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<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/e22?rss=1">
<title><![CDATA[[Electronic pages] British Society for Cardiovascular Research: Joint Late Spring Meeting with the British Cardiovascular Society]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/e22?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/</dc:identifier>
<dc:title><![CDATA[[Electronic pages] British Society for Cardiovascular Research: Joint Late Spring Meeting with the British Cardiovascular Society]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>e22</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>e22</prism:startingPage>
<prism:section>Electronic pages</prism:section>
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<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1105?rss=1">
<title><![CDATA[[Featured editorial] What explains declining coronary mortality? Lessons and warnings]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1105?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Capewell, S., O'Flaherty, M.]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2008.149930</dc:identifier>
<dc:title><![CDATA[[Featured editorial] What explains declining coronary mortality? Lessons and warnings]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1108</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1105</prism:startingPage>
<prism:section>Featured editorial</prism:section>
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<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1109?rss=1">
<title><![CDATA[[Editorials] Stroke risk in the elderly: it's not all about visible clot]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1109?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kanagaratnam, P.]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.126318</dc:identifier>
<dc:title><![CDATA[[Editorials] Stroke risk in the elderly: it's not all about visible clot]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1110</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1109</prism:startingPage>
<prism:section>Editorials</prism:section>
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<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1110?rss=1">
<title><![CDATA[[Miscellanea] Optimising device imaging in atrial septal closure by three-dimensional transoesophageal echocardiography]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1110?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Budts, W, Troost, E, Voigt, J-U]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2008.142828</dc:identifier>
<dc:title><![CDATA[[Miscellanea] Optimising device imaging in atrial septal closure by three-dimensional transoesophageal echocardiography]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1110</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1110</prism:startingPage>
<prism:section>Miscellanea</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1111?rss=1">
<title><![CDATA[[Editorials] Low-density lipoprotein and aortic stenosis]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1111?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rajamannan, N. M]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.130971</dc:identifier>
<dc:title><![CDATA[[Editorials] Low-density lipoprotein and aortic stenosis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1112</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1111</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1113?rss=1">
<title><![CDATA[[Editorials] Alternatives to warfarin in atrial fibrillation: drugs and devices]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1113?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bayard, Y. L, Ostermayer, S. H, Sievert, H.]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.118844</dc:identifier>
<dc:title><![CDATA[[Editorials] Alternatives to warfarin in atrial fibrillation: drugs and devices]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1116</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1113</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1116?rss=1">
<title><![CDATA[[Miscellanea] Contrast-enhanced magnetic resonance imaging of endomyocardial fibrosis secondary to Bancroftian filariasis]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1116?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Martin, T N, Weir, R A P, Dargie, H J]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.140392</dc:identifier>
<dc:title><![CDATA[[Miscellanea] Contrast-enhanced magnetic resonance imaging of endomyocardial fibrosis secondary to Bancroftian filariasis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1116</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1116</prism:startingPage>
<prism:section>Miscellanea</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1117?rss=1">
<title><![CDATA[[Editorials] Myocardial oedema: a forgotten entity essential to the understanding of regional function after ischaemia or reperfusion injury]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1117?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bijnens, B., Sutherland, G. R]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.135392</dc:identifier>
<dc:title><![CDATA[[Editorials] Myocardial oedema: a forgotten entity essential to the understanding of regional function after ischaemia or reperfusion injury]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1119</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1117</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1120?rss=1">
<title><![CDATA[[Editorials] Secundum atrial septal defects: time to close them all?]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1120?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sharp, A., Malik, I.]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.133264</dc:identifier>
