<?xml version="1.0" encoding="UTF-8"?>

<rdf:RDF
 xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
 xmlns="http://purl.org/rss/1.0/"
 xmlns:content="http://purl.org/rss/1.0/modules/content/"
 xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/"
 xmlns:dc="http://purl.org/dc/elements/1.1/"
 xmlns:syn="http://purl.org/rss/1.0/modules/syndication/"
 xmlns:prism="http://purl.org/rss/1.0/modules/prism/"
 xmlns:admin="http://webns.net/mvcb/"
>

<channel rdf:about="http://heart.bmj.com">
<title>Heart current issue</title>
<link>http://heart.bmj.com</link>
<description>Heart RSS feed -- current issue</description>
<prism:coverDisplayDate>Jul  1 2013 12:00:00:000AM</prism:coverDisplayDate>
<prism:publicationName>Heart</prism:publicationName>
<prism:issn>1355-6037</prism:issn>
<items>
 <rdf:Seq>
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/897?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/899?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/901?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/904?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/909?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/911?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/914?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/921?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/932?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/938?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/944?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/949?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/954?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/960?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/968?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/968-a?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/969?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/970-a?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/971?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/972?rss=1" />
  <rdf:li rdf:resource="http://heart.bmj.com/cgi/content/short/99/13/972-a?rss=1" />
 </rdf:Seq>
</items>
<image rdf:resource="http://hwmaint.heart.bmj.com/homepage/Heart_95x60.gif" />
</channel>
<image rdf:about="http://hwmaint.heart.bmj.com/homepage/Heart_95x60.gif">
<title>Heart</title>
<url>http://hwmaint.heart.bmj.com/homepage/Heart_95x60.gif</url>
<link>http://heart.bmj.com</link>
</image>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/897?rss=1">
<title><![CDATA[The coronary collateral circulation--clinical relevances and therapeutic options]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/897?rss=1</link>
<description><![CDATA[ <p>The coronary arteries were once thought of as end-arteries. Certainly, they often behave like functional end-arteries, as illustrated by the ischaemia induced by single vessel coronary artery disease. However, we now know that there are interconnecting branches between the main arteries although their clinical relevance has been disputed, since the anastomoses are often incapable of restoring flow to normal levels (<cross-ref type="fig" refid="HEARTJNL2012303426F1">figure 1</cross-ref>).</p> <p> <fig loc="float" id="HEARTJNL2012303426F1"><no>Figure&nbsp;1</no><caption><p>Left side: Heart with well-developed coronary collateral circulation and, therefore, much smaller area at risk compared with the heart on the right side with poorly developed collaterals. (Illustration by Anne Wadmore, Medical Illustrations Ltd, UK).</p> </caption> <link locator="heartjnl2012303426f01"></fig> </p> <p>Hitherto, 12 studies have investigated the effect of collaterals on survival, the first in 1971,<cross-ref type="bib" refid="R1">1</cross-ref> but only three have demonstrated a clear benefit leaving unresolved the dispute about their functional relevance.<cross-ref type="bib" refid="R2">2</cross-ref> The inconsistency is partially explained by the method...]]></description>
<dc:creator><![CDATA[Meier, P., Seiler, C.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303426</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303426</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Bradyarrhythmias and heart block, Drugs: cardiovascular system, Interventional cardiology, Clinical diagnostic tests, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The coronary collateral circulation--clinical relevances and therapeutic options]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>897</prism:startingPage>
<prism:endingPage>898</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/899?rss=1">
<title><![CDATA[The diagnostic utility of CT coronary angiography in patients with acute chest pain]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/899?rss=1</link>
<description><![CDATA[ <sec> <p>Acute chest pain is a common cause of attendance at emergency departments and of emergency admission. Some patients have coronary artery disease or some other life-threatening condition, but many do not. Some have other conditions, but not all have an identifiable cause. There is an increasing drive to avoid unnecessary admission to hospital and to reduce length of stay when admission does occur, and new ways to do so are constantly being looked for. Simple clinical assessment in the patient with acute chest pain permits estimation of the likelihood of coronary disease but is not sufficiently sensitive to use in isolation for exclusion of an acute coronary syndrome<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> without additional diagnostic testing. The ECG is a pivotal early diagnostic test and should be undertaken as soon as possible even before a detailed clinical history, and ideally before arrival at hospital. In those with...]]></description>
<dc:creator><![CDATA[Skinner, J. S.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302971</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302971</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[The diagnostic utility of CT coronary angiography in patients with acute chest pain]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>899</prism:startingPage>
