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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.onlinejcf.com/?rss=yes"><title>Journal of Cardiac Failure</title><description>Journal of Cardiac Failure RSS feed: Current Issue.    
 
 
 
 Journal of Cardiac Failure  publishes original, peer-reviewed communications of scientific excellence 
and review articles on clinical research, basic human studies, animal studies, and bench research with potential clinical applications 
to 
heart failure -pathogenesis, etiology, epidemiology, pathophysiological mechanisms, assessment, prevention, and treatment.   </description><link>http://www.onlinejcf.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:issn>1071-9164</prism:issn><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:publicationDate>May 2012</prism:publicationDate><prism:copyright> © 2012 Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000425/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000371/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000395/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000383/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000759/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412001169/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS107191641200053X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000437/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000401/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000516/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000528/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412000784/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412001248/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS107191641200125X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412001261/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916412001273/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000425/abstract?rss=yes"><title>Plasma Copeptin Levels and Prediction of Outcome in Heart Failure Outpatients: Relation to Hyponatremia and Loop Diuretic Doses</title><link>http://www.onlinejcf.com/article/PIIS1071916412000425/abstract?rss=yes</link><description>Abstract: Background: Copeptin, a stable fragment of the vasopressin prohormone, has been shown to be a significant biomarker for morbidity and mortality in heart failure. The aims of this study were to evaluate the influence of plasma sodium on the prognostic significance of copeptin concentrations in heart failure outpatients and to determine whether increased copeptin concentrations predict future development of hyponatremia.Methods and Results: A total of 340 heart failure patients with left ventricular systolic dysfunction were followed for 55 months (median) in a Danish heart failure clinic. A baseline measurement of plasma copeptin, N-terminal pro–B-type natriuretic peptide (NT-proBNP), and sodium was performed, and the sodium concentrations were recorded during 3 months after the baseline visit in the heart failure clinic. Patients were divided into 3 groups according to copeptin tertiles. In multivariate Cox proportional hazard models adjusted for confounders, including plasma sodium, loop diuretic dose, and NT-proBNP, copeptin was a significant predictor of hospitalization or death (hazard ratio 1.4, 95% confidence interval 1.1–1.9; P &lt; .019) but did not predict mortality independently from NT-proBNP. Additionally, copeptin concentrations did not predict future development of hyponatremia.Conclusions: Plasma copeptin levels predict mortality in outpatients with chronic heart failure independently from clinical variables, plasma sodium, and loop diuretic doses. Furthermore, copeptin predicts the combined end point of hospitalization or death independently from NT-proBNP.</description><dc:title>Plasma Copeptin Levels and Prediction of Outcome in Heart Failure Outpatients: Relation to Hyponatremia and Loop Diuretic Doses</dc:title><dc:creator>Louise Balling, Caroline Kistorp, Morten Schou, Michael Egstrup, Ida Gustafsson, Jens Peter Goetze, Per Hildebrandt, Finn Gustafsson</dc:creator><dc:identifier>10.1016/j.cardfail.2012.01.019</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Trials</prism:section><prism:startingPage>351</prism:startingPage><prism:endingPage>358</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000371/abstract?rss=yes"><title>Dyads Affected by Chronic Heart Failure: A Randomized Study Evaluating Effects of Education and Psychosocial Support to Patients With Heart Failure and Their Partners</title><link>http://www.onlinejcf.com/article/PIIS1071916412000371/abstract?rss=yes</link><description>Abstract: Background: Chronic heart failure (CHF) causes great suffering for both patients and their partners. The aim of this study was to evaluate the effects of an integrated dyad care program with education and psychosocial support to patients with CHF and their partners during a postdischarge period after acute deterioration of CHF.Methods: One hundred fifty-five patient-caregiver dyads were randomized to usual care (n = 71) or a psychoeducation intervention (n = 84) delivered in 3 modules through nurse-led face-to-face counseling, computer-based education, and other written teaching materials to assist dyads to develop problem-solving skills. Follow-up assessments were completed after 3 and 12 months to assess perceived control, perceived health, depressive symptoms, self-care, and caregiver burden.Results: Baseline sociodemographic and clinical characteristics of dyads in the experimental and control groups were similar at baseline. Significant differences were observed in patients’ perceived control over the cardiac condition after 3 (P &lt; .05) but not after 12 months, and no effect was seen for the caregivers.No group differences were observed over time in dyads’ health-related quality of life and depressive symptoms, patients’ self-care behaviors, and partners’ experiences of caregiver burden.Conclusions: Integrated dyad care focusing on skill-building and problem-solving education and psychosocial support was effective in initially enhancing patients’ levels of perceived control. More frequent professional contact and ongoing skills training may be necessary to have a higher impact on dyad outcomes and warrants further research.</description><dc:title>Dyads Affected by Chronic Heart Failure: A Randomized Study Evaluating Effects of Education and Psychosocial Support to Patients With Heart Failure and Their Partners</dc:title><dc:creator>Susanna Ågren, Lorraine S. Evangelista, Carina Hjelm, Anna Strömberg</dc:creator><dc:identifier>10.1016/j.cardfail.2012.01.014</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-05</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-05</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Trials</prism:section><prism:startingPage>359</prism:startingPage><prism:endingPage>366</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000395/abstract?rss=yes"><title>