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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/99/12/821?rss=1">
<title><![CDATA[Coronary bypass grafting with bilateral internal thoracic arteries]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/821?rss=1</link>
<description><![CDATA[ <sec id="s1"> <p>In 1999, a seminal paper from the Cleveland Clinic demonstrated that patients treated with two versus one internal thoracic artery (ITA) coronary grafts have better long-term survival and freedom from reoperation.<cross-ref type="bib" refid="R1">1</cross-ref> This finding was later confirmed in a systematic review<cross-ref type="bib" refid="R2">2</cross-ref> and in a number of more recent studies.<cross-ref type="bib" refid="R3">3&ndash;5</cross-ref><cross-ref type="bib" refid="R4"></cross-ref><cross-ref type="bib" refid="R5"></cross-ref> Puskas and colleagues<cross-ref type="bib" refid="R3">3</cross-ref> have reported an impressive (35%) reduction in the long-term hazard of death in patients with and without diabetes undergoing bilateral internal thoracic artery (BITA) grafting. In a propensity-matched analysis of 1856 patients Grau <I>et al</I><cross-ref type="bib" refid="R4">4</cross-ref> showed a 10% survival benefit at 10&nbsp;years, and 18% at 15&nbsp;years for BITA grafting. Glineur <I>et al</I><cross-ref type="bib" refid="R5">5</cross-ref> showed that the survival benefit following BITA grafting is sustained up to 25&nbsp;years. The available data consistently show better survival with two ITA grafts, especially when the second...]]></description>
<dc:creator><![CDATA[Falk, V.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303961</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303961</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology]]></dc:subject>
<dc:title><![CDATA[Coronary bypass grafting with bilateral internal thoracic arteries]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>821</prism:startingPage>
<prism:endingPage>821</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/822?rss=1">
<title><![CDATA[Transcatheter aortic valve implantation: what's the bleeding problem?]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/822?rss=1</link>
<description><![CDATA[ <sec id="s1"> <p>The importance of bleeding and its sequelae have been increasingly recognised by interventional cardiologists. We are undertaking increasingly complex percutaneous interventions, performed upon higher-risk patients, who are more elderly with a greater range of comorbidities,<cross-ref type="bib" refid="R1">1</cross-ref> and using multiple anticoagulant pharmacotherapies,<cross-ref type="bib" refid="R2">2</cross-ref> which may all increase susceptibility to bleeding. The advent of transcatheter aortic valve implantation (TAVI) has allowed cardiologists and surgeons to offer treatment for aortic valve disease to a similarly high-risk cohort of patients. The PARTNER randomised trial having demonstrated a survival benefit,<cross-ref type="bib" refid="R3">3</cross-ref> the challenge is now to improve the safety profile of the procedure, and addressing the risk of bleeding is paramount to this.</p> <p>Borz <I>et al</I><cross-ref type="bib" refid="R4">4</cross-ref> present data from a single centre using the Edwards bioprosthesis (Edwards Lifesciences, Irvine, California, USA). They report notable bleeding and life-threatening bleeding (LTB) rates of 27.6% and 13.2%, respectively. Their survival...]]></description>
<dc:creator><![CDATA[Khawaja, M. Z., Redwood, S. R.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303437</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303437</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Interventional cardiology, Acute coronary syndromes, Aortic valve disease, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Transcatheter aortic valve implantation: what's the bleeding problem?]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>822</prism:startingPage>
<prism:endingPage>823</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/824?rss=1">
<title><![CDATA[Can NICE prevent diabetes?]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/824?rss=1</link>
<description><![CDATA[ <sec id="s1"><st>The rising tide</st> <p>Diabetes (diagnosed or undiagnosed) currently affects 7.4% of the UK population, and is projected to reach 10% by 2030.<cross-ref type="bib" refid="R1">1</cross-ref> Conventional wisdom (with just a hint of moral censure) attributes the rising prevalence of diabetes to obesity and physical inactivity. It would however be just as true to lay the blame on increasing longevity, for glucose tolerance deteriorates with age, and we live much longer than we did. By their ninth decade, 55% of European males and 74% of females will have diabetes, undiagnosed diabetes or some form of glucose intolerance.<cross-ref type="bib" refid="R2">2</cross-ref> Diabetes is also on the increase because of simpler diagnostic tests, lower diagnostic thresholds and health policies that reward primary care physicians for finding new cases. Last but not least, those with diabetes now live longer following diagnosis, whether due to better care or lead-time bias,<cross-ref type="bib" refid="R3">3</cross-ref> thus adding to...]]></description>