<prism:endingPage>900</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/901?rss=1">
<title><![CDATA[Transient loss of consciousness: summary of NICE guidance]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/901?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,...]]></description>
<dc:creator><![CDATA[Petkar, S., Bullock, I., Davis, S., Cooper, P.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303403</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;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>2013-07-01</prism:publicationDate>
<prism:section>Editorials</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>901</prism:startingPage>
<prism:endingPage>903</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/904?rss=1">
<title><![CDATA[Vagally mediated atrioventricular block: pathophysiology and diagnosis]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/904?rss=1</link>
<description><![CDATA[
<p>Vagally mediated atrioventricular (AV) block is defined as a paroxysmal AV block, localised within the AV node, associated with slowing of the sinus rate. All types of second-degree AV block, including pseudo-Mobitz II block, and complete AV block, may be present. Most of the patients have normal AV conduction. Differential diagnosis with intrinsic AV block is based on the behaviour of the sinus rate. Vagally mediated AV block is benign; it can be recorded as an asymptomatic or symptomatic event (syncope/presyncope). Syncope due to this form of AV block should be diagnosed and managed as neurally mediated syncope. When this block is fortuitously recorded in asymptomatic patients, pacemaker implantation is not indicated.</p>
]]></description>
<dc:creator><![CDATA[Alboni, P., Holz, A., Brignole, M.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303220</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303220</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Vagally mediated atrioventricular block: pathophysiology and diagnosis]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Reviews</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>904</prism:startingPage>
<prism:endingPage>908</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/909?rss=1">
<title><![CDATA[Cardiac rehabilitation and mortality reduction after myocardial infarction: the emperor's new clothes?: Evidence in favour of cardiac rehabilitation ]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/909?rss=1</link>
<description><![CDATA[
<p>This piece highlights the strength of evidence in favour of cardiac rehabilitation (CR) and postulates that the emperor is indeed well dressed. The reason why a single negative trial, in the UK, has caused such hullabaloo in the literature and clinical practice is examined against overwhelming evidence from over 40 positive randomised controlled trials. The lack of motivation to promote lifestyle change and the role of patients in determining outcome is also explored. To conclude, we set the scene for the final chapter of this story by outlining what needs to be done to answer the question about the real-world effectiveness of CR.</p>
]]></description>
<dc:creator><![CDATA[Lewin, R., Doherty, P.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303704</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303704</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[Cardiac rehabilitation and mortality reduction after myocardial infarction: the emperor's new clothes?: Evidence in favour of cardiac rehabilitation ]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Point-Counterpoint</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>909</prism:startingPage>
<prism:endingPage>911</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/911?rss=1">
<title><![CDATA[Cardiac rehabilitation and mortality reduction after myocardial infarction: the emperor's new clothes?: Evidence against cardiac rehabilitation]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/911?rss=1</link>
<description><![CDATA[
<p>No trial of cardiac rehabilitation (CR) following myocardial infarction (MI) (not even the WHO European collaborative) demonstrates significant reduction of mortality, as do trials of secondary prevention. There is potential conflict of interest when therapists report self-evaluations. Reviews of published reports exaggerate publication bias. Meta-analyses show no significant effect of CR on mortality in recent years &ndash; since 1990, 23 trials, 6527 patients, relative risk 1.01 (0.88&ndash;1.15). It does no service to MI patients &ndash; or rehabilitation therapists &ndash; to repeat claims derived from poolings of historic trials, undertaken before many significant advances in diagnosis, acute treatment and effective secondary prevention. While CR has a role in good medical/nursing practice and continuity of care, rehabilitation therapists could be more effective elsewhere in the NHS.</p>
]]></description>
<dc:creator><![CDATA[West, R., Jones, D.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303705</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303705</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[Cardiac rehabilitation and mortality reduction after myocardial infarction: the emperor's new clothes?: Evidence against cardiac rehabilitation]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Point-Counterpoint</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>911</prism:startingPage>
<prism:endingPage>913</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/914?rss=1">
