var org = {p3k: ({url:"http://content.onlinejacc.org/rss/current.xml", xml:"<?xml version=\"1.0\" encoding=\"ISO-8859-1\"?>\n\n<rdf:RDF\n xmlns:rdf=\"http://www.w3.org/1999/02/22-rdf-syntax-ns#\"\n xmlns=\"http://purl.org/rss/1.0/\"\n xmlns:taxo=\"http://purl.org/rss/1.0/modules/taxonomy/\"\n xmlns:dc=\"http://purl.org/dc/elements/1.1/\"\n xmlns:syn=\"http://purl.org/rss/1.0/modules/syndication/\"\n xmlns:prism=\"http://purl.org/rss/1.0/modules/prism/\"\n xmlns:admin=\"http://webns.net/mvcb/\"\n>\n\n<channel rdf:about=\"http://content.onlinejacc.org\">\n<title>Journal of the American College of Cardiology current issue</title>\n<link>http://content.onlinejacc.org</link>\n<description>Journal of the American College of Cardiology RSS feed -- current issue</description>\n<prism:coverDisplayDate>September 7, 2010</prism:coverDisplayDate>\n<prism:publicationName>Journal of the American College of Cardiology</prism:publicationName>\n<items>\n <rdf:Seq>\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/e21?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/A23?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/827?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/838?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/845?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/855?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/864?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/867?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/875?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/888?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/890?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/897?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/899?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/900?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/903?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/903-a?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/904?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/905?rss=1\" />\n  <rdf:li rdf:resource=\"http://content.onlinejacc.org/cgi/content/short/56/11/910?rss=1\" />\n </rdf:Seq>\n</items>\n<image rdf:resource=\"http://content.onlinejacc.org/icons/banner/title.gif\" />\n</channel>\n\n<image rdf:about=\"http://content.onlinejacc.org/icons/banner/title.gif\">\n<title>Journal of the American College of Cardiology</title>\n<url>http://content.onlinejacc.org/icons/banner/title.gif</url>\n<link>http://content.onlinejacc.org</link>\n</image>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/e21?rss=1\">\n<title><![CDATA[Saddle Pulmonary Embolism Visualized by Transthoracic Echocardiography]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/e21?rss=1</link>\n<description><![CDATA[]]></description>\n<dc:creator><![CDATA[Kanjanauthai, S., Couture, L. A., Fissha, M., Gentry, M., Sharma, G. K.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:05 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2009.10.097</dc:identifier>\n<dc:title><![CDATA[Saddle Pulmonary Embolism Visualized by Transthoracic Echocardiography]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>e21</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>e21</prism:startingPage>\n<prism:section>IMAGES IN CARDIOLOGY</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/A23?rss=1\">\n<title><![CDATA[Inside This Issue]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/A23?rss=1</link>\n<description><![CDATA[]]></description>\n<dc:creator><![CDATA[]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:05 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/S0735-1097(10)02841-X</dc:identifier>\n<dc:title><![CDATA[Inside This Issue]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>A23</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>A23</prism:startingPage>\n<prism:section>Inside This Issue</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/827?rss=1\">\n<title><![CDATA[Age as a Risk Factor for Stroke in Atrial Fibrillation Patients: Implications for Thromboprophylaxis]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/827?rss=1</link>\n<description><![CDATA[\n<sec>\n<p>The prevalence of atrial fibrillation (AF) is related to age and is projected to rise exponentially as the population ages and the prevalence of cardiovascular risk factors increases. The risk of ischemic stroke is significantly increased in AF patients, and there is evidence of a graded increased risk of stroke associated with advancing age. Oral anticoagulation (OAC) is far more effective than antiplatelet agents at reducing stroke risk in patients with AF. Therefore, increasing numbers of elderly patients are candidates for, and could benefit from, the use of anticoagulants. However, elderly people with AF are less likely to receive OAC therapy. This is mainly due to concerns about a higher risk of OAC-associated hemorrhage in the elderly population. Until recently, older patients were under-represented in randomized controlled trials of OAC versus placebo or antiplatelet therapy, and therefore the evidence base for the value of OAC in the elderly population was not known. However, analyses of the available trial data indicate that the expected net clinical benefit of warfarin therapy is highest among patients with the highest untreated risk for stroke, which includes the oldest age category. An important caveat with warfarin treatment is maintenance of a therapeutic international normalized ratio, regardless of the age of the patient, where time in therapeutic range should be &ge;65%. Therefore, age alone should not prevent prescription of OAC in elderly patients, given an appropriate stroke and bleeding risk stratification.