<dc:title><![CDATA[[Editorials] Secundum atrial septal defects: time to close them all?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1122</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1120</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1122?rss=1">
<title><![CDATA[[Miscellanea] WEB TOP 10]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1122?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:title><![CDATA[[Miscellanea] WEB TOP 10]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1122</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1122</prism:startingPage>
<prism:section>Miscellanea</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1123?rss=1">
<title><![CDATA[[Editorials] Three-dimensional echocardiography: coming of age]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1123?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sugeng, L., Mor-Avi, V., Lang, R. M]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.133702</dc:identifier>
<dc:title><![CDATA[[Editorials] Three-dimensional echocardiography: coming of age]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1125</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1123</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1126?rss=1">
<title><![CDATA[[Global burden of cardiovascular disease] Coronary heart disease in China]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1126?rss=1</link>
<description><![CDATA[
<p>Coronary heart disease (CHD) is the second leading cause of cardiovascular death in the Chinese population. It accounts for 22% of cardiovascular deaths in urban areas and 13% in rural areas. Although mortality from CHD in China is relatively low compared with Western levels, the burden of CHD has been increasing. This is partly because of a worsening profile of risk factors, such as an increased prevalence of hypertension, hyperlipidaemia, overweight/obesity, diabetes, etc and partly because of an increase in the aged population. Large-scale, randomised controlled trials on thrombolytic, blood-pressure-lowering, antiplatelet and blood-cholesterol-lowering treatment as well as cardiac intervention have been conducted for Chinese patients with myocardial infarction. The studies provide important information for the prevention and management of chronic CHD and acute myocardial infarction in the Chinese population.</p>
]]></description>
<dc:creator><![CDATA[Zhang, X-H, Lu, Z L, Liu, L]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.132423</dc:identifier>
<dc:title><![CDATA[[Global burden of cardiovascular disease] Coronary heart disease in China]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1131</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1126</prism:startingPage>
<prism:section>Global burden of cardiovascular disease</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1132?rss=1">
<title><![CDATA[[Rapid communication] Low-dose CT coronary angiography in the step-and-shoot mode: diagnostic performance]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1132?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p>To investigate the performance of low-dose, dual-source computed tomography (DSCT) coronary angiography in the step-and-shoot (SAS) mode for the diagnosis of significant coronary artery stenoses in comparison with conventional coronary angiography (CCA).</p>
</sec>
<sec><st>Design, setting and patients:</st>
<p>Prospective, single-centre study conducted in a referral centre enrolling 120 patients (71 men, mean (SD) age 68 (9) years, mean (SD) body mass index 26.2 (3.2) kg/m<cross-ref type="bib" refid="b2">2</cross-ref>). All study participants underwent DSCT in the SAS mode and CCA within 14 days. Twenty-seven patients were given intravenous &beta; blockers for heart rate reduction before CT. Patients were excluded if a target heart rate &lt;=70 bpm could not be achieved by &beta; blockers or when the patients were in non-sinus rhythm. Two blinded readers independently evaluated coronary artery segments for assessability and for the presence of significant (&gt;50%) stenoses. Sensitivity, specificity, negative (NPV) and positive predictive values (PPV) were determined, with CCA being the standard of reference. Radiation dose values were calculated.</p>
</sec>
<sec><st>Results:</st>
<p>DSCT coronary angiography in the SAS mode was successfully performed in all 120 patients. Mean (SD) heart rate during scanning was 59 (6) bpm (range 44&ndash;69). 1773/1803 coronary segments (98%) were depicted with a diagnostic image quality in 109/120 patients (91%). The overall patient-based sensitivity, specificity, PPV and NPV for the diagnosis of significant stenoses were 100%, 93%, 94% and 100%, respectively. The mean (SD) effective dose of the CT protocol was 2.5 (0.8) mSv (range 1.2&ndash;4.4).</p>
</sec>
<sec><st>Conclusions:</st>
<p>DSCT coronary angiography in the SAS mode allows, in selected patients with a regular heart rate, the accurate diagnosis of significant coronary stenoses at a low radiation dose.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Scheffel, H, Alkadhi, H, Leschka, S, Plass, A, Desbiolles, L, Guber, I, Krauss, T, Gruenenfelder, J, Genoni, M, Luescher, T F, Marincek, B, Stolzmann, P]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:subject><![CDATA[Editor's choice]]></dc:subject>
<dc:identifier>info:doi/10.1136/hrt.2008.149971</dc:identifier>
<dc:title><![CDATA[[Rapid communication] Low-dose CT coronary angiography in the step-and-shoot mode: diagnostic performance]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1137</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1132</prism:startingPage>
<prism:section>Rapid communication</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1138?rss=1">
<title><![CDATA[[Viewpoints] Who does not need a statin: too late in end-stage renal disease or heart failure?]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1138?rss=1</link>
<description><![CDATA[