<dc:creator><![CDATA[Gale, E. A. M.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302763</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302763</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Clinical diagnostic tests, Epidemiology, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Can NICE prevent diabetes?]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>824</prism:startingPage>
<prism:endingPage>826</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/827?rss=1">
<title><![CDATA[Thalassaemia major and the heart: a toxic cardiomyopathy tamed?]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/827?rss=1</link>
<description><![CDATA[ <sec id="s1"><st>Introduction</st> <p>Disorders of haemoglobin synthesis, such as thalassaemia, are the most common monogenetic disorders worldwide. When first described, thalassaemia major (TM) was universally fatal in childhood, but after the adoption of regular blood transfusion, survival until early teenage and adulthood was to be expected. Sadly as these individuals aged organ failure followed, due to the accumulated iron secondary to regular blood transfusion. Principal among the tissues affected by iron overload is the heart and even to the present day, heart disease accounts for the overwhelming majority of premature deaths in this population. For nearly four decades the only available treatment was the demanding regime of parenteral chelation therapy, required on a daily basis, to achieve growth, development and survival with limited or no organ damage. Despite the adoption of these treatment strategies the outlook for thalassaemia patients remained poor, with a 30% to 40% mortality occurring between late...]]></description>
<dc:creator><![CDATA[Walker, J. M.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302857</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302857</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Thalassaemia major and the heart: a toxic cardiomyopathy tamed?]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Reviews</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>827</prism:startingPage>
<prism:endingPage>834</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/835?rss=1">
<title><![CDATA[Are arterial grafts superior to vein grafts for revascularisation of the right coronary system? A systematic review]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/835?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>The optimal conduit choice in revascularisation of the right coronary system (RCA) remains uncertain. This study aims to identify if arterial grafts are superior to saphenous vein (SV) grafts and whether graft failure rates vary between proximal and distal RCA anastomoses.</p>
</sec>
<sec><st>Methods</st>
<p>29 studies identified by systematic review were analysed for study quality and length of follow-up using Bayesian hierarchical random effects modelling. Heterogeneity was assessed and sensitivity analysis performed. Primary endpoints were graft patency at early, mid and late-term follow-up when compared with SV grafts.</p>
</sec>
<sec><st>Results</st>
<p>There was no difference in early failure of radial artery (RA) or right gastroepiploic artery grafts when compared with SV (OR 0.82, 95% CI (0.14 to 2.68) and OR 1.19 (0.08 to 4.66), respectively). However, mid-term ORs based on observational study data demonstrated increased graft failure with right gastroepiploic artery and right internal thoracic artery compared with SV (OR 2.76 (1.26 to 5.48) and OR 2.07 (0.96 to 3.98), respectively), although right internal thoracic artery did not achieve statistical significance. No significant difference was observed in late graft failure for RA compared with SV (OR 0.47 (0.09 to 1.41)) without study-type disparity. However, simplified statistical pooling revealed significantly lower graft failure was observed with RA grafts to the proximal RCA when compared with SV (<sup>2</sup> 6.15, p=0.01).</p>
</sec>
<sec><st>Conclusions</st>
<p>Arterial grafts do not demonstrate a beneficial reduction of angiographic graft failure when compared with SV grafts on the RCA with the exception of RA to the proximal RCA. Future research should focus on clinical and patient-reported endpoints to identify any benefits of RCA arterial revascularisation.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Athanasiou, T., Ashrafian, H., Mukherjee, D., Harling, L., Okabayashi, K.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303225</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303225</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Are arterial grafts superior to vein grafts for revascularisation of the right coronary system? A systematic review]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Systematic review</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>835</prism:startingPage>