<title><![CDATA[The cost-effectiveness of transcatheter aortic valve implantation versus surgical aortic valve replacement in patients with severe aortic stenosis at high operative risk]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/914?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To determine the cost-effectiveness of transcatheter aortic valve implantation (TAVI) compared with surgical aortic valve replacement (SAVR) in a high-risk aortic stenosis (AS) population.</p>
</sec>
<sec><st>Design</st>
<p>A cost-utility analysis employing the National Institute of Clinical Excellence (NICE) reference case design for technology appraisals.</p>
</sec>
<sec><st>Setting</st>
<p>The perspective of the UK National Health Service.</p>
</sec>
<sec><st>Patients</st>
<p>Utility data from a UK high-risk AS population. TAVI and SAVR effectiveness was taken from the PARTNER A randomised controlled trial.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Costs modelled over a 10&nbsp;year horizon using a Markov model. Incremental cost-effectiveness ratios and cost-effectiveness acceptability curve were calculated with reference to the NICE willingness to pay per quality adjusted life year (QALY) gain threshold. Deterministic and probabilistic sensitivity analyses performed.</p>
</sec>
<sec><st>Results</st>
<p>Despite greater procedural costs (&pound;16&nbsp;500 vs &pound;9,256), TAVI was cost-effective compared with SAVR over the 10&nbsp;year model horizon (costs &pound;52&nbsp;593 vs &pound;53&nbsp;943 and QALYs 2.81 vs 2.75), indicating that TAVI dominated SAVR. This appeared to be due to greater postsurgical costs, related to the length and cost of hospital stay. The results appeared robust to a number of deterministic sensitivity and probabilistic analyses. The cost-effectiveness acceptability curve indicated that at the NICE &pound;20&nbsp;000 willingness to pay threshold per QALY gained, TAVI had a 64.6% likelihood of being cost-effective, compared with 35.4% for SAVR.</p>
</sec>
<sec><st>Conclusions</st>
<p>TAVI is likely to be a cost-effective treatment for high-risk patients with AS compared with the reference standard of SAVR. However, uncertainty surrounding the long-term outcomes for TAVI patients remains; this could have a substantive impact on estimates of cost-effectiveness.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Fairbairn, T. A., Meads, D. M., Hulme, C., Mather, A. N., Plein, S., Blackman, D. J., Greenwood, J. P.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303722</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303722</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Editor's choice, Drugs: cardiovascular system, Aortic valve disease, Epidemiology]]></dc:subject>
<dc:title><![CDATA[The cost-effectiveness of transcatheter aortic valve implantation versus surgical aortic valve replacement in patients with severe aortic stenosis at high operative risk]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Valvular heart disease</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>914</prism:startingPage>
<prism:endingPage>920</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/921?rss=1">
<title><![CDATA[Inconsistent echocardiographic grading of aortic stenosis: is the left ventricular outflow tract important?]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/921?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>Discrepancy in the echocardiographic severity grading of aortic stenosis (AS) based on current guidelines has been reported. We sought to investigate the left ventricular outflow tract diameter (LVOTd) as a source of inconsistencies, and to explore hypothetical alternatives for discrepancy improvement.</p>
</sec>
<sec><st>Design</st>
<p>Retrospective echocardiographic cross-sectional analysis.</p>
</sec>
<sec><st>Setting</st>
<p>From 2000 to 2010, we identified all AS patients with left ventricular EF &ge;50%, mean gradient (MG) &ge;20&nbsp;mm&nbsp;Hg, aortic valve area (AVA) &le;2.5&nbsp;cm<sup>2</sup>, &lt;moderate (2+) aortic regurgitation; and divided them into three groups: patients with &lsquo;small &rsquo; LVOTd 1.7&ndash;1.9&nbsp;cm, &lsquo;average&rsquo; LVOTd 2.0&ndash;2.2&nbsp;cm and &lsquo;large&rsquo; LVOTd &ge;2.3&nbsp;cm. In each group, inconsistency of data for classification of severity of AS was assessed and alternative thresholds explored.</p>
</sec>
<sec><st>Results</st>
<p>Of 9488 total patients, 58% were men, LVOTd 2.18&plusmn;0.19&nbsp;cm, peak velocity (Vmax) 3.9&plusmn;0.8&nbsp;m/s, MG 37&plusmn;16&nbsp;mm&nbsp;Hg, and AVA 1.09&plusmn;0.34&nbsp;cm<sup>2</sup>. Small LVOTd patients were older women (91%) with worse systemic haemodynamics and more prevalent paradoxical low-flow, compared with average and large LVOTd patients (all parameters p &lt;0.001). Despite clinically similar MG and Vmax across all groups, mean AVA ranged from 0.88 to 1.25&nbsp;cm<sup>2</sup> (p &lt;0.001), classifying small LVOTd patients as severe, average LVOTd as moderate-severe and large LVOTd as moderate. For patients with large, average and small LVOTd, an AVA of 1&nbsp;cm<sup>2</sup> corresponded to MG of 42, 35 and 29&nbsp;mm&nbsp;Hg, Vmax of 4.1, 3.8 and 3.5&nbsp;m/s and dimensionless index (DI) of 0.22, 0.29 and 0.36, respectively. An AVA cut-off of 0.8&nbsp;cm<sup>2</sup> reduced severe AS inconsistency from 48% to 26% for small LVOTd patients. An AVA cut-off of 0.9&nbsp;cm<sup>2</sup> reduced severe AS inconsistency from 37% to 26% for average LVOTd patients. The current AVA cut-off of 1&nbsp;cm<sup>2</sup> was consistent for large LVOTd patients.</p>
</sec>
<sec><st>Conclusions</st>