<p>Current guidelines from large randomised trials recommend that all patients with diabetes type 2 or coronary artery disease after myocardial infarction should be treated with statin drugs. However, the recent 4D and CORONA trials show no improvement in mortality in elderly patients with ischaemic heart failure and patients with diabetes and end-stage renal disease receiving haemodialysis with the onset of statin treatment. The survival benefit from statin treatment appears to stem primarily from the prevention of progression of coronary artery disease. In clinical conditions where coronary artery disease does not significantly contribute to the cause of death statins seem to be less effective. In patients at risk for organ damage, statin treatment, therefore, has to be started early in the course of the disease. The effect of statin withdrawal in ischaemic heart failure or in patients with advanced renal disease is not known. On the basis of the available evidence, current statin treatment should not be stopped in these patients.</p>
]]></description>
<dc:creator><![CDATA[Laufs, U, Custodis, F, Bohm, M]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.125013</dc:identifier>
<dc:title><![CDATA[[Viewpoints] Who does not need a statin: too late in end-stage renal disease or heart failure?]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1140</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1138</prism:startingPage>
<prism:section>Viewpoints</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1141?rss=1">
<title><![CDATA[[Original articles] Impact on mortality following first acute myocardial infarction of distance between home and hospital: cohort study]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1141?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p>To investigate the effect of distance between home and acute hospital on mortality outcome of patients experiencing an incident myocardial infarction (MI).</p>
</sec>
<sec><st>Design:</st>
<p>Cohort study using a record linkage database.</p>
</sec>
<sec><st>Setting:</st>
<p>Tayside, Scotland, UK.</p>
</sec>
<sec><st>Patients:</st>
<p>10 541 patients with incident acute MI between 1994 and 2003 were identified from Tayside hospital discharge data and from death certification data.</p>
</sec>
<sec><st>Main outcome measures:</st>
<p>MI mortality in the community, all-cause mortality in hospital and all-cause mortality during follow-up.</p>
</sec>
<sec><st>Results:</st>
<p>4133 subjects died following incident MI in the community (that is, were not hospitalised), 6408 patients survived to be hospitalised and 1010 of these (15.8%) died in hospital. Of 5398 discharged from hospital, 1907 (35.3%) died during a median of 3.2 years of follow-up. After adjustment for rurality and other known risk factors, distance between home and admitting hospital was significantly associated with increased mortality both before hospital admission (adjusted odds ratio (OR), 2.05, 95% CI 1.00 to 4.21 for &gt;9 miles and 1.46, 1.09 to 1.95 for 3&ndash;9 miles when compared to &lt;3 miles) and after hospitalisation (adjusted hazard ratio (HR) 1.90, 1.19 to 3.02 and 1.27, 0.96 to 1.68). However, there was no effect of distance on in-hospital mortality (adjusted OR 0.95, 0.45 to 2.03 and 1.02, 0.66 to 1.58).</p>
</sec>
<sec><st>Conclusion:</st>
<p>The distance between home and hospital of admission may predict mortality in subjects experiencing a first acute MI. This association was found both before and after hospitalisation. Further studies are needed to explore the reasons for this association. However these data provide support for policies that locate services for acute MI closer to where patients live.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Wei, L, Lang, C C, Sullivan, F M, Boyle, P, Wang, J, Pringle, S D, MacDonald, T M]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.123612</dc:identifier>
<dc:title><![CDATA[[Original articles] Impact on mortality following first acute myocardial infarction of distance between home and hospital: cohort study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1146</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1141</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1147?rss=1">
<title><![CDATA[[Original articles] Administration of intracoronary bone marrow mononuclear cells on chronic myocardial infarction improves diastolic function]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1147?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p>Regeneration of the myocardium and improved ventricular function have been demonstrated in patients with acute myocardial infarction (MI) treated by intracoronary delivery of autologous bone marrow mononuclear cells (BMC) a few days after successful myocardial reperfusion by percutaneous coronary intervention (PCI); however, the effects of intracoronary cell infusion in chronic MI patients are still unknown.</p>
</sec>
<sec><st>Aims:</st>
<p>To investigate whether intracoronary infusion of BMC into the infarct-related artery in patients with healed MI could lead to improvement in left ventricular (LV) function.</p>
</sec>
<sec><st>Methods:</st>
<p>Among 47 patients with stable ischaemic heart disease due to a previous MI (13 (SD 8) months previously), 24 were randomised to intracoronary infusion of BMC (BMC group) and 23 to a saline infusion (control group) into the target vessel after successful PCI within 12 hours after chest pain occurred. LV systolic and diastolic function, infarct size and myocardial perfusion defect were assessed with the use of echocardiography, magnetic resonance imaging (MRI) or <sup>201</sup>Tl single-photon-emission computed tomography (SPECT) at baseline and repeated at the 6-month follow-up examination.</p>
</sec>
<sec><st>Results:</st>