<prism:endingPage>842</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/843?rss=1">
<title><![CDATA[CHADS2 and CHA2DS2-VASc score to assess risk of stroke and death in patients paced for sick sinus syndrome]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/843?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>The risk of stroke in patients with atrial fibrillation (AF) can be assessed by use of the CHADS<SUB>2</SUB> and the CHA<SUB>2</SUB>DS<SUB>2</SUB>-VASc score system. We hypothesised that these risk scores and their individual components could also be applied to patients paced for sick sinus syndrome (SSS) to evaluate risk of stroke and death.</p>
</sec>
<sec><st>Design</st>
<p>Prospective cohort study.</p>
</sec>
<sec><st>Settings</st>
<p>All Danish pacemaker centres and selected centres in the UK and Canada.</p>
</sec>
<sec><st>Patients</st>
<p>Risk factors were recorded prior to pacemaker implantation in 1415 patients with SSS participating in the Danish Multicenter Randomized Trial on Single Lead Atrial Pacing versus Dual Chamber Pacing in Sick Sinus Syndrome (Danpace) trial. Development of stroke was assessed at follow-up visits and by evaluation of patient charts. Mortality was assessed from the civil registration system.</p>
</sec>
<sec><st>Interventions</st>
<p>Patients were randomised to AAIR (N=707) or DDDR pacing (N=708).</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Stroke and death during follow-up.</p>
</sec>
<sec><st>Results</st>
<p>Mean follow-up was 4.3&plusmn;2.5&nbsp;years. In the AAIR group 6.9% patients developed stroke versus 6.1% in the DDDR group (NS). There was a significant association between CHADS<SUB>2</SUB> score and the development of stroke (HR 1.41; 95% CI 1.22 to 1.64, p&lt;0.001). CHA<SUB>2</SUB>DS<SUB>2</SUB>-VASc score was also significantly associated with stroke (HR 1.25; CI 1.12 to 1.40, p&lt;0.001). CHADS<SUB>2</SUB> score (HR 1.46; CI 1.36 to 1.56, p&lt;0.001) and CHA<SUB>2</SUB>DS<SUB>2</SUB>-VASc score (HR 1.39; CI 1.31 to 1.46, p&lt;0.001) were associated with mortality. Results were still significant after adjusting for AF and anticoagulation therapy.</p>
</sec>
<sec><st>Conclusions</st>
<p>CHADS<SUB>2</SUB> and CHA<SUB>2</SUB>DS<SUB>2</SUB>-VASc score are associated with increased risk of stroke and death in patients paced for SSS irrespective of the presence of AF.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Svendsen, J. H., Nielsen, J. C., Darkner, S., Jensen, G. V. H., Mortensen, L. S., Andersen, H. R., on behalf of the DANPACE Investigators]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303695</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303695</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[CHADS2 and CHA2DS2-VASc score to assess risk of stroke and death in patients paced for sick sinus syndrome]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Clinical trials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>843</prism:startingPage>
<prism:endingPage>848</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/849?rss=1">
<title><![CDATA[Bilateral internal mammary artery grafts, mortality and morbidity: an analysis of 1 526 360 coronary bypass operations]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/849?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>The objective of this study was to investigate the impact of bilateral internal mammary artery (BIMA) on early outcomes after coronary artery bypass grafting.</p>
</sec>
<sec><st>Design</st>
<p>Retrospective database analysis.</p>
</sec>
<sec><st>Setting</st>
<p>US hospitals.</p>
</sec>
<sec><st>Patients</st>
<p>1&nbsp;526&nbsp;360 patients (mean age 65&nbsp;years, 73% male) from the Nationwide Inpatient Sample from 2002&ndash;2008 who underwent isolated coronary artery bypass grafting with at least one internal mammary artery.</p>
</sec>
<sec><st>Interventions</st>
<p>Single versus BIMA bypass grafting.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Inhospital mortality, deep sternal wound infection (DSWI).</p>
</sec>
<sec><st>Results</st>
<p>The rate of BIMA use was 3.9%. Use of BIMA was independently associated with slightly lower inhospital mortality (unadjusted rate 1.1% vs 1.7%, adjusted OR 0.86, 95% CI 0.79 to 0.93). The DSWI rate was 1.4%. The independent predictors of DSWI were female gender (OR 1.06), congestive heart failure (OR 6.22), chronic pulmonary disease (OR 1.57), obesity (OR 1.17), diabetes mellitus (OR 1.04; OR 1.51 with chronic complication) and chronic renal failure (OR 2.13; OR 2.63 with dialysis). The use of BIMA was not an independent predictor of DSWI (OR 1.03, 95% CI 0.96 to 1.10). BIMA was associated with higher incidence of DSWI in patients with chronic complications of diabetes mellitus (OR 1.90, 95% CI 1.51 to 2.41).</p>
</sec>
<sec><st>Conclusions</st>