<p>The LVOTd is associated with significant inconsistencies in AS assessment by current guidelines. For patients with normal EF and normal flow, current guideline definition of severe AS is most consistent for patients with large LVOTd, but not so for patients with average or small LVOTd in whom lower AVA cut-offs should be further studied. The DI cut-off for severe AS is highly variable depending on the LVOTd and guideline revision of this threshold should be considered.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Michelena, H. I., Margaryan, E., Miller, F. A., Eleid, M., Maalouf, J., Suri, R., Messika-Zeitoun, D., Pellikka, P. A., Enriquez-Sarano, M.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-302881</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-302881</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[Inconsistent echocardiographic grading of aortic stenosis: is the left ventricular outflow tract important?]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Valvular heart disease</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>921</prism:startingPage>
<prism:endingPage>931</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/932?rss=1">
<title><![CDATA[Human non-contrast T1 values and correlation with histology in diffuse fibrosis]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/932?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Aortic stenosis (AS) leads to diffuse fibrosis in the myocardium, which is linked to adverse outcome. Myocardial T1 values change with tissue composition.</p>
</sec>
<sec><st>Objective</st>
<p>To test the hypothesis that our recently developed non-contrast cardiac magnetic resonance (CMR) T1 mapping sequence could identify myocardial fibrosis without contrast agent.</p>
</sec>
<sec><st>Design, setting and patients</st>
<p>A prospective CMR non-contrast T1 mapping study of 109 patients with moderate and severe AS and 33 age- and gender-matched controls.</p>
</sec>
<sec><st>Methods</st>
<p>CMR at 1.5&nbsp;T, including non-contrast T1 mapping using a shortened modified Look&ndash;Locker inversion recovery sequence, was carried out. Biopsy samples for histological assessment of collagen volume fraction (CVF%) were obtained in 19 patients undergoing aortic valve replacement.</p>
</sec>
<sec><st>Results</st>
<p>There was a significant correlation between T1 values and CVF% (r=0.65, p=0.002). Mean T1 values were significantly longer in all groups with severe AS (972&plusmn;33&nbsp;ms in severe asymptomatic, 1014&plusmn;38&nbsp;ms in severe symptomatic) than in normal controls (944&plusmn;16&nbsp;ms) (p&lt;0.05). The strongest associations with T1 values were for aortic valve area (r=&ndash;0.40, p=0.001) and left ventricular mass index (LVMI) (r=0.36, p=0.008), and these were the only independent predictors on multivariate analysis.</p>
</sec>
<sec><st>Conclusions</st>
<p>Non-contrast T1 values are increased in patients with severe AS and further increase in symptomatic compared with asymptomatic patients. T1 values lengthened with greater LVMI and correlated with the degree of biopsy-quantified fibrosis. This may provide a useful clinical assessment of diffuse myocardial fibrosis in the future.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Bull, S., White, S. K., Piechnik, S. K., Flett, A. S., Ferreira, V. M., Loudon, M., Francis, J. M., Karamitsos, T. D., Prendergast, B. D., Robson, M. D., Neubauer, S., Moon, J. C., Myerson, S. G.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303052</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303052</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access, Drugs: cardiovascular system, Aortic valve disease, Clinical diagnostic tests]]></dc:subject>
<dc:title><![CDATA[Human non-contrast T1 values and correlation with histology in diffuse fibrosis]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Cardiovascular imaging</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>932</prism:startingPage>
<prism:endingPage>937</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/938?rss=1">
<title><![CDATA[Cardiac symptoms before sudden cardiac death caused by coronary artery disease: a nationwide study among young Danish people]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/938?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>The aim of this nationwide case&ndash;control study was to identify and characterise symptoms before sudden death of young persons who had died due to coronary artery disease (CAD).</p>
</sec>
<sec><st>Methods</st>
<p>We have previously investigated the incidence of sudden cardiac death (SCD) in young Danish people aged 1&ndash;35&nbsp;years in Denmark during 2000&ndash;2006. We included all deaths (n=6629) and identified 314 autopsied cases of SCD, 40 of whom (13%) died from CAD. To compare symptoms before death, the CAD case group was sex- and age-matched 1:2 with a control group randomly sampled from a population of 1497 individuals who had died in accidents. We used data from the National Patient Registry on previous contacts with the healthcare system for all persons and read all available patient records, including death certificates and autopsy reports.</p>
</sec>
<sec><st>Results</st>
<p>A total of 31 (79%) persons with CAD-SCD had cardiac symptoms such as angina pectoris (n=24, 62%) and dyspnoea during the 12&nbsp;months before death, and this was significantly higher than in the control group (p&lt;0.001). In the case group, 18 persons (46%) had contacts with the healthcare system for cardiac symptoms before death, and this was also significantly higher than the control group (p&lt;0.001).</p>
</sec>
<sec><st>Conclusions</st>
<p>In this nationwide study we found that 62% of young persons with SCD experienced angina before death, and nearly half of them who died of CAD had sought medical attention within the last year before death.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Jabbari, R., Risgaard, B., Holst, A. G., Nielsen, J. B., Glinge, C., Engstrom, T., Bundgaard, H., Svendsen, J. H., Haunso, S., Winkel, B. G., Tfelt-Hansen, J.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303534</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303534</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Stable coronary heart disease, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Cardiac symptoms before sudden cardiac death caused by coronary artery disease: a nationwide study among young Danish people]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Sudden cardiac death</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>938</prism:startingPage>