<p>BMC treatment did not result in a significant increase in LV ejection fraction in any of the groups by any of the methods used, and the apparent tendency of an improvement was not statistically different between the two groups. The two groups also did not differ significantly in changes of LV end-diastolic and systolic volume, infarct size or myocardial perfusion. However, there was an overall effect of BMC transfer compared with the control group with respect to early/late (E/A) (p&lt;0.001), early diastolic velocity/late diastolic (Aa) velocity (Ea/Aa) ratio (p = 0.002) and isovolumetric relaxation time (p = 0.038) after 6 months, as evaluated by tissue Doppler echocardiography. We noted no complications associated with BMS transfer.</p>
</sec>
<sec><st>Conclusion:</st>
<p>Intracoronary transfer of autologous BMC in patients with healed MI did not lead to significant improvement of cardiac systolic function, infarct size or myocardial perfusion, but did lead to improvement in diastolic function.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Yao, K, Huang, R, Qian, J, Cui, J, Ge, L, Li, Y, Zhang, F, Shi, H, Huang, D, Zhang, S, Sun, A, Zou, Y, Ge, J]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.137919</dc:identifier>
<dc:title><![CDATA[[Original articles] Administration of intracoronary bone marrow mononuclear cells on chronic myocardial infarction improves diastolic function]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1153</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1147</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1154?rss=1">
<title><![CDATA[[Original articles] Combining dual-source computed tomography coronary angiography and calcium scoring: added value for the assessment of coronary artery disease]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1154?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p>To prospectively investigate the diagnostic accuracy of dual-source 64-slice computed tomography coronary angiography (CTCA), calcium scoring (CS) and both methods combined for assessing significant coronary artery stenoses relative to conventional coronary angiography (CCA).</p>
</sec>
<sec><st>Design, setting and patients:</st>
<p>Prospective, single-centre study conducted in a referral centre enrolling 74 consecutive patients (24 women; mean age 62 (SD 12) years) from August-October 2006. All study participants underwent CS, CTCA and CCA. Diagnostic accuracy was calculated for CS, CTCA and both methods combined relative to CCA. Not-evaluative segments at computed tomography were considered false positive.</p>
</sec>
<sec><st>Results:</st>
<p>CCA identified 139 stenoses in 36 patients. Average heart rate during CTCA was 68 (13) bpm (range 35&ndash;102 bpm), and 2% of segments (21/1001) in 11% of patients (8/74) were not evaluative. Considering these as false positives, per-patient sensitivity and specificity was 98% and 87%. When using CS cut-off values of 0 to exclude and &gt;=400 to predict stenosis, sensitivity and specificity of CS was 100% and 70%, respectively. Combining CS and CTCA in all patients correctly reclassified five patients, while six were falsely classified as stenotic, all of them correctly classified with CTCA alone. Using CS only in patients with not-evaluative segments correctly reclassified five patients while avoiding misclassifications (sensitivity 98%, specificity 100%).</p>
</sec>
<sec><st>Conclusion:</st>
<p>Dual-source CTCA allows the diagnosis of significant stenoses with a high diagnostic accuracy. Selectively combining CS with CTCA in patients with not-evaluative coronary segments improves specificity from 87% to 100% without decreasing the high sensitivity of 98%.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Leschka, S, Scheffel, H, Desbiolles, L, Plass, A, Gaemperli, O, Stolzmann, P, Genoni, M, Luescher, T, Marincek, B, Kaufmann, P, Alkadhi, H]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.124800</dc:identifier>
<dc:title><![CDATA[[Original articles] Combining dual-source computed tomography coronary angiography and calcium scoring: added value for the assessment of coronary artery disease]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1161</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1154</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1162?rss=1">
<title><![CDATA[[Original articles] The impact of lesion length and vessel size on outcomes after sirolimus-eluting stent implantation for in-stent restenosis]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1162?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>We evaluated the predictors of recurrent restenosis and the impact of lesion length and vessel size on outcomes in patients treated with routine sirolimus-eluting stent (SES) implantation for in-stent restenosis (ISR) of bare-metal stent (BMS).</p>
</sec>
<sec><st>Methods:</st>
<p>In this study, 250 consecutive patients with 275 lesions after SES implantation for ISR of BMS were enrolled. Follow-up angiogram was obtained in 239 patients with 258 lesions eight months after implantation (follow-up rate: 95.6%). We compared characteristics of patients and lesions between the two groups (the recurrent restenosis group and the no-restenosis group).</p>
</sec>
<sec><st>Results:</st>
<p>Recurrent restenosis was angiographically documented in 43 lesions (16.7%). Recurrent restenosis was found in 30.4% with small vessel lesions (reference diameter of less than 2.5 mm, 92 lesions) and 23% with the diffuse type lesions (106 lesions). Seventy-two per cent of patients had a focal pattern of recurrent restenosis. Previously recurrent ISR lesions (odds ratio (OR) 1.94, 95% confidence interval (CI) 0.94 to 4.06, p = 0.05), reference diameter of less than 2.5 mm (OR 2.41, CI 1.05 to 5.41, p = 0.03), diffuse type restenosis (OR 4.48, CI 2.12 to 9.94, p = 0.0001) and dialysis patients (OR 4.72, CI 1.42 to 15.7, p = 0.01) were independent predictors of recurrent restenosis.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Small vessels, diffuse type restenosis and dialysis patients were still the predictors of recurrent restenosis in patients treated with SES for ISR of BMS.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Habara, S, Mitsudo, K, Goto, T, Kadota, K, Fujii, S, Yamamoto, H, Kato, H, Takenaka, S, Fuku, Y, Hosogi, S, Hirono, A, Yamamoto, K, Tanaka, H, Hasegawa, D, Nakamura, Y, Tasaka, H, Otsuru, S, Okamoto, Y, Yamada, C, Miyamoto, M, Inoue, K]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.128595</dc:identifier>