<p>BIMA grafting is associated with increased risk of DSWI only in patients with severe, chronic diabetes. The incremental morbidity and mortality of DSWI does not justify denial of BIMA in the majority of patients.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Itagaki, S., Cavallaro, P., Adams, D. H., Chikwe, J.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303672</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303672</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Heart failure, Interventional cardiology, Epidemiology, Diabetes, Metabolic disorders]]></dc:subject>
<dc:title><![CDATA[Bilateral internal mammary artery grafts, mortality and morbidity: an analysis of 1 526 360 coronary bypass operations]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Cardiovascular surgery</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>849</prism:startingPage>
<prism:endingPage>853</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/854?rss=1">
<title><![CDATA[Bilateral internal mammary artery bypass grafting: long-term clinical benefits in a series of 1000 patients]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/854?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>Bilateral internal mammary arteries (BIMA) remain widely underused in coronary artery bypass grafting (CABG). In this study, we aim to investigate the early and long-term outcomes of BIMA grafts in isolated CABGs.</p>
</sec>
<sec><st>Design</st>
<p>Single-centre retrospective observational study.</p>
</sec>
<sec><st>Setting</st>
<p>University Hospital, Nancy.</p>
</sec>
<sec><st>Patients</st>
<p>1000 consecutive patients undergoing elective, isolated, primary, multiple CABGs using BIMA grafts and supplemental venous grafts for multi-vessel coronary disease.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>In-hospital mortality and major morbidity, and long-term all-cause mortality.</p>
</sec>
<sec><st>Results</st>
<p>Mean age of the overall population was 60&plusmn;15&nbsp;years. A left ventricular ejection fraction (LVEF) &le;45% was found in 28% of the patients and 27.1% of the patients were diabetics. Comorbidities were represented by chronic renal failure, chronic obstructive pulmonary disease and peripheral artery disease in 11, 11.7 and 27.3% of the cases, respectively. The in-hospital mortality rate was 2.8%. Early postoperative morbidity included myocardial infarction (2.2%), stroke (0.9%), mesenteric ischaemia (0.7%) and mediastinitis (2.2%).</p>
<p>The Kaplan&ndash;Meier 8-year survival rates for patients less than 65 and between 65 and 74&nbsp;years of age were 88% and 66%, respectively (p&lt;0.01). Multiple regression analysis showed that patients&rsquo; age 65&nbsp;years or greater at baseline (OR 2.3; 95% CI 1.3 to 4, p&lt;0.001), acute coronary syndrome (OR 1.9; 95% CI 1.1 to 3.4, p=0.02), chronic renal failure (OR 2.7; 95% CI 1.4 to 5.2, p&lt;0.001), peripheral artery disease (OR 3.1; 95% CI 1.8 to 5.5, p&lt;0.001) and LVEF &le;45% (OR 2.6; 95% CI 1.4 to 4.5, p&lt;0.001) were independent predictors of long-term cardiovascular mortality.</p>
</sec>
<sec><st>Conclusions</st>
<p>Our longitudinal analysis presents encouraging data concerning operative risk of BIMA grafting and provides excellent long-term survival in appropriately selected patients.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Popovic, B., Voillot, D., Maureira, P., Vanhuyse, F., Agrinier, N., Aliot, E., Folliguet, T., Villemot, J. P.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303466</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303466</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[Bilateral internal mammary artery bypass grafting: long-term clinical benefits in a series of 1000 patients]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Cardiovascular surgery</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>854</prism:startingPage>
<prism:endingPage>859</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/860?rss=1">
<title><![CDATA[Incidence, predictors and impact of bleeding after transcatheter aortic valve implantation using the balloon-expandable Edwards prosthesis]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/860?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To evaluate the incidence, predictors and impact of bleeding after transcatheter aortic valve implantation (TAVI).</p>
</sec>
<sec><st>Design</st>
<p>Single-centre prospective observational study.</p>
</sec>
<sec><st>Setting</st>
<p>Charles Nicolle University Hospital, Rouen, France.</p>
</sec>
<sec><st>Interventions</st>
<p>We included 250 consecutive patients who underwent TAVI between May 2006 and October 2011. All procedures were performed using Edwards SAPIEN and SAPIEN XT valves via transfemoral (TF) and transapical (TA) routes. Surgical cutdown was used for TF access when implanting the SAPIEN valve, while percutaneous access was used for SAPIEN XT implantation. Life-threatening bleeding (LTB), major and minor bleeding and other complications were defined using Valve Academic Research Consortium criteria.</p>
</sec>
<sec><st>Results</st>