</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[Marinigh, R., Lip, G. Y. H., Fiotti, N., Giansante, C., Lane, D. A.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.05.028</dc:identifier>\n<dc:title><![CDATA[Age as a Risk Factor for Stroke in Atrial Fibrillation Patients: Implications for Thromboprophylaxis]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>837</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>827</prism:startingPage>\n<prism:section>STATE-OF-THE-ART PAPER</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/838?rss=1\">\n<title><![CDATA[Differential Associations Between Specific Depressive Symptoms and Cardiovascular Prognosis in Patients With Stable Coronary Heart Disease]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/838?rss=1</link>\n<description><![CDATA[\n<sec><st>Objectives</st>\n<p>The purpose of this research was to evaluate the relationship between cognitive and somatic depressive symptoms and cardiovascular prognosis.</p>\n</sec>\n<sec><st>Background</st>\n<p>Depression in patients with stable coronary heart disease (CHD) is associated with poor cardiac prognosis. Whether certain depressive symptoms are more cardiotoxic than others is unknown.</p>\n</sec>\n<sec><st>Methods</st>\n<p>In the Heart and Soul Study, 1,019 patients with stable CHD were assessed using the Patient Health Questionnaire to determine the presence of the 9 depressive symptoms included in the Diagnostic and Statistical Manual of Mental Disorders&ndash;Fourth Edition. The mean age of the patients was 67 years, and 82% were men. A comparison was made on a new cardiovascular event (myocardial infarction, stroke, transient ischemic attack, or congestive heart failure) or death (mean follow-up duration 6.1 &plusmn; 2.0 years) on the basis of cognitive and somatic sum scores and for patients with or without each of those specific depressive symptoms. Demographic characteristics, cardiac risk factors, and cardiac medications were controlled for.</p>\n</sec>\n<sec><st>Results</st>\n<p>After adjustment for demographic data and cardiac risk factors, each somatic symptom was associated with 14% greater risk for events (hazard ratio [HR]: 1.14; 95% confidence interval [CI]: 1.05 to 1.24; p = 0.002). Fatigue (HR: 1.34; 95% CI: 1.07 to 1.67; p = 0.01), appetite problems (HR: 1.46; 95% CI: 1.12 to 1.91; p = 0.005), and sleeping difficulties (HR: 1.26; 95% CI: 1.00 to 1.58; p = 0.05) were most strongly predictive of cardiovascular events. In contrast, cognitive symptoms (HR: 1.08; 95% CI: 0.99 to 1.17; p = 0.09) were not significantly associated with cardiovascular events.</p>\n</sec>\n<sec><st>Conclusions</st>\n<p>In patients with stable CHD, somatic symptoms of depression were more strongly predictive of cardiovascular events than cognitive symptoms, although the CIs surrounding these estimates had substantial overlap. These findings are highly consistent with those of previous studies. Further research is needed to understand the pathophysiological processes by which somatic depressive symptoms contribute to prognosis in patients with CHD.</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[Hoen, P. W., Whooley, M. A., Martens, E. J., Na, B., van Melle, J. P., de Jonge, P.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.03.080</dc:identifier>\n<dc:title><![CDATA[Differential Associations Between Specific Depressive Symptoms and Cardiovascular Prognosis in Patients With Stable Coronary Heart Disease]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>844</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>838</prism:startingPage>\n<prism:section>Coronary Artery Disease</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/845?rss=1\">\n<title><![CDATA[Global Cardiovascular Reserve Dysfunction in Heart Failure With Preserved Ejection Fraction]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/845?rss=1</link>\n<description><![CDATA[\n<sec><st>Objectives</st>\n<p>The purpose of this study was to comprehensively examine cardiovascular reserve function with exercise in patients with heart failure and preserved ejection fraction (HFpEF).</p>\n</sec>\n<sec><st>Background</st>\n<p>Optimal exercise performance requires an integrated physiologic response, with coordinated increases in heart rate, contractility, lusitropy, arterial vasodilation, endothelial function, and venous return. Cardiac and vascular responses are coupled, and abnormalities in several components may interact to promote exertional intolerance in HFpEF.</p>\n</sec>\n<sec><st>Methods</st>\n<p>Subjects with HFpEF (n = 21), hypertension without heart failure (n = 19), and no cardiovascular disease (control, n = 10) were studied before and during exercise with characterization of cardiovascular reserve function by Doppler echocardiography, peripheral arterial tonometry, and gas exchange.</p>\n</sec>\n<sec><st>Results</st>\n<p>Exercise capacity and tolerance were reduced in HFpEF compared with hypertensive subjects and controls, with lower VO<SUB>2</SUB> and cardiac index at peak, and more severe dyspnea and fatigue at matched low-level workloads. Endothelial function was impaired in HFpEF and in hypertensive subjects as compared with controls. However, blunted exercise-induced increases in chronotropy, contractility, and vasodilation were unique to HFpEF and resulted in impaired dynamic ventricular-arterial coupling responses during exercise. Exercise capacity and symptoms of exertional intolerance were correlated with abnormalities in each component of cardiovascular reserve function, and HFpEF subjects were more likely to display multiple abnormalities in reserve.