<dc:title><![CDATA[[Original articles] The impact of lesion length and vessel size on outcomes after sirolimus-eluting stent implantation for in-stent restenosis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1165</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1162</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1166?rss=1">
<title><![CDATA[[Original articles] Occluding the left atrial appendage: anatomical considerations]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1166?rss=1</link>
<description><![CDATA[
<sec><st>Background:</st>
<p>Occlusion of the left atrial appendage (LAA) is thought to reduce the risk of thromboembolic events in patients with atrial fibrillation.</p>
</sec>
<sec><st>Objective:</st>
<p>To examine the LAA and its relationship to neighbouring structures that may be put at risk when intervening to occlude its os.</p>
</sec>
<sec><st>Methods:</st>
<p>31 heart specimens were examined grossly. Four of the LAAs were processed for histological examination and endocasts were made from 11 appendages. The diameters of the LAA os and proximity to the left superior pulmonary vein, mitral valve and left anterior descending artery were measured and areas of thin atrial wall in the vicinity were noted.</p>
</sec>
<sec><st>Results:</st>
<p>The LAA orifice was oval shaped in all cases with a mean (SD) diameter of 17.4 (4) mm (range 10&ndash;24.1). The mean (SD) distances of the LAA orifice to the left superior pulmonary vein and mitral valve were 11.1 (4.1) mm and 10.7 (2.4) mm, respectively. The left anterior descending, circumflex artery and, in 6 cases, the sinus node artery, were in close proximity to the LAA. Pits or troughs and areas of thin atrial wall were found in 57.7% of hearts within a 20.9 mm radius from the os. Histology showed small crevices and areas of very thin wall within the trabeculated appendage.</p>
</sec>
<sec><st>Conclusions:</st>
<p>The LAA orifice is oval shaped and thin areas of appendage wall and atrial wall are common. Potentially, the left superior pulmonary vein, mitral valve and anterior descending coronary artery can be at risk during occlusion of the os.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Su, P, McCarthy, K P, Ho, S Y]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2006.111989</dc:identifier>
<dc:title><![CDATA[[Original articles] Occluding the left atrial appendage: anatomical considerations]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1170</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1166</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1171?rss=1">
<title><![CDATA[[Original articles] Homocysteine, migration and early vascular impairment in people of African descent]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1171?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>A gradient of increased vascular risk with migration exists across the African diaspora. We investigated the hypothesis that differences in homocysteine/folic acid status contribute to this increased risk.</p>
</sec>
<sec><st>Design:</st>
<p>Community cohort study of 73 Afro-Caribbeans in the United Kingdom and 151 matched Afro-Caribbeans in Jamaica with no conventional vascular risk factors.</p>
</sec>
<sec><st>Methods:</st>
<p>Subjects were compared for baseline characteristics, vascular risk profile, homocysteine (tHcy), folate and B<SUB>12</SUB> concentrations. Endothelium-dependent vasodilatation was assessed by measuring the absolute change from baseline in the reflection index (RI) of the digital volume pulse during intravenous infusion of albuterol (5 &micro;g/min, RI<SUB>ALB</SUB>) and glyceryltrinitrate (GTN) (5 &micro;g/min, RI<SUB>GTN</SUB>). Carotid intima media thickness (CIMT) was measured ultrasonographically in the distal 1 cm of the common carotid artery.</p>
</sec>
<sec><st>Results:</st>
<p>UK Afro-Caribbeans had higher tHcy (mean difference 2.3 (95% confidence interval 1.3 to 3.4) &micro;mol/l) and lower folate (mean difference 3.2 (95% CI 1.8 to 4.7) &micro;g/l) levels. RI<SUB>ALB</SUB> was 5.1 (95% CI 2.5 to 7.6) percentage points lower and CIMT 0.124 (95% CI 0.075 to 0.173) mm greater in UK Afro-Caribbeans. Higher tHcy and lower folate concentrations correlated with impaired RI<SUB>ALB</SUB> and increased CIMT. A 1 &micro;g/l increase in folate concentration was associated with 0.3 (95% CI 0.1 to 0.5) percentage point increase in RI<SUB>ALB</SUB> and 0.002 (95% CI 0.001 to 0.006) mm decrease in CIMT, independent of blood pressure, smoking and vascular risk profile.</p>
</sec>
<sec><st>Conclusions:</st>
<p>Lower folate concentrations in UK compared with West Indian African-Caribbeans may contribute to the higher stroke risk seen in UK African-Caribbean people.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kalra, L, Iveson, E, Rambaran, C, Sherwood, R, Chowienczyk, P, Ritter, J, Shah, A, Forrester, T]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.132670</dc:identifier>
<dc:title><![CDATA[[Original articles] Homocysteine, migration and early vascular impairment in people of African descent]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1174</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1171</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1175?rss=1">
<title><![CDATA[[Original articles] Association between circulating oxidised low-density lipoprotein and fibrocalcific remodelling of the aortic valve in aortic stenosis]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1175?rss=1</link>
<description><![CDATA[
<sec><st>Introduction:</st>
