25.6% women) were interviewed. In general practice, 943 people at high CVD risk were identified and 446 (46.5% women) were interviewed.</p>
</sec>
<sec><st>Results</st>
<p>The prevalence of risk factors in patients with CHD and high-risk individuals was, respectively: smoking 14.1%, 13.3%; obesity 38%, 50.2%; not reaching physical activity target 83.3%, 85.4%; blood pressure &ge;130/80&nbsp;mm&nbsp;Hg (patients with CHD and self-reported diabetes) or &ge;140/85&nbsp;mm&nbsp;Hg (high-risk individuals) 46.9%, 51.3%; total cholesterol &ge;4&nbsp;mmol/l 52.6%, 78.7%; and diabetes 17.8%, 43.8%.</p>
</sec>
<sec><st>Conclusions</st>
<p>The potential among patients with CHD and individuals at high risk of developing CVD in the UK to achieve the JBS2 lifestyle and risk factor targets is considerable. CVD prevention needs a comprehensive multidisciplinary approach, addressing all aspects of lifestyle and risk factor management. The challenge is to engage and motivate cardiologists, physicians and other health professionals to routinely practice high quality preventive cardiology in a healthcare system which must invest in prevention.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kotseva, K., Jennings, C. S., Turner, E. L., Mead, A., Connolly, S., Jones, J., Bowker, T. J., Wood, D. A., On behalf of the ASPIRE-2-PREVENT Study Group]]></dc:creator>
<dc:date>2012-05-12T00:35:47-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-301603</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-301603</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Tobacco use]]></dc:subject>
<dc:title><![CDATA[ASPIRE-2-PREVENT: a survey of lifestyle, risk factor management and cardioprotective medication in patients with coronary heart disease and people at high risk of developing cardiovascular disease in the UK]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Secondary prevention of coronary disease</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>865</prism:startingPage>
<prism:endingPage>871</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/872?rss=1">
<title><![CDATA[Clinical prediction model for death prior to appropriate therapy in primary prevention implantable cardioverter defibrillator patients with ischaemic heart disease: the FADES risk score]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/872?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To construct a risk score out of baseline variables to estimate the risk of death without prior implantable cardioverter defibrillator (ICD) in primary prevention ICD patients with ischaemic heart disease.</p>
</sec>
<sec><st>Design</st>
<p>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 with ischaemic heart disease who received an ICD for primary prevention of sudden cardiac death at the Leiden University Medical Center, Leiden, The Netherlands in the period 1996&ndash;2009.</p>
</sec>
<sec><st>Main outcome measure</st>
<p>All-cause mortality without prior appropriate ICD therapy (anti-tachycardia pacing or shock).</p>
</sec>
<sec><st>Results</st>
<p>900 patients (87% men, mean age 64&plusmn;10&nbsp;years) were included in the analysis. During a median follow-up of 669&nbsp;days (IQR 363&ndash;1322&nbsp;days), 150 patients (17%) died and 191 (21%) patients received appropriate device therapy. 114 (13%) patients died without prior appropriate therapy. Stratification of the risk for death without prior appropriate therapy resulted in risk categorisation of patients as low, intermediate or high risk. NYHA &ge;III, advanced age, diabetes mellitus, left ventricular ejection fraction &le;25% and a history of smoking were significant independent predictors of death without appropriate ICD therapy. 5-year cumulative incidence for death without prior appropriate therapy ranged from 10% (95% CI 6% to 16%) in low-risk patients to 41% (95% CI 33% to 51%) in high-risk patients.</p>
</sec>
<sec><st>Conclusions</st>
<p>The risk of death without prior appropriate ICD therapy can be predicted in primary prevention ICD patients with ischaemic heart disease, which facilitates patient-tailored risk estimation.</p>
</sec>
]]></description>
<dc:creator><![CDATA[van Rees, J. B., Borleffs, C. J. W., van Welsenes, G. H., van der Velde, E. T., Bax, J. J., van Erven, L., Putter, H., van der Bom, J. G., Schalij, M. J.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-300632</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-300632</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology, Diabetes, Metabolic disorders, Tobacco use]]></dc:subject>
<dc:title><![CDATA[Clinical prediction model for death prior to appropriate therapy in primary prevention implantable cardioverter defibrillator patients with ischaemic heart disease: the FADES risk score]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Sudden cardiac death</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>872</prism:startingPage>
<prism:endingPage>877</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/878?rss=1">
<title><![CDATA[Heart transplantation: organisational aspects and current trends in immunosuppression--a view from Spain]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/878?rss=1</link>