</p>\n</sec>\n<sec><st>Conclusions</st>\n<p>HFpEF is characterized by depressed reserve capacity involving multiple domains of cardiovascular function, which contribute in an integrated fashion to produce exercise limitation. Appreciation of the global nature of reserve dysfunction in HFpEF will better inform optimal design for future diagnostic and therapeutic strategies.</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[Borlaug, B. A., Olson, T. P., Lam, C. S. P., Flood, K. S., Lerman, A., Johnson, B. D., Redfield, M. M.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.03.077</dc:identifier>\n<dc:title><![CDATA[Global Cardiovascular Reserve Dysfunction in Heart Failure With Preserved Ejection Fraction]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>854</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>845</prism:startingPage>\n<prism:section>Heart Failure</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/855?rss=1\">\n<title><![CDATA[Hemodynamic Basis of Exercise Limitation in Patients With Heart Failure and Normal Ejection Fraction]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/855?rss=1</link>\n<description><![CDATA[\n<sec><st>Objectives</st>\n<p>The purpose of this study was to invasively investigate the hemodynamic response to exercise in patients with heart failure with normal ejection fraction (HFNEF) and to evaluate the ability of the peak early diastolic transmitral velocity to peak early diastolic annular velocity ratio (E/e') to reflect exercise hemodynamics.</p>\n</sec>\n<sec><st>Background</st>\n<p>There is little information regarding the hemodynamic response to exercise in HFNEF.</p>\n</sec>\n<sec><st>Methods</st>\n<p>Patients with HFNEF (n = 14) and asymptomatic controls (n = 8) underwent right-side heart catheterization at rest and during supine cycle ergometer exercise and echocardiography with measurement of resting and peak exercise E/e'.</p>\n</sec>\n<sec><st>Results</st>\n<p>Resting pulmonary capillary wedge pressure (PCWP) (10 &plusmn; 4 mm Hg vs. 10 &plusmn; 4 mm Hg; p = 0.94) was similar in HFNEF patients and controls, but stroke volume index (SVI) (p = 0.02) was lower, and systemic vascular resistance index (SVRI) (p = 0.01) was higher in patients. Patients stopped exercise at lower work rate (0.63 &plusmn; 0.29 W/kg vs. 1.13 &plusmn; 0.49 W/kg; p = 0.006). Although peak exercise PCWP was similar in both groups (23 &plusmn; 6 mm Hg vs. 20 &plusmn; 7 mm Hg; p = 0.31), the peak PCWP/work rate ratio was higher in patients compared with controls (46 &plusmn; 31 mm Hg/W/kg vs. 20 &plusmn; 9 mm Hg/W/kg; p = 0.03). Peak exercise SVI (p = 0.001) was lower and SVRI was higher (p = 0.01) in patients. Resting E/e' was modestly elevated in patients (13.2 &plusmn; 4.1 vs. 9.5 &plusmn; 3.4; p = 0.04). Peak exercise E/e' did not differ between the groups (11.1 &plusmn; 3.4 vs. 9.4 &plusmn; 3.4; p = 0.28).</p>\n</sec>\n<sec><st>Conclusions</st>\n<p>The HFNEF patients achieved a similar peak exercise PCWP to that of asymptomatic controls, at a much lower workload. This occurs at a lower SVI and in the setting of higher SVRI. The E/e' does not reflect the hemodynamic changes during exercise in HFNEF patients.</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[Maeder, M. T., Thompson, B. R., Brunner-La Rocca, H.-P., Kaye, D. M.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.04.040</dc:identifier>\n<dc:title><![CDATA[Hemodynamic Basis of Exercise Limitation in Patients With Heart Failure and Normal Ejection Fraction]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>863</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>855</prism:startingPage>\n<prism:section>Heart Failure</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/864?rss=1\">\n<title><![CDATA[Culprit Mechanism(s) for Exercise Intolerance in Heart Failure With Normal Ejection Fraction]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/864?rss=1</link>\n<description><![CDATA[]]></description>\n<dc:creator><![CDATA[Paulus, W. J.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.04.041</dc:identifier>\n<dc:title><![CDATA[Culprit Mechanism(s) for Exercise Intolerance in Heart Failure With Normal Ejection Fraction]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>866</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>864</prism:startingPage>\n<prism:section>Editorial Comment</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/867?rss=1\">\n<title><![CDATA[Prognostic Significance of Myocardial Fibrosis in Hypertrophic Cardiomyopathy]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/867?rss=1</link>\n<description><![CDATA[\n<sec><st>Objectives</st>\n<p>We investigated the significance of fibrosis detected by late gadolinium enhancement cardiovascular magnetic resonance for the prediction of major clinical events in hypertrophic cardiomyopathy (HCM).</p>\n</sec>\n<sec><st>Background</st>\n<p>The role of myocardial fibrosis in the prediction of sudden death and heart failure in HCM is unclear with a lack of prospective data.</p>\n</sec>\n<sec><st>Methods</st>\n<p>We assessed the presence and amount of myocardial fibrosis in HCM patients and prospectively followed them for the development of morbidity and mortality in patients over 3.1 &plusmn; 1.7 years.