<p>Aortic stenosis (AS) is the most common valvular heart disease in westernised societies. AS is a disease process akin to atherosclerosis in which calcification and tissue remodelling play a crucial role. In patients with moderate/severe AS, we sought to determine whether the remodelling process would be in relationship with transvalvular gradients and circulating oxidised low-density lipoprotein (ox-LDL) levels.</p>
</sec>
<sec><st>Methods:</st>
<p>In 105 patients with AS, the aortic valve and blood plasma were collected at the time of valve replacement surgery. The degree of valve tissue remodelling was assessed using a scoring system (Score: 1-4) and the amount of calcium within the valve cusps was determined. The standard plasma lipid profile, the size of LDL particles and the plasma level of circulating ox-LDL (4E6 antibody) were determined.</p>
</sec>
<sec><st>Results:</st>
<p>After adjustment for covariables, aortic remodelling score was significantly related to transvalvular gradients measured by Doppler echocardiography before surgery. Patients with higher valve remodelling score had higher circulating ox-LDL levels (score 2: 27.3 (SEM 2.6) U/l; score 3: 32.2 (SEM 2.3) U/l; score 4: 38.3 (SEM 2.3) U/l; p = 0.02). After correction for age, gender, hypertension and HDL-C, the plasma level of ox-LDL remained significantly associated with the aortic valve remodelling score (p&lt;0.001). The plasma level of ox-LDL was significantly associated with LDL-C (r = 0.41; p&lt;0.001), apoB (r = 0.59; p&lt;0.001), triglyceride (r = 0.39; p&lt;0.001), Apo A-I (r = 0.23; p = 0.01) and cholesterol in small (&lt;255 &Aring;) LDL particles (r = 0.22; p = 0.02). After correction for covariables, circulating ox-LDL levels remained significantly associated with apoB (p&lt;0.001) and triglyceride (p = 0.01) levels.</p>
</sec>
<sec><st>Conclusion:</st>
<p>Increased level of circulating ox-LDL is associated with worse fibrocalcific remodelling of valvular tissue in AS. It remains to be determined whether circulating ox-LDL is a risk marker for a highly atherogenic profile and/or a circulating molecule which is actively involved in the pathogenesis of calcific aortic valve disease.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Cote, C, Pibarot, P, Despres, J-P, Mohty, D, Cartier, A, Arsenault, B J, Couture, C, Mathieu, P]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.125740</dc:identifier>
<dc:title><![CDATA[[Original articles] Association between circulating oxidised low-density lipoprotein and fibrocalcific remodelling of the aortic valve in aortic stenosis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1180</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1175</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1180?rss=1">
<title><![CDATA[[Miscellanea] ST-segment elevation myocardial infarction with concomitant multiple coronary arteries thromboses in a young patient with hyperhomocysteinaemia]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1180?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Politi, L, Monopoli, D E, Modena, M G]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2008.144246</dc:identifier>
<dc:title><![CDATA[[Miscellanea] ST-segment elevation myocardial infarction with concomitant multiple coronary arteries thromboses in a young patient with hyperhomocysteinaemia]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1180</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1180</prism:startingPage>
<prism:section>Miscellanea</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1181?rss=1">
<title><![CDATA[[Original articles] Valve type and long-term outcomes after aortic valve replacement in older patients]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1181?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p>To compare outcomes after aortic valve replacement (AVR) according to valve type specifically in older patients since valve-related risks are age-dependent; two randomised trials comparing mechanical and bioprosthetic valves found better outcomes with mechanical valves, but the samples were small and the patients were considerably younger than most who undergo AVR.</p>
</sec>
<sec><st>Design:</st>
<p>Cohort study.</p>
</sec>
<sec><st>Setting:</st>
<p>1199 US hospitals.</p>
</sec>
<sec><st>Patients:</st>
<p>Patients 65 years and older undergoing AVR during 1991&ndash;2003 (n = 307 054) identified through Medicare claims data.</p>
</sec>
<sec><st>Main outcome measures:</st>
<p>Relative hazard ratios associated with bioprosthetic valves of (1) death (n = 131 719); (2) readmission for haemorrhage (n = 31 186), stroke (n = 25 051) or embolism (n = 5870); (3) reoperation (n = 4216); and (4) death or reoperation (reoperation free survival) in Cox regression analyses adjusting for demographic and clinical factors and hospital-level effects.</p>
</sec>
<sec><st>Results:</st>
<p>Overall, 36% of AVR patients received bioprosthetic valves. Bioprosthetic valve recipients were older (77 vs 75 years, p&lt;0.001) and generally had higher comorbidity. Bioprosthetic valve recipients had a slightly lower adjusted hazard ratios of death (HR = 0.97; 95% CI 0.95 to 0.98); readmission for haemorrhage, stroke or embolism (HR = 0.90, 95% CI 0.88 to 0.92); and death or reoperation (HR = 0.97, 95% CI 0.96 to 0.98), but a higher hazard ratio of reoperation (HR = 1.25, 95% CI 1.16 to 1.35). However, overall mortality and complication rates were more than 20 and 10 times higher, respectively, than the overall reoperation rate.</p>
</sec>
<sec><st>Conclusions:</st>
<p>In older patients undergoing AVR, bioprosthetic valve recipients had slightly lower risks of death and complications, but a higher risk of reoperation. Given the low reoperation rate, these data suggest that bioprosthetic valves may be preferred in older patients.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Schelbert, E B, Vaughan-Sarrazin, M S, Welke, K F, Rosenthal, G E]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.127506</dc:identifier>