<prism:endingPage>943</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/944?rss=1">
<title><![CDATA[Fatty acid binding protein 4 predicts left ventricular mass and longitudinal function in overweight and obese women]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/944?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To explore whether increased adipocyte-derived serum fatty acid binding protein 4 (FABP4) predisposes to cardiac remodelling and left ventricular dysfunction in human obesity.</p>
</sec>
<sec><st>Design</st>
<p>Cross-sectional investigation.</p>
</sec>
<sec><st>Setting</st>
<p>Academic clinical research centre.</p>
</sec>
<sec><st>Patients</st>
<p>108 overweight and obese non-diabetic women (body-mass index 33&plusmn;5&nbsp;kg/m&sup2;).</p>
</sec>
<sec><st>Interventions</st>
<p>None.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Relationship between serum FABP4 and abdominal adipose tissue quantified by MRI. Relationship between serum FABP4 and left ventricular morphology and function assessed by cardiac MRI.</p>
</sec>
<sec><st>Results</st>
<p>FABP4 was independently associated with visceral abdominal adipose tissue (&beta;=0.34, p&lt;0.01) and subcutaneous abdominal adipose tissue (&beta;=0.22, p&lt;0.05). After stratification into serum FABP4 tertiles, left ventricular masses were 92&plusmn;16&nbsp;g, 86&plusmn;13&nbsp;g and 81&plusmn;12&nbsp;g in women with high, intermediate and low FABP4 concentrations (p&lt;0.01), respectively. Longitudinal systolic function was reduced by 8% in women with intermediate and high versus low FABP4 concentrations (p&lt;0.01), whereas ejection fraction did not differ among tertiles (p=0.5). In multivariate linear analysis FABP4 remained an independent predictor of left ventricular mass (&beta;=0.17, p&lt;0.05) and reduced longitudinal fractional shortening (&beta;=0.21, p&lt;0.05).</p>
</sec>
<sec><st>Conclusions</st>
<p>In overweight and obese women, FABP4 showed an independent association with parameters of left ventricular remodelling.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Engeli, S., Utz, W., Haufe, S., Lamounier-Zepter, V., Pofahl, M., Traber, J., Janke, J., Luft, F. C., Boschmann, M., Schulz-Menger, J., Jordan, J.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303735</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303735</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system]]></dc:subject>
<dc:title><![CDATA[Fatty acid binding protein 4 predicts left ventricular mass and longitudinal function in overweight and obese women]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Biomarkers and heart disease</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>944</prism:startingPage>
<prism:endingPage>948</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/949?rss=1">
<title><![CDATA[Smoking and obesity associated BDNF gene variance predicts total and cardiovascular mortality in smokers]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/949?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>The brain derived neurotrophic factor (BDNF) locus has been implicated in psychiatric and substance related disorders. Recent genome-wide association studies (GWAS) have shown strong associations between single nucleotide polymorphisms in BDNF, smoking behaviour and high body mass index (BMI). Our aim was to test whether genetic BDNF variation alters the risk of smoking related morbidity and mortality.</p>
</sec>
<sec><st>Design</st>
<p>Cox proportional hazards models were used to relate the BDNF rs4923461(A/G) polymorphisms to all-cause, cancer and cardiovascular mortality and cardiovascular disease (CVD) incidence adjusted for age, sex, BMI, and smoking quantity.</p>
</sec>
<sec><st>Setting</st>
<p>The Malm&ouml; Diet and Cancer Study (MDCS), a population based prospective cohort study (n=30&nbsp;447).</p>
</sec>
<sec><st>Patients</st>
<p>We obtained complete data on 25&nbsp;071 subjects, of whom 6507 were current smokers and 18&nbsp;564 were non-smokers who underwent a baseline examination from 1991&ndash;1996.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>During a mean follow-up time of 12&nbsp;years, 1049 deaths (346 cardiovascular deaths and 492 cancer deaths) and 802 incident CVD events occurred among current smokers.</p>
</sec>
<sec><st>Results</st>
<p>The major allele (A) of rs4923461 was significantly associated with ever having smoked (p=0.03) and high BMI (p=0.001). The A-allele was associated with risk of all-cause (HR=1.12, 95% CI 1.00 to 1.25; p&lt;0.05) and CVD (HR=1.23, 95% CI 1.01 to 1.49; p=0.04) mortality. There was no significant association between the rs4923461 and cancer mortality or CVD incidence.</p>
</sec>
<sec><st>Conclusions</st>
<p>Our data suggest that smoking- and obesity-associated variation of the <I>BDNF</I> gene affects the risk of death, especially due to cardiovascular causes, in smokers. Determination of the BDNF genotype in smokers may guide the need for smoking cessation interventions.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Hallden, S., Sjogren, M., Hedblad, B., Engstrom, G., Narkiewicz, K., Hoffmann, M., Wahlstrand, B., Hedner, T., Melander, O.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303634</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303634</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology, Health effects of tobacco use, Smoking cessation, Tobacco use]]></dc:subject>
<dc:title><![CDATA[Smoking and obesity associated BDNF gene variance predicts total and cardiovascular mortality in smokers]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>949</prism:startingPage>
<prism:endingPage>953</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/954?rss=1">