<description><![CDATA[ <sec><st>Impact and limitations of heart transplantation: organisational aspects</st> <p>In spite of recent advances in the treatment of patients with end stage heart failure, heart transplantation (HTx) still remains the best option for patients under 70&nbsp;years of age suffering from this condition. It provides not only a dramatic change in expected survival, unequalled by any other intervention, but also a substantial improvement in the quality of life of patients.<cross-ref type="bib" refid="b1">1&ndash;3</cross-ref><cross-ref type="bib" refid="b2"></cross-ref><cross-ref type="bib" refid="b3"></cross-ref> <sup>w1</sup></p> <p>According to the <I>Global Observatory on Donation and Transplantation</I>, approximately 100 000 solid organ transplants are performed every year in the world, 5000 of which are HTx.<cross-ref type="bib" refid="b3">3</cross-ref> <sup>w2</sup> Data derived from the voluntary Registry of the International Society for Heart and Lung Transplantation (ISHLT) show that median survival after HTx is 10&nbsp;years, and &gt;90% of recipients live without significant activity limitations.<cross-ref type="bib" refid="b2">2</cross-ref> <sup>w1</sup> Similar results are shown in the exhaustive Spanish National...]]></description>
<dc:creator><![CDATA[Alonso-Pulpon, L., Segovia, J., Gomez-Bueno, M., Garcia-Pavia, P.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-300479</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-300479</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Education in Heart, Dilated cardiomyopathy, Cardiac surgery, Hypertrophic cardiomyopathy, Congenital heart disease, Drugs: cardiovascular system, Heart failure, Interventional cardiology, Acute coronary syndromes]]></dc:subject>
<dc:title><![CDATA[Heart transplantation: organisational aspects and current trends in immunosuppression--a view from Spain]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>878</prism:startingPage>
<prism:endingPage>889</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/890?rss=1">
<title><![CDATA[Cardiovascular highlights from non-cardiology journals]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/890?rss=1</link>
<description><![CDATA[ <sec><st>General cardiology</st><sec><st>Epinephrine use and cardiac arrest survival</st> <p>Whist epinephrine (epinephrine) is commonly used during cardiopulmonary resuscitation, both in and out of hospital, its effectiveness is poorly established. Although some animal studies have suggested a short term benefit due to increased cerebral and coronary perfusion, an increase in myocardial oxygen consumption and ventricular arrhythmias has also been documented. The purpose of this analysis was to determine how the use of epinephrine in cardiopulmonary resuscitation performed before hospital arrival (out-of-hospital arrest) was associated with immediate and 1-month survival.</p> <p>The study was a prospective, non-randomised, observational propensity analysis of data from 417 188 out-of-hospital cardiac arrests in Japan between 2005 and 2008. The main outcome measures were the return of spontaneous circulation before hospital arrival, survival at one month after cardiac arrest, survival with good or moderate cerebral performance, and survival with no, mild, or only moderate neurological disability. Outcomes were compared between...]]></description>
<dc:creator><![CDATA[Lindsay, A. C.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302289</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302289</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cardiovascular highlights from non-cardiology journals]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Journal scan</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>890</prism:startingPage>
<prism:endingPage>890</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/891-a?rss=1">
<title><![CDATA[It is usually the cigarettes that do it]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/891-a?rss=1</link>
<description><![CDATA[ <p><b>To the Editor</b> It should be remembered that in the INTERHEART study, nine risk factors accounted for 90% of the population attributable risk of a myocardial infarction in men and 94% in women&mdash;these did not include family history.<cross-ref type="bib" refid="b1">1</cross-ref> Thus, on a population basis, I would disagree with the authors that &lsquo;A positive family history of premature coronary artery disease (CAD) is an important risk factor for cardiovascular disease (CVD)&rsquo;. It is, however, obvious that &lsquo;The associated risk increases further when relatives are affected at a younger age&rsquo;&mdash;and thus the paper asks an important question in trying to ascertain whether arterial stiffness might play a role in risk prediction within families with genuinely premature CAD.</p> <p>On that point of genuineness, rarely do my colleagues ask the patient whether that relative who suffered a heart attack in their 50s smoked or had diabetes. The &lsquo;positive family history&rsquo; of CAD...]]></description>
<dc:creator><![CDATA[Zaman, M. J. S.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301944</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301944</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[It is usually the cigarettes that do it]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>891</prism:startingPage>
<prism:endingPage>891</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/891-b?rss=1">
<title><![CDATA[The Authors' reply]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/891-b?rss=1</link>
<description><![CDATA[ <p><b>The Authors' reply</b> Recently, we reported a case-control study in which we found that both patients with premature coronary artery disease (CAD) and their &lsquo;healthy&rsquo; asymptomatic first degree relatives had increased arterial stiffness compared with controls.<cross-ref type="bib" refid="b1">1</cross-ref> Noteworthy, these patients and their first degree relatives had at least two prematurely affected relatives within their family. With interest we read the comment by Zaman<cross-ref type="bib" refid="b2">2</cross-ref> who disputes that a family history of premature CAD is an important risk factor on a population base, for which he refers to the INTERHEART study.<cross-ref type="bib" refid="b3">3</cross-ref> However, we have several arguments to oppose his statement.</p> <p>We agree that the INTERHEART study shows that a combination of nine risk factors accounts for 90% of the population attributable risk for myocardial infarction, which did not include family history. However, even in the INTERHEART study, family history was an independent risk factor for myocardial...]]></description>