<p>TAVI was performed via TF access in 190 cases (76%) and the SAPIEN XT valve was used in 123 cases (49.2%). Bleeding after TAVI was noted in 68 patients (27.2%): LTB in 33 (13.2%), major bleeding in 23 (9.2%) and minor bleeding in 12 (4.8%). By multivariate analysis, only TA access was an independent predictor of LTB (OR 3.7, 95% CI 1.73 to 7.9, p=0.001). Patients presenting with LTB after TAVI had a higher 30-day mortality (33.3% vs 3.7%, p&lt;0.001) and 1-year mortality (54% vs 18%, p&lt;0.001). LTB was an independent predictive factor of 1-year mortality (HR 2.54, 95% CI 1.3 to 4.9, p=0.002).</p>
</sec>
<sec><st>Conclusions</st>
<p>Bleeding is a frequent complication of TAVI, occurring in 27% of cases. LTB is associated with higher 30-day and 1-year mortality.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Borz, B., Durand, E., Godin, M., Tron, C., Canville, A., Litzler, P.-Y., Bessou, J.-P., Cribier, A., Eltchaninoff, H.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303095</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303095</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Incidence, predictors and impact of bleeding after transcatheter aortic valve implantation using the balloon-expandable Edwards prosthesis]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Valvular heart disease</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>860</prism:startingPage>
<prism:endingPage>865</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/866?rss=1">
<title><![CDATA[Development and validation of a prediction rule for recurrent vascular events based on a cohort study of patients with arterial disease: the SMART risk score]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/866?rss=1</link>
<description><![CDATA[
<sec><st>Objectives</st>
<p>To enable risk stratification of patients with various types of arterial disease by the development and validation of models for prediction of recurrent vascular event risk based on vascular risk factors, imaging or both.</p>
</sec>
<sec><st>Design</st>
<p>Prospective cohort study.</p>
</sec>
<sec><st>Setting</st>
<p>University Medical Centre.</p>
</sec>
<sec><st>Patients</st>
<p>5788 patients referred with various clinical manifestations of arterial disease between January 1996 and February 2010.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>788 recurrent vascular events (ie, myocardial infarction, stroke or vascular death) that were observed during 4.7 (IQR 2.3 to 7.7) years&rsquo; follow-up.</p>
</sec>
<sec><st>Results</st>
<p>Three Cox proportional hazards models for prediction of 10-year recurrent vascular event risk were developed based on age and sex in addition to clinical parameters (model A), carotid ultrasound findings (model B) or both (model C). Clinical parameters were medical history, current smoking, systolic blood pressure and laboratory biomarkers. In a separate part of the dataset, the concordance statistic of model A was 0.68 (95% CI 0.64 to 0.71), compared to 0.64 (0.61 to 0.68) for model B and 0.68 (0.65 to 0.72) for model C. Goodness-of-fit and calibration of model A were adequate, also in separate subgroups of patients having coronary, cerebrovascular, peripheral artery or aneurysmal disease. Model A predicted &lt;20% risk in 59% of patients, 20&ndash;30% risk in 19% and &gt;30% risk in 23%.</p>
</sec>
<sec><st>Conclusions</st>
<p>Patients at high risk for recurrent vascular events can be identified based on readily available clinical characteristics.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Dorresteijn, J. A. N., Visseren, F. L. J., Wassink, A. M. J., Gondrie, M. J. A., Steyerberg, E. W., Ridker, P. M., Cook, N. R., van der Graaf, Y., on behalf of the SMART Study Group, Algra, Grobbee, Rutten, Moll, Kappelle, Mali, Doevendans]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303640</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303640</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Hypertension, Acute coronary syndromes, Clinical diagnostic tests, Epidemiology, Tobacco use]]></dc:subject>
<dc:title><![CDATA[Development and validation of a prediction rule for recurrent vascular events based on a cohort study of patients with arterial disease: the SMART risk score]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Prognosis research</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>866</prism:startingPage>
<prism:endingPage>872</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/873?rss=1">
<title><![CDATA[Cost-effectiveness of cardiovascular magnetic resonance in the diagnosis of coronary heart disease: an economic evaluation using data from the CE-MARC study]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/873?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To evaluate the cost-effectiveness of diagnostic strategies for coronary heart disease (CHD) derived from the CE-MARC study.</p>
</sec>
<sec><st>Design</st>
<p>Cost-effectiveness analysis using a decision analytic model to compare eight strategies for the diagnosis of CHD.</p>
</sec>