<dc:title><![CDATA[[Original articles] Valve type and long-term outcomes after aortic valve replacement in older patients]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1188</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1181</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1189?rss=1">
<title><![CDATA[[Original articles] Outcomes in patients with pulmonary hypertension undergoing percutaneous atrial septal defect closure]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1189?rss=1</link>
<description><![CDATA[
<sec><st>Objectives:</st>
<p>To examine the outcomes in patients with moderate or severe pulmonary arterial hypertension (PAH) undergoing percutaneous atrial septal defect (ASD) closure.</p>
</sec>
<sec><st>Design:</st>
<p>Retrospective study.</p>
</sec>
<sec><st>Setting:</st>
<p>Teaching hospital-based study.</p>
</sec>
<sec><st>Patients:</st>
<p>Fifty-four patients with moderate (n = 34) or severe PAH (n = 20) who underwent successful device implantation between 1999 and 2004 were included in the study. Clinical and transthoracic echocardiographic data were reviewed. Pulmonary hypertension was classified as moderate (50&ndash;59 mm Hg) or severe (&gt;=60 mm Hg) according with the right ventricular systolic pressure (RVSP) calculated by echocardiography.</p>
</sec>
<sec><st>Results:</st>
<p>At the early follow-up (mean (SD) 2.3 (1.2) months) all patients were alive and the baseline RVSP decreased from 57 (11) mm Hg to 51 (17) mm Hg (p = 0.003). At the late follow-up (n = 39, mean (SD) duration 31 (15) months) two patients had died and the baseline RVSP decreased from 58 (10) mm Hg to 44 (16) mm Hg (p = 0.004). Although the overall mean RVSP decreased at late follow-up, only 43.6% (17/39) of patients had normalisation (&lt;40 mm Hg) of the RVSP and 15.4% (6/39) had persistent severe PAH.</p>
</sec>
<sec><st>Conclusion:</st>
<p>Transcatheter closure in patients with secundum ASD and PAH can be successfully performed in selected subjects and is associated with good outcomes. Early improvements in RVSP are seen in patients with moderate or severe PAH undergoing transcatheter ASD closure. Continued improvement in RVSP occurs in late follow-up. Despite decreases in the mean RVSP in late follow-up, many patients do not have complete normalisation of pressures.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Balint, O H, Samman, A, Haberer, K, Tobe, L, McLaughlin, P, Siu, S C, Horlick, E, Granton, J, Silversides, C K]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2006.114660</dc:identifier>
<dc:title><![CDATA[[Original articles] Outcomes in patients with pulmonary hypertension undergoing percutaneous atrial septal defect closure]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1193</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1189</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1194?rss=1">
<title><![CDATA[[Original articles] Comorbidity, healthcare utilisation and process of care measures in patients with congenital heart disease in the UK: cross-sectional, population-based study with case-control analysis]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1194?rss=1</link>
<description><![CDATA[
<sec><st>Objective:</st>
<p>To determine the prevalence of comorbidities, patterns of healthcare utilisation and primary care recording of clinical indicators in patients with congenital heart disease.</p>
</sec>
<sec><st>Patients and methods:</st>
<p>A population-based case&ndash;control study using data from general practices across the UK contributing data to the QRESEARCH primary care database. The subjects comprised 9952 patients with congenital heart disease and 29 837 matched controls. Outcome measures were prevalence of selected comorbidities; adjusted odds ratios for risk of comorbidities, healthcare utilisation and clinical indicator recording.</p>
</sec>
<sec><st>Results:</st>
<p>The overall crude prevalence of congenital heart disease was 3.05 per 1000 patients (95% CI 2.99 to 3.11). Prevalence of key comorbidities in patients with congenital heart disease ranged from 2.4% (95% CI 2.1% to 2.7%) for epilepsy to 9.3% (95% CI 8.8% to 9.9%) for hypertension. After adjusting for smoking and deprivation, cases were significantly more likely than controls to have each of the cardiovascular comorbidities and an increased risk of diabetes, epilepsy and renal disease. Patients with congenital heart disease were more frequent users of primary care than controls. Patients with congenital heart disease were also more likely than controls to have lifestyle and risk factor measurements recorded in primary care, although overall levels of recording were low.</p>
</sec>
<sec><st>Conclusions:</st>
<p>There is a significant burden of comorbidity associated with congenital heart disease, and levels of primary care utilisation and referral to secondary care are high in this patient group. The predicted future expansion in the numbers of adults with congenital heart disease owing to improvements in survival will have implications for primary and secondary care, and not just tertiary centres offering specialist care.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Billett, J, Cowie, M R, Gatzoulis, M A, Vonder Muhll, I F, Majeed, A]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.122671</dc:identifier>
<dc:title><![CDATA[[Original articles] Comorbidity, healthcare utilisation and process of care measures in patients with congenital heart disease in the UK: cross-sectional, population-based study with case-control analysis]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1199</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1194</prism:startingPage>
<prism:section>Original articles</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1200?rss=1">