<dc:creator><![CDATA[Mulders, T. A., Pinto-Sietsma, S.-J.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301945</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301945</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[The Authors' reply]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>891</prism:startingPage>
<prism:endingPage>891</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/891-c?rss=1">
<title><![CDATA[Balloons and atrial fibrillation]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/891-c?rss=1</link>
<description><![CDATA[ <p><b>To the Editor</b> This excellent short review article<cross-ref type="bib" refid="b1">1</cross-ref> is written by someone who has a self-declared interest in the manufacturer of the &lsquo;laser balloon&rsquo; (Cardiofocus Inc, Marlborough, MA, USA). It is unsurprising therefore to see that he gives the cryoballoon, a rival technology, short shrift by dismissing it as &lsquo;having problems&rsquo;. In fact, there are published data showing that it is probably the most successful approach to paroxysmal atrial fibrillation (PAF) so-far invented.<cross-ref type="bib" refid="b2">2</cross-ref> Acute success was achieved in over 98% of 924 patients. The one year freedom from PAF rate is over 70% discounting recurrences inside a 3-month blanking period.</p> <p>Clinical pulmonary vein stenosis was 0.17%. Persistent phrenic nerve palsy beyond one year occurred in only 0.37%. It is also a very simple technique not involving any ancillary technology such as angioscopy and no additional certification is required (in the UK, laser training and certification...]]></description>
<dc:creator><![CDATA[Ward, D. E.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301956</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301956</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Balloons and atrial fibrillation]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>891</prism:startingPage>
<prism:endingPage>892</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/892?rss=1">
<title><![CDATA[The Author's reply]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/892?rss=1</link>
<description><![CDATA[ <p><b>The Author's reply</b> Dr Ward feels that I have given &lsquo;short shrift&rsquo; to the cryoballoon in my commentary on the National Institute of Health and Clinical Excellence (NICE) guidelines for laser balloon ablation.<cross-ref type="bib" refid="b1">1</cross-ref> <cross-ref type="bib" refid="b2">2</cross-ref> I certainly welcome Dr Wards' comments and summary of cryoballoon efficacy, but feel a few additional comments are necessary.</p> <p>First, Dr Ward points out that my comments may be biased because I have a &lsquo;vested interest&rsquo; in the laser balloon. It should be noted that while I have received an investigator initiated research grant to perform preclinical work with the laser balloon (as declared in the editorial), I have no other consulting role with the company nor have I received any payment for work with the company. As a physician who spends a large part of my time performing atrial fibrillation (AF) ablations, my main goal is to help develop any...]]></description>
<dc:creator><![CDATA[Gerstenfeld, E. P.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301957</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301957</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[The Author's reply]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>892</prism:startingPage>
<prism:endingPage>892</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/98/11/893?rss=1">
<title><![CDATA[Left ventricular apical mechanics during ectopy in an asymptomatic athlete]]></title>
<link>http://heart.bmj.com/cgi/content/short/98/11/893?rss=1</link>
<description><![CDATA[ <p>The frequent occurrence of ventricular ectopics in athletes is thought to be a part of the physiological adaptation process as a consequence of regular exercise training.<cross-ref type="bib" refid="b1">1</cross-ref> However, the acute impact of a premature ventricular contraction (PVC) on the mechanical sequence of the myocardium has never been shown. Here, we present data of left ventricular (LV) apical function during a PVC in a 20-year-old healthy, asymptomatic male triathlete (body mass: 76&nbsp;kg; height: 1.81&nbsp;m; maximal oxygen uptake (VO<SUB>2</SUB>max): 66.4&nbsp;ml/kg/min). Data were analysed using novel speckle tracking echocardiography (video 1). LV apical rotation and strain were normal prior to the PVC (<cross-ref type="fig" refid="fig1">figure 1</cross-ref>). Spontaneous ectopy during repolarisation caused a brief reversal of the normal diastolic mechanics (arrow A). Furthermore, reversed apical rotation was immediately followed by an over-rotation of the apex within the same cardiac cycle (arrow B). The following cardiac cycle was characterised by a markedly enhanced...]]></description>
<dc:creator><![CDATA[Stohr, E. J., Shave, R.]]></dc:creator>
<dc:date>2012-05-12T00:35:48-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301737</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301737</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Left ventricular apical mechanics during ectopy in an asymptomatic athlete]]></dc:title>
<prism:publicationDate>2012-06-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>98</prism:volume>
<prism:number>11</prism:number>
<prism:startingPage>893</prism:startingPage>
<prism:endingPage>894</prism:endingPage>
</item>
</rdf:RDF>