</p>\n</sec>\n<sec><st>Results</st>\n<p>Of 217 consecutive HCM patients, 136 (63%) showed fibrosis. Thirty-four of the 136 patients (25%) in the fibrosis group but only 6 of 81 (7.4%) patients without fibrosis reached the combined primary end point of cardiovascular death, unplanned cardiovascular admission, sustained ventricular tachycardia or ventricular fibrillation, or appropriate implantable cardioverter-defibrillator discharge (hazard ratio [HR]: 3.4, p = 0.006). In the fibrosis group, overall risk increased with the extent of fibrosis (HR: 1.18/5% increase, p = 0.008). The risk of unplanned heart failure admissions, deterioration to New York Heart Association functional class III or IV, or heart failure-related death was greater in the fibrosis group (HR: 2.5, p = 0.021), and this risk increased as the extent of fibrosis increased (HR: 1.16/5% increase, p = 0.017). All relationships remained significant after multivariate analysis. The extent of fibrosis and nonsustained ventricular tachycardia were univariate predictors for arrhythmic end points (sustained ventricular tachycardia or ventricular fibrillation, appropriate implantable cardioverter-defibrillator discharge, sudden cardiac death) (HR: 1.30, p = 0.014). Nonsustained ventricular tachycardia remained an independent predictor of arrhythmic end points after multivariate analysis, but the extent of fibrosis did not.</p>\n</sec>\n<sec><st>Conclusions</st>\n<p>In patients with HCM, myocardial fibrosis as measured by late gadolinium enhancement cardiovascular magnetic resonance is an independent predictor of adverse outcome. (The Prognostic Significance of Fibrosis Detection in Cardiomyopathy; <inter-ref locator=\"http://www.clinicaltrials.gov/ct2/show/NCT00930735%3Fterm%3DNCT00930735%26rank%3D1\" locator-type=\"url\">NCT00930735</inter-ref>)</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[O'Hanlon, R., Grasso, A., Roughton, M., Moon, J. C., Clark, S., Wage, R., Webb, J., Kulkarni, M., Dawson, D., Sulaibeekh, L., Chandrasekaran, B., Bucciarelli-Ducci, C., Pasquale, F., Cowie, M. R., McKenna, W. J., Sheppard, M. N., Elliott, P. M., Pennell, D. J., Prasad, S. K.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.05.010</dc:identifier>\n<dc:title><![CDATA[Prognostic Significance of Myocardial Fibrosis in Hypertrophic Cardiomyopathy]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>874</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>867</prism:startingPage>\n<prism:section>Hypertrophic Cardiomyopathy</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/875?rss=1\">\n<title><![CDATA[Myocardial Scar Visualized by Cardiovascular Magnetic Resonance Imaging Predicts Major Adverse Events in Patients With Hypertrophic Cardiomyopathy]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/875?rss=1</link>\n<description><![CDATA[\n<sec><st>Objectives</st>\n<p>We sought to establish the prognostic value of a comprehensive cardiovascular magnetic resonance (CMR) examination in risk stratification of hypertrophic cardiomyopathy (HCM) patients.</p>\n</sec>\n<sec><st>Background</st>\n<p>With annual mortality rates ranging between 1% and 5%, depending on patient selection, a small but significant number of HCM patients are at risk for an adverse event. Therefore, the identification of and prophylactic therapy (i.e., defibrillator placement) in patients with HCM who are at risk of dying are imperative.</p>\n</sec>\n<sec><st>Methods</st>\n<p>Two-hundred forty-three consecutive patients with HCM were prospectively enrolled. All patients underwent initial CMR, and 220 were available for clinical follow-up. The mean follow-up time was 1,090 days after CMR. End points were all-cause and cardiac mortality.</p>\n</sec>\n<sec><st>Results</st>\n<p>During follow-up 20 of the 220 patients died, and 2 patients survived sudden cardiac death due to adequate implantable cardioverter-defibrillator discharge. Most events (n = 16) occurred for cardiac reasons; the remaining 6 events were related to cancer and accidents. Our data indicate that the presence of scar visualized by CMR yields an odds ratio of 5.47 for all-cause mortality and of 8.01 for cardiac mortality. This might be superior to classic clinical risk factors, because in our dataset the presence of 2 risk factors yields an odds ratio of 3.86 for all-cause and of 2.20 for cardiac mortality, respectively. Multivariable analysis also revealed the presence of late gadolinium enhancement as a good independent predictor of death in HCM patients.</p>\n</sec>\n<sec><st>Conclusions</st>\n<p>Among our population of largely low or asymptomatic HCM patients, the presence of scar indicated by CMR is a good independent predictor of all-cause and cardiac mortality.</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[Bruder, O., Wagner, A., Jensen, C. J., Schneider, S., Ong, P., Kispert, E.-M., Nassenstein, K., Schlosser, T., Sabin, G. V., Sechtem, U., Mahrholdt, H.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.05.007</dc:identifier>\n<dc:title><![CDATA[Myocardial Scar Visualized by Cardiovascular Magnetic Resonance Imaging Predicts Major Adverse Events in Patients With Hypertrophic Cardiomyopathy]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>887</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>875</prism:startingPage>\n<prism:section>Hypertrophic Cardiomyopathy</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/888?rss=1\">\n<title><![CDATA[Prognosis in Hypertrophic Cardiomyopathy With Contrast-Enhanced Cardiac Magnetic Resonance: The Future Looks Bright]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/888?rss=1</link>\n<description><![CDATA[]]></description>\n<dc:creator><![CDATA[Salerno, M., Kramer, C. M.