<title><![CDATA[[Technology and guidelines] Cardiac optical coherence tomography]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1200?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Raffel, O C, Akasaka, T, Jang, I-K]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2007.130765</dc:identifier>
<dc:title><![CDATA[[Technology and guidelines] Cardiac optical coherence tomography]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1210</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1200</prism:startingPage>
<prism:section>Technology and guidelines</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1211?rss=1">
<title><![CDATA[[Featured correspondence] Secondary prevention of coronary heart disease and heart failure in primary care]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1211?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jaarsma, T]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/</dc:identifier>
<dc:title><![CDATA[[Featured correspondence] Secondary prevention of coronary heart disease and heart failure in primary care]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1211</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1211</prism:startingPage>
<prism:section>Featured correspondence</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1211-a?rss=1">
<title><![CDATA[[Featured correspondence] The authors' reply:]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1211-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Khunti, K, Stone, M, Paul, S, Turner, D A, Squire, I]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:title><![CDATA[[Featured correspondence] The authors' reply:]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1211</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1211</prism:startingPage>
<prism:section>Featured correspondence</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1211-b?rss=1">
<title><![CDATA[[Featured correspondence] Care with single-coil automated implantable cardio-defibrillator leads]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1211-b?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Curtis, S L, Stuart, A G]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/</dc:identifier>
<dc:title><![CDATA[[Featured correspondence] Care with single-coil automated implantable cardio-defibrillator leads]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1212</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1211</prism:startingPage>
<prism:section>Featured correspondence</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1212?rss=1">
<title><![CDATA[[Featured correspondence] Accuracy of real-time, three-dimensional Doppler echocardiography for stroke volume estimation compared with phase-encoded MRI: an in vivo study]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1212?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Pemberton, J, Jerosch-Herold, M, Li, X, Hui, L, Silberbach, M, Woodward, W, Thiele, K, Kenny, A, Sahn, D J]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2008.147751</dc:identifier>
<dc:title><![CDATA[[Featured correspondence] Accuracy of real-time, three-dimensional Doppler echocardiography for stroke volume estimation compared with phase-encoded MRI: an in vivo study]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1213</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1212</prism:startingPage>
<prism:section>Featured correspondence</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1214?rss=1">
<title><![CDATA[[Education in Heart] Cell therapy for ischaemic heart disease]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1214?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Beeres, S. L M A, Atsma, D. E, van Ramshorst, J., Schalij, M. J, Bax, J. J]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2008.149476</dc:identifier>
<dc:title><![CDATA[[Education in Heart] Cell therapy for ischaemic heart disease]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1226</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1214</prism:startingPage>
<prism:section>Education in Heart</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1227?rss=1">
<title><![CDATA[[Education in Heart] Transposition of the great arteries: from fetus to adult]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1227?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Skinner, J., Hornung, T., Rumball, E.]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2006.104737</dc:identifier>
<dc:title><![CDATA[[Education in Heart] Transposition of the great arteries: from fetus to adult]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1235</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1227</prism:startingPage>
<prism:section>Education in Heart</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1236?rss=1">
<title><![CDATA[[Education in Heart] Intraoperative echocardiography]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1236?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Oxorn, D. C]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:identifier>info:doi/10.1136/hrt.2008.148510</dc:identifier>
<dc:title><![CDATA[[Education in Heart] Intraoperative echocardiography]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1243</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1236</prism:startingPage>
<prism:section>Education in Heart</prism:section>
</item>

<item rdf:about="http://heart.bmj.com/cgi/content/full/94/9/1244?rss=1">
<title><![CDATA[[Journal scan] Cardiovascular highlights from non-cardiology journals]]></title>
<link>http://heart.bmj.com/cgi/content/full/94/9/1244?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lindsay, A.]]></dc:creator>
<dc:date>2008-08-14</dc:date>
<dc:title><![CDATA[[Journal scan] Cardiovascular highlights from non-cardiology journals]]></dc:title>
<dc:publisher>BMJ Publishing Group Ltd</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>94</prism:volume>
<prism:endingPage>1246</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1244</prism:startingPage>
<prism:section>Journal scan</prism:section>
</item>

</rdf:RDF>