<title><![CDATA[Aging of the population may not lead to an increase in the numbers of acute coronary events: a community surveillance study and modelled forecast of the future]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/954?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To examine the incidence, mortality and case fatality of acute coronary syndrome (ACS) in Finland during 1993&ndash;2007 and to create forecasts of the absolute numbers of ACS cases in the future, taking into account the aging of the population.</p>
</sec>
<sec><st>Design</st>
<p>Community surveillance study and modelled forecasts of the future.</p>
</sec>
<sec><st>Setting and methods</st>
<p>Two sets of population-based coronary event register data from Finland (FINAMI and the National Cardiovascular Disease Register (CVDR)). Bayesian age&ndash;period&ndash;cohort (APC) modelling.</p>
</sec>
<sec><st>Participants</st>
<p>24&nbsp;905 observed ACS events in the FINAMI register and 364&nbsp;137 in CVDR.</p>
</sec>
<sec><st>Main outcome measures</st>
<p>Observed trends of ACS events during 1993&ndash;2007, forecasted numbers of ACS cases, and the prevalence of ACS survivors until the year 2050.</p>
</sec>
<sec><st>Results</st>
<p>In the FINAMI register, the average annual declines in age-standardised incidence of ACS were 1.6% (p&lt;0.001) in men and 1.8% (p&lt;0.001) in women. For 28-day case fatality of incident ACS, the average annual declines were 4.1% (p&lt;0.001) in men and 6.7% (p&lt;0.001) in women. Findings in the country-wide CVDR data were consistent with the FINAMI register. The APC model, based on the CVDR data, suggested that both the absolute numbers of ACS events and the prevalence of ACS survivors reached their peak in Finland around 1990, have declined since then, and very likely will continue to decline until 2050.</p>
</sec>
<sec><st>Conclusions</st>
<p>The ACS event rates and absolute numbers of cases have declined steeply in Finland. The declining trends are likely to continue in the future despite the aging of the population.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Salomaa, V., Havulinna, A. S., Koukkunen, H., Karja-Koskenkari, P., Pietila, A., Mustonen, J., Ketonen, M., Lehtonen, A., Immonen-Raiha, P., Lehto, S., Airaksinen, J., Kesaniemi, Y. A.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303216</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303216</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Drugs: cardiovascular system, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Aging of the population may not lead to an increase in the numbers of acute coronary events: a community surveillance study and modelled forecast of the future]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Epidemiology</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>954</prism:startingPage>
<prism:endingPage>959</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/960?rss=1">
<title><![CDATA[Transcatheter heart valve implantation for failing surgical bioprostheses: technical considerations and evidence for valve-in-valve procedures]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/960?rss=1</link>
<description><![CDATA[ <p>Transcatheter aortic valve implantation (TAVI) represents a novel technology for treating patients with severe symptomatic calcific aortic stenosis at high or prohibitive surgical risk. In patients at excessive surgical risk, TAVI substantially reduces mortality compared to medical treatment,<cross-ref type="bib" refid="R1">1</cross-ref> and in high risk cohorts provides similar safety and efficacy to surgical aortic valve (SAV) replacement.<cross-ref type="bib" refid="R2">2</cross-ref></p> <p>More recently, the remit of transcatheter heart valve (THV) technology has been expanded beyond that initially conceived: patients at lower surgical risk are being treated despite a lack of evidence in this patient population<sup>w1</sup>; and novel implantation techniques, such as the transaortic approach, have been developed.<sup>w2</sup> Perhaps the most notable adaptation of this technology is the treatment of patients with failing surgical bioprosthetic valves. In 2007, Wenaweser and colleagues reported the implantation of a Medtronic CoreValve (Medtronic CV, Luxembourg S.a.r.l.) into a degenerated surgical aortic bioprosthesis.<cross-ref type="bib" refid="R3">3</cross-ref> Since this first...]]></description>
<dc:creator><![CDATA[Mylotte, D., Lange, R., Martucci, G., Piazza, N.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-301673</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-301673</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Valvular heart disease, Education in Heart, Interventional cardiology, Epidemiology]]></dc:subject>
<dc:title><![CDATA[Transcatheter heart valve implantation for failing surgical bioprostheses: technical considerations and evidence for valve-in-valve procedures]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Education in Heart</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>960</prism:startingPage>
<prism:endingPage>967</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/968?rss=1">
<title><![CDATA[Cardiac rehabilitation mortality trends: how far from a true picture are we?]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/968?rss=1</link>