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.06.004</dc:identifier>\n<dc:title><![CDATA[Prognosis in Hypertrophic Cardiomyopathy With Contrast-Enhanced Cardiac Magnetic Resonance: The Future Looks Bright]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>889</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>888</prism:startingPage>\n<prism:section>Editorial Comment</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/890?rss=1\">\n<title><![CDATA[Arrhythmias in a Contemporary Fontan Cohort: Prevalence and Clinical Associations in a Multicenter Cross-Sectional Study]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/890?rss=1</link>\n<description><![CDATA[\n<sec><st>Objectives</st>\n<p>Our aim was to examine the prevalence of arrhythmias and identify independent associations of time to arrhythmia development.</p>\n</sec>\n<sec><st>Background</st>\n<p>Since introduction of the Fontan operation in 1971, long-term results have steadily improved with newer modifications. However, atrial arrhythmias are frequent and contribute to ongoing morbidity and mortality. Data are lacking regarding the prevalence of arrhythmias and risk factors for their development in the current era.</p>\n</sec>\n<sec><st>Methods</st>\n<p>The Pediatric Heart Network Fontan Cross-Sectional study evaluated data from 7 centers, with 520 patients age 6 to 18 years (mean 8.6 &plusmn; 3.4 years after the Fontan operation), including echocardiograms, electrocardiograms, exercise testing, parent-reported Child Health Questionnaire (CHQ) results, and medical history.</p>\n</sec>\n<sec><st>Results</st>\n<p>Supraventricular tachycardias were present in 9.4% of patients. Intra-atrial re-entrant tachycardia (IART) was present in 7.3% (32 of 520). The hazard of IART decreased until 4 to 6 years post-Fontan, and then increased with age thereafter. Cardiac anatomy and resting heart rate (including marked bradycardia) were not associated with IART. We identified 3 independent associations of time to occurrence of IART: lower CHQ physical summary score (p &lt; 0.001); predominant rhythm (p = 0.002; highest risk with paced rhythm), and type of Fontan operation (p = 0.037; highest risk with atriopulmonary connection). Time to IART did not differ between patients with lateral tunnel and extracardiac conduit types of Fontan repair. Ventricular tachycardia was noted in 3.5% of patients.</p>\n</sec>\n<sec><st>Conclusions</st>\n<p>Overall prevalence of IART was lower in this cohort (7.3%) than previously reported. Lower functional status, an atriopulmonary connection, and paced rhythm were determined to be independently associated with development of IART after Fontan. (Relationship Between Functional Health Status and Ventricular Performance After Fontan&ndash;Pediatric Heart Network; <inter-ref locator=\"http://www.clinicaltrials.gov/ct2/show/NCT00132782%3Fterm%3DNCT00132782%26rank%3D1\" locator-type=\"url\">NCT00132782</inter-ref>)</p>\n</sec>\n]]></description>\n<dc:creator><![CDATA[Stephenson, E. A., Lu, M., Berul, C. I., Etheridge, S. P., Idriss, S. F., Margossian, R., Reed, J. H., Prakash, A., Sleeper, L. A., Vetter, V. L., Blaufox, A. D., for the Pediatric Heart Network Investigators]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.03.079</dc:identifier>\n<dc:title><![CDATA[Arrhythmias in a Contemporary Fontan Cohort: Prevalence and Clinical Associations in a Multicenter Cross-Sectional Study]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>896</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>890</prism:startingPage>\n<prism:section>Congenital Heart Disease</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/897?rss=1\">\n<title><![CDATA[On the Evolution of the Fontan Operation: From an Electrophysiologist's Perspective]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/897?rss=1</link>\n<description><![CDATA[]]></description>\n<dc:creator><![CDATA[Van Hare, G. F.]]></dc:creator>\n<dc:date>Mon, 30 Aug 2010 13:21:04 PDT</dc:date>\n<dc:identifier>info:doi/10.1016/j.jacc.2010.03.078</dc:identifier>\n<dc:title><![CDATA[On the Evolution of the Fontan Operation: From an Electrophysiologist's Perspective]]></dc:title>\n<dc:publisher>American College of Cardiology</dc:publisher>\n<prism:number>11</prism:number>\n<prism:volume>56</prism:volume>\n<prism:endingPage>898</prism:endingPage>\n<prism:publicationDate>2010-09-07</prism:publicationDate>\n<prism:startingPage>897</prism:startingPage>\n<prism:section>Editorial Comment</prism:section>\n</item>\n\n<item rdf:about=\"http://content.onlinejacc.org/cgi/content/short/56/11/899?rss=1\">\n<title><![CDATA[Ebstein's Anomaly With Left Ventricular Noncompaction and Bicuspid Aortic Valve]]></title>\n<link>http://content.onlinejacc.org/cgi/content/short/56/11/899?rss=1</link>\n<description><![CDATA[]]></description>\n<dc:creator><![CDATA[Thani, K. B., Khadivi, B., Kahn, A. 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         ref.width = getText(getNode(channel, "imageWidth"));
         ref.height = getText(getNode(channel, "imageHeight"));
         ref.description = getText(getNode(channel, "imageCaption"));
      }
   } else {
      var channel = getNode(xml, "channel");
      rss.format = "RSS";
      rss.version = (type === "rdf:RDF") ? "1.0" : 
            root.getAttribute("version");
      rss.title = getText(getNode(channel, "title"));
      rss.description = getText(getNode(channel, "description"));
      rss.link = getText(getNode(channel, "link"));
      var image = getNode(xml, "image");
      if (image) {
         ref = rss.image = {};
         ref.source = getText(getNode(image, "url"));
         ref.title = getText(getNode(image, "title"));
         ref.link = getText(getNode(image, "link"));
         ref.width = getText(getNode(image, "width"));
         ref.height = getText(getNode(image, "height"));
         ref.description = getText(getNode(image, "description"));
      }
   }
   