<sec><st>Setting</st>
<p>Secondary care out-patients (Cardiology Department).</p>
</sec>
<sec><st>Patients</st>
<p>Patients referred to cardiologists for the further evaluation of symptoms thought to be angina pectoris.</p>
</sec>
<sec><st>Interventions</st>
<p>Eight different strategies were considered, including different combinations of exercise treadmill testing (ETT), single-photon emission CT (SPECT), cardiovascular magnetic resonance (CMR) and coronary angiography (CA).</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Costs expressed as UK sterling in 2010&ndash;2011 prices and health outcomes in quality-adjusted life-years (QALYs). The time horizon was 50&nbsp;years.</p>
</sec>
<sec><st>Results</st>
<p>Based on the characteristics of patients in the CE-MARC study, only two strategies appear potentially cost-effective for diagnosis of CHD, both including CMR. The choice is between two strategies: one in which CMR follows a positive or inconclusive ETT, followed by CA if CMR is positive or inconclusive (Strategy 3 in the model); and the other where CMR is followed by CA if CMR is positive or inconclusive (Strategy 5 in the model). The more cost-effective of these two rests on the threshold cost per QALY gained below which health systems define an intervention as cost-effective. Strategy 3 appears cost-effective at the lower end of the threshold range used in the UK (&pound;20&nbsp;000 per QALY gained), while Strategy 5 appears cost-effective at the higher end of the threshold range (&pound;30&nbsp;000 per QALY). The results are robust to various sources of uncertainty although prior likelihood of CHD requiring revascularisation and the rate at which false negative patients are eventually appropriately identified do impact upon the results.</p>
</sec>
<sec><st>Conclusions</st>
<p>The CE-MARC study showed that CMR had superior diagnostic accuracy to SPECT and concluded that CMR should be more widely used in the investigation of patients with CHD. The economic evaluation results show that using CMR is also a cost-effective strategy and supports the wider adoption of this modality.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Walker, S., Girardin, F., McKenna, C., Ball, S. G., Nixon, J., Plein, S., Greenwood, J. P., Sculpher, M.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303624</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303624</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Stable coronary heart disease, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Cost-effectiveness of cardiovascular magnetic resonance in the diagnosis of coronary heart disease: an economic evaluation using data from the CE-MARC study]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Cardiovascular imaging</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>873</prism:startingPage>
<prism:endingPage>881</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/882?rss=1">
<title><![CDATA[Elevated resting heart rate, physical fitness and all-cause mortality: a 16-year follow-up in the Copenhagen Male Study]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/882?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To examine whether elevated resting heart rate (RHR) is an independent risk factor for mortality or a mere marker of physical fitness (VO<SUB>2</SUB>Max).</p>
</sec>
<sec><st>Methods</st>
<p>This was a prospective cohort study: the Copenhagen Male Study, a longitudinal study of healthy middle-aged employed men. Subjects with sinus rhythm and without known cardiovascular disease or diabetes were included. RHR was assessed from a resting ECG at study visit in 1985&ndash;1986. VO<SUB>2</SUB>Max was determined by the &Aring;strand bicycle ergometer test in 1970&ndash;1971. Subjects were classified into categories according to level of RHR. Associations with mortality were studied in multivariate Cox models adjusted for physical fitness, leisure-time physical activity and conventional cardiovascular risk factors.</p>
</sec>
<sec><st>Results</st>
<p>2798 subjects were followed for 16&nbsp;years. 1082 deaths occurred. RHR was inversely related to physical fitness (p&lt;0.001). Overall, increasing RHR was highly associated with mortality in a graded manner after adjusting for physical fitness, leisure-time physical activity and other cardiovascular risk factors. Compared to men with RHR &le;50, those with RHR &gt;90 had an HR (95% CI) of 3.06 (1.97 to 4.75). With RHR as a continuous variable, risk of mortality increased with 16% (10&ndash;22) per 10 beats per minute (bpm). There was a borderline interaction with smoking (p=0.07); risk per 10&nbsp;bpm increase in RHR was 20% (12&ndash;27) in smokers, and 14% (4&ndash;24) in non-smokers.</p>
</sec>
<sec><st>Conclusions</st>
<p>Elevated RHR is a risk factor for mortality independent of physical fitness, leisure-time physical activity and other major cardiovascular risk factors.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Jensen, M. T., Suadicani, P., Hein, H. O., Gyntelberg, F.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303375</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303375</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Epidemiology, Tobacco use]]></dc:subject>