<description><![CDATA[ <p><b>To the Editor</b>, Thank you for the opportunity to respond to this editorial,<cross-ref type="bib" refid="R1">1</cross-ref> which questions our findings of a greater mortality risk of 58% for cardiac rehabilitation (CR) non-attenders compared to attenders.<cross-ref type="bib" refid="R1">1</cross-ref> <cross-ref type="bib" refid="R2">2</cross-ref> While this effect size is larger than some reports, benefits of this magnitude have been seen by other studies with patient samples comparable to ours. These recent studies found similar effect sizes of 45&ndash;59%.<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></p> <p>The authors also comment that &lsquo;it may be that Melbourne CR programmes are really that good&rsquo;.<cross-ref type="bib" refid="R1">1</cross-ref> A 1996 survey of Victorian CR programmes conducted by the Heart Research Centre (including all 43 programmes in our study)<cross-ref type="bib" refid="R2">2</cross-ref> found that best practice was routinely implemented. For example, 72% undertook programme evaluation and 87% had a registered nurse or physiotherapist as coordinator (data available on request). Since 1993, intensive...]]></description>
<dc:creator><![CDATA[Beauchamp, A., Worcester, M., Murphy, B., Tatoulis, J., Ng, A.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303724</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303724</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Cardiac rehabilitation mortality trends: how far from a true picture are we?]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>968</prism:startingPage>
<prism:endingPage>968</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/968-a?rss=1">
<title><![CDATA[Impaired endothelial function in obstructive sleep apnoea: Allometric scaling can help estimate the true difference in flow-mediated response]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/968-a?rss=1</link>
<description><![CDATA[ <p><b>To the Editor</b> One of the most consistent findings in research on percentage flow-mediated dilation (FMD%) is the negative correlation between baseline arterial diameter (Dbase) and FMD% itself. The study by Namtvedt <I>et al</I><cross-ref type="bib" refid="heartjnl-2013-303772R1">1</cross-ref> is no exception in this respect. FMD% is obviously already an attempt to &lsquo;normalise&rsquo; the measured change in arterial diameter (in millimetre) for variability in Dbase, but seems to do this job poorly.<cross-ref type="bib" refid="heartjnl-2013-303772R2">2</cross-ref> <cross-ref type="bib" refid="heartjnl-2013-303772R3">3</cross-ref></p> <p>In a well-designed study, Namtvedt <I>et al</I><cross-ref type="bib" refid="heartjnl-2013-303772R1">1</cross-ref> reported that FMD% was 3.7% lower in patients with obstructive sleep apnoea (OSA) versus healthy controls. However, Dbase was 0.4&nbsp;mm higher in the OSA patients. This higher Dbase in clinical versus healthy samples is common. Put together with the negative correlation between Dbase and FMD%, the impact of this can be damaging to research. It seems rare, even in recent studies, that sample differences in Dbase...]]></description>
<dc:creator><![CDATA[Atkinson, G.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303772</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303772</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Impaired endothelial function in obstructive sleep apnoea: Allometric scaling can help estimate the true difference in flow-mediated response]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>968</prism:startingPage>
<prism:endingPage>969</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/969?rss=1">
<title><![CDATA[Impaired endothelial function in persons with obstructive sleep apnoea: impact of obesity--the response]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/969?rss=1</link>
<description><![CDATA[ <p><b>The Authors' reply</b> We appreciate Dr Atkinson's letter<cross-ref type="bib" refid="heartjnl-2013-303771R1">1</cross-ref> discussing our recent paper on endothelial function and impact of obesity in persons with obstructive sleep apnoea.<cross-ref type="bib" refid="heartjnl-2013-303771R2">2</cross-ref> In our study, flow-mediated dilatation (FMD) in the brachial artery was used to measure endothelial function. The FMD method was introduced in 1992 by Celermajer and coworkers and has subsequently been used to investigate endothelial function in numerous studies. Several other non-invasive techniques have also been employed to test endothelial function, but the FMD method has been the most widely used over the years. Since the introduction of the FMD method in 1992, the procedures and guidelines to obtain reliable and valid results gradually have been developed to standardise the recordings and eliminate potential confounding factors.</p> <p>Our study had a rather extensive protocol starting with a screening questionnaire for sleep apnoea being mailed to 30&nbsp;000 randomly selected individuals. The FMD...]]></description>
<dc:creator><![CDATA[Hisdal, J., Agewall, S., Omland, T.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303771</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303771</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Impaired endothelial function in persons with obstructive sleep apnoea: impact of obesity--the response]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>PostScript</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>969</prism:startingPage>
<prism:endingPage>969</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/970-a?rss=1">
<title><![CDATA[Two-vessel spontaneous coronary artery dissection as a rare cause of acute coronary syndrome]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/970-a?rss=1</link>
<description><![CDATA[ <p>A 50-year-old hypertensive female presented to us with her first episode of anginal sounding chest discomfort at rest. Her 12-lead ECG demonstrated sinus rhythm with evolving antero-lateral T-wave inversion. Twelve-h Troponin-I was raised at 11.14&nbsp;ng/ml (normal range 0&ndash;0.08&nbsp;ng/ml).</p> <p>Coronary angiography revealed two-vessel spontaneous coronary artery dissection (SCAD) involving the right coronary artery extending into the postero-lateral artery (<cross-ref type="fig" refid="HEARTJNL2012303507F1">figure 1</cross-ref>), and the proximal segment of the first diagonal of the left anterior descending artery (<cross-ref type="fig" refid="HEARTJNL2012303507F2">figure 2</cross-ref>).</p> <p> <fig loc="float" id="HEARTJNL2012303507F1"><no>Figure&nbsp;1</no><caption><p>Reveals a dissection within the right coronary artery extending into the postero-lateral artery.</p> </caption> <link locator="heartjnl2012303507f01"></fig> </p> <p> <fig loc="float" id="HEARTJNL2012303507F2"><no>Figure&nbsp;2</no><caption><p>Reveals a dissection within the proximal segment of the first diagonal branch of the left anterior descending artery.</p> </caption> <link locator="heartjnl2012303507f02"></fig> </p> <p>SCAD is a rare cause of an acute coronary syndrome. It is more common in females between the ages of 30 and 50&nbsp;years, and hypertensive...]]></description>
<dc:creator><![CDATA[Plonczak, A., Luther, V., Kaprielian, R.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303507</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303507</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Two-vessel spontaneous coronary artery dissection as a rare cause of acute coronary syndrome]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>970</prism:startingPage>
<prism:endingPage>970</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/971?rss=1">
<title><![CDATA[Transfemoral TAVI and aortic calcification: the destructive impact of endogenous calcium]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/971?rss=1</link>
<description><![CDATA[ <p>Transfemoral transcatheter aortic valve implantation (TAVI) procedure was performed in an elderly patient with degenerative aortic stenosis using a 23&nbsp;mm-Edwards-Sapien XT bioprosthesis (Edwards Lifesciences, Irvine, California, USA). In addition to degenerative aortic stenosis, the patient also had severe calcification in the descending aorta. After positioning the 16F-e-sheath through the right femoral artery, the bioprosthesis was advanced with a retroflex catheter to the ascending aorta in the usual fashion. Just before crossing the aortic valve, a deformation of the cobalt&ndash;chromium stent with an outward bending of two struts was observed, which had been caused by resistance of endogenous calcium plaques in the descending aorta during catheter introduction (<cross-ref type="fig" refid="HEARTJNL2012303482F1">figure 1</cross-ref>A and D). The device was therefore retracted into the descending aorta and a &lsquo;reshaping&rsquo; manoeuvre was attempted by balloon inflation alongside the valve (figure 1B). This, however, failed due to repetitive balloon rupture. To retract the device into the...]]></description>
<dc:creator><![CDATA[Lauten, A., Figulla, H. R., Ferrari, M.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2012-303482</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2012-303482</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:subject><![CDATA[Open access]]></dc:subject>
<dc:title><![CDATA[Transfemoral TAVI and aortic calcification: the destructive impact of endogenous calcium]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>971</prism:startingPage>
<prism:endingPage>971</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/972?rss=1">
<title><![CDATA[Retraction]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/972?rss=1</link>
<description><![CDATA[
<sec id="s1">
<p>G Foldes, M Mioulane, M N Chahine <I>et al</I>. Human induced pluripotent stem cell-derived cardiomyocytes serve as in vitro model of cardiac hypertrophy. <I>Heart</I>;2011:97.e7. The authors have requested that their abstract is retracted.</p>
</sec>
]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2011-300920b.29ret</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2011-300920b.29ret</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Retraction]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Retraction</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>972</prism:startingPage>
<prism:endingPage>972</prism:endingPage>
</item>
<item rdf:about="http://heart.bmj.com/cgi/content/short/99/13/972-a?rss=1">
<title><![CDATA[Giant unruptured Sinus of Valsalva aneurysm: an unusual cause of aortic regurgitation]]></title>
<link>http://heart.bmj.com/cgi/content/short/99/13/972-a?rss=1</link>
<description><![CDATA[ <sec> <p>Sinus of Valsalva aneurysm (SVA) is rare (0.15%&ndash;1.5% of cardiopulmonary bypass cases) and usually presents acutely following rupture. Unruptured SVA is usually asymptomatic, but can lead to symptoms secondary to compression of adjacent cardiac structures. Ruptured SVA can lead to aortocardiac shunts and heart failure. About 65%&ndash;85% of SVAs originate from the right sinus, 10%&ndash;30% from non-coronary sinus and less than 5% from left sinus. SVA is often congenital. Causes of acquired SVA include atherosclerosis, infection and trauma. SVA is associated with increased morbidity and mortality and should be corrected by surgery or percutaneous device closure.</p> <p>A 79-year-old man was referred to the cardiology clinic with 6&nbsp;months history of progressive breathlessness. On examination, he had an early diastolic murmur in the aortic area and signs of right heart failure. Transthoracic echo showed severe aortic regurgitation and a very large unruptured SVA, arising from the right coronary sinus and...]]></description>
<dc:creator><![CDATA[Lutaaya, M., Rajagopal, R., More, R. S.]]></dc:creator>
<dc:date>2013-06-05T02:33:04-07:00</dc:date>
<dc:identifier>info:doi/10.1136/heartjnl-2013-303758</dc:identifier>
<dc:identifier>hwp:master-id:heartjnl;heartjnl-2013-303758</dc:identifier>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<dc:title><![CDATA[Giant unruptured Sinus of Valsalva aneurysm: an unusual cause of aortic regurgitation]]></dc:title>
<prism:publicationDate>2013-07-01</prism:publicationDate>
<prism:section>Miscellanea</prism:section>
<prism:volume>99</prism:volume>
<prism:number>13</prism:number>
<prism:startingPage>972</prism:startingPage>
<prism:endingPage>972</prism:endingPage>
</item>
</rdf:RDF>