   if (type === "rdf:RDF") {
      rss.date = renderDate(getText(getNode(channel, "date", "dc")) || data.modified);
      rss.rights = getText(getNode(channel, "creator", "dc"));
      var input = getNode(root, "textinput");
      if (input && !getNode(input, "link")) {
         input = root.getElementsByTagName("textinput")[1];
      }
      if (input) {
         ref = rss.input = {};
         ref.link = getText(getNode(input, "link"));
         ref.description = getText(getNode(input, "description"));
         ref.name = getText(getNode(input, "name"));
         ref.title = getText(getNode(input, "title"));
      }
   } else {
      rss.date = renderDate(getText(getNode(channel, "lastBuildDate") || getText(getNode(channel, "pubDate"))) || data.modified);
      rss.rights = getText(getNode(channel, "copyright"));
   }
   
   var item, text, node;
   var items = xml.getElementsByTagName("item");

   for (var i=0; i<Math.min(items.length, param.maxItems); i+=1) {
      item = items[i];

      if (type === "scriptingNews") {
         ref = {title: ""};
         ref.description = getText(getNode(item, "text")).replace(/\n/g, " ");
         ref.link = getText(getNode(item, "link"));
         if (text = trim(getText(getNode(item, "linetext")).replace(/\n/g, " "))) {
            ref.description = ref.description.replace(new RegExp(text), 
                  '<a href="' + getText(getNode(item, "url")) + '">' + text + '</a>');
         }
      } else {
         ref = {
            title: getText(getNode(item, "title")),
            description: getText(getNode(item, "description")),
            link: getText(getNode(item, "link") || getNode(item, "guid"))
         };
     }