<dc:title><![CDATA[Elevated resting heart rate, physical fitness and all-cause mortality: a 16-year follow-up in the Copenhagen Male Study]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>882</prism:startingPage>
<prism:endingPage>887</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/888?rss=1">
<title><![CDATA[Surgical ablation in atrial fibrillation: in which patients?]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/888?rss=1</link>
<description><![CDATA[ <sec id="s1"><st>Concomitant atrial fibrillation</st> <p>It has been 21&nbsp;years since the first description of the maze procedure by James Cox.<cross-ref type="bib" refid="R1">1</cross-ref> At that time the hypothesis of multiple independent wavelets propagating randomly through both atria was the most accepted dominant atrial fibrillation (AF) mechanism; there was no knowledge of the importance of focal triggers within the pulmonary veins, the influence of different local activation rates, frequency gradients, the autonomic nervous system, or genetics in the genesis of AF. The Cox maze procedure was designed basically with two aims: to reconduct the electrical impulse into dead-end paths, and to avoid its rotation on round structures like the mitral and tricuspid annuli, both venae cavae and atrial appendages. Interestingly, it still is the most successful therapy for controlling AF, with over 90% of sinus rhythm (SR) recovery in patients with lone AF,<cross-ref type="bib" refid="R2">2</cross-ref> but the aggressiveness of the original procedure...]]></description>
<dc:creator><![CDATA[Castella, M.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302044</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302044</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Atrial fibrillation, Education in Heart, Drugs: cardiovascular system, Interventional cardiology]]></dc:subject>
<dc:title><![CDATA[Surgical ablation in atrial fibrillation: in which patients?]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>888</prism:startingPage>
<prism:endingPage>892</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/893?rss=1">
<title><![CDATA[Cardiovascular highlights from non-cardiology journals]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/893?rss=1</link>
<description><![CDATA[ <sec id="s1"><st>Heart failure, cardiovascular imaging, general cardiology, electrophysiology, molecular cardiology</st><sec id="s1a"><st>Long QT syndrome mutations and intrauterine fetal death</st> <p>Intrauterine fetal death occurs in approximately 1 in every 160 pregnancies; postmortem evaluation often fails to find an underlying cause. The objective of this paper was to determine the spectrum and prevalence of mutations in the three most common Long QT syndrome (LQTS) susceptible genes in a cohort of cases of unexplained intrauterine death.</p> <p>Retrospective post-mortem genetic testing was carried out on 91 unexplained intrauterine fetal deaths collected between 2006 and 2012. Publically available exome databases were assessed for the general population frequency of identified genetic variants. Mutations analysis was performed by liquid chromatography and DNA sequencing. Functional analysis of novel mutations was performed using heterologous expression and patch-clamp recording.</p> <p>The three LQTS missense mutations (KCNQ1, p.A283T; KCNQ1, p.R397W; and KCNH2[1b], p.R25W) were discovered in three intrauterine fetal deaths. Both KV7.1-A283T...]]></description>
<dc:creator><![CDATA[Lindsay, A. C.]]></dc:creator>
<dc:date>2013-05-13T22:40:08-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-304193</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-304193</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cardiovascular highlights from non-cardiology journals]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Journal scan</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>893</prism:startingPage>
<prism:endingPage>893</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/894?rss=1">
<title><![CDATA[Response: Raised troponin levels in COPD: a possible mechanism]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/894?rss=1</link>
<description><![CDATA[ <sec> <p><b>The Authors' reply</b> We appreciate Dr Orde&rsquo;s interest in potential mechanisms underlying the raised circulating troponin levels in COPD.<cross-ref type="bib" refid="heartjnl-2013-303662R1">1&ndash;4</cross-ref><cross-ref type="bib" refid="heartjnl-2013-303662R2"></cross-ref><cross-ref type="bib" refid="heartjnl-2013-303662R3"></cross-ref><cross-ref type="bib" refid="heartjnl-2013-303662R4"></cross-ref> Based on his own work,<cross-ref type="bib" refid="heartjnl-2013-303662R4">4</cross-ref> Dr Orde speculates that right ventricular myocardial necrosis and inflammation may represent a possible mechanism for troponin rise in stable COPD and COPD exacerbations. The study by Orde <I>et al</I>, which included a selected sample of 28 patients with significant pulmonary thromboembolism and isolated right ventricular pathology, observed the histological presence of right ventricular myocardial inflammation and necrosis in 18 (64%) of these patients and postulated that this may be due to pulmonary thromboembolism.</p> <p>We agree that acute right ventricular strain and inflammation, as observed after acute pulmonary embolism, may cause troponin release, and that this mechanism may be operative in some patients with COPD. However, patients with haemodynamically significant pulmonary thromboembolism differ significantly...]]></description>
<dc:creator><![CDATA[Neukamm, A., Soyseth, V., Omland, T.]]></dc:creator>
<dc:date>2013-05-13T22:40:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303662</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303662</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Response: Raised troponin levels in COPD: a possible mechanism]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>894</prism:startingPage>
<prism:endingPage>894</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/894-a?rss=1">
<title><![CDATA[Raised troponin levels in COPD: a possible mechanism]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/894-a?rss=1</link>
<description><![CDATA[ <p><b>To the Editor</b> I read with interest the recent papers and editorial concerning elevated levels of troponin in chronic obstructive pulmonary disease (COPD).<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> The authors proffered a variety of possible mechanisms which could account at least in part for the troponin rises detected in instances of both acute exacerbation of COPD and stable COPD, but appear to have overlooked the possibility of right ventricular myocardial necrosis and inflammation thought secondary to increased right ventricular stretch and strain&mdash;as described by myself and coworkers in a previous article.<cross-ref type="bib" refid="R4">4</cross-ref> As alluded to in that paper, we are also aware of instances in which similar right ventricular myocardial necroinflammatory changes were identified in the absence of pulmonary thromboembolism (PTE), but in which there were other potential causes of increased right ventricular strain. COPD in both stable and acute guises would of course have such potential,...]]></description>
<dc:creator><![CDATA[Orde, M. M.]]></dc:creator>
<dc:date>2013-05-13T22:40:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303665</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303665</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Raised troponin levels in COPD: a possible mechanism]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>894</prism:startingPage>
<prism:endingPage>894</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/12/895?rss=1">
<title><![CDATA[Ventricular fibrillation caused by extrinsic compression of the left main coronary artery]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/12/895?rss=1</link>
<description><![CDATA[ <sec id="s1"><st>Case-report</st> <p>A 43-year-old woman with a history of ventricular septal defect (VSD) closure, pulmonary hypertension and partial Eisenmenger's physiology presented with in-field v-fib arrest. She was defibrillated to normal sinus rhythm. Echocardiography revealed dilated right ventricle (RV), right ventricular hypertrophy (RVH) and right ventricular systolic pressure (RVSP) of 88&nbsp;mm&nbsp;Hg. A robust right-to-left shunt through a patent foramen ovale (PFO) was seen. A coronary CT angiogram revealed compressed left main coronary artery (LMCA) by severely dilated main pulmonary artery with ostium measuring 6.2<FONT FACE="arial,helvetica">x</FONT>2.6&nbsp;mm (<cross-ref type="fig" refid="HEARTJNL2012303408F1">figure 1</cross-ref>). Coronary artery catheterisation confirmed the compression of LMCA with normal rest of the coronaries. A bare metal stent was placed in the LMCA at the site of compression (<cross-ref type="fig" refid="HEARTJNL2012303408F2">figure 2</cross-ref>).</p> <p> <fig loc="float" id="HEARTJNL2012303408F1"><no>Figure&nbsp;1</no><caption><p>Coronary CT angiogram showing the compression of the left main coronary artery (LMCA). Panel A shows the extrinsic compression of the LMCA by the enlarged pulmonary artery....]]></description>
<dc:creator><![CDATA[Sahay, S., Tonelli, A. R.]]></dc:creator>
<dc:date>2013-05-13T22:40:09-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303408</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303408</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Ventricular fibrillation caused by extrinsic compression of the left main coronary artery]]></dc:title>
<prism:publicationDate>2013-06-15</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>99</prism:volume>
<prism:number>12</prism:number>
<prism:startingPage>895</prism:startingPage>
<prism:endingPage>896</prism:endingPage>
</item>
</rdf:RDF>