     if (node = getNode(item, "source")) {
        ref.source = {
           link: node.getAttribute("url"),
           title: getText(node)
        }
     }
     
     if (node = getNode(item, "enclosure")) {
        ref.enclosure = {
           link: node.getAttribute("url"),
           length: node.getAttribute("length"),
           type: node.getAttribute("type")
        }
     }
     
     if (node = getNode(item, "category")) {
        ref.category = {
           domain: node.getAttribute("domain") || "",
           content: getText(node)
        }
     }
     
     rss.items.push(ref);
   }
   
   var item, items = "";
   for (var i=0; i<rss.items.length; i+=1) {
      item = rss.items[i];
      items += render(data.item, {
         title: new function() {
            var title = (!param.compact ? "<strong>" : "");
            if (item.link) {
               title += render(data.link, {
                  link: encodeURI(item.link),
                  text: item.title,
                  'class': "rssBoxItemTitle"
               });
            } else {
               title += item.title;
            }
            !param.compact && (title += "</strong>");
            return new String(title); // FIXME: Funny, title alone will be rendered as [object]
         }(),
         'break': item.title && item.description ? "<br />" : "",
         description: (!param.compact || !item.title) && item.description,
         buttons: renderButtons(item.enclosure, item.source)
      });
   }
   
   var box = render(data.box, {
      title: rss.link ? render(data.link, {
         link: encodeURI(rss.link),
         text: rss.title,
         'class': "rssBoxTitle",
         style: "color: " + param.titleBarTextColor
      }) : rss.title,
      description: rss.description,
      items: items,

      xmlButton: param.showXmlButton && render(data.image, {
         link: param.url,
         source: baseUri + "rss.png",
         title: rss.format + " " + rss.version,
         width: 16,
         height: 16,
         align: "right",
         hspace: 3
      }),
      
      image: !param.compact && rss.image && render(data.image, {
         link: encodeURI(rss.image.link),
         source: rss.image.source,
         width: rss.image.width,
         height: rss.image.height,
         title: rss.image.title,
         align: "right",
         valign: "baseline",
         hspace: 5,
         vspace: 5
      }),
      
      input: !param.compact && rss.input && render(data.input, {
         link: encodeURI(rss.input.link),
         description: rss.input.description,
         name: rss.input.name,
         title: rss.input.title
      }),
      
      date: rss.date,
      width: param.width,
      frameColor: param.frameColor,
      fontFace: param.fontFace,
      align: param.align,
      titleBarColor: param.titleBarColor,
      titleBarTextColor: param.titleBarTextColor,
      boxFillColor: param.boxFillColor,
      textColor: param.textColor
   });

   if (!window.rssBoxSetup) {
      document.write(box);
   }
   
   return box;
};

org.p3k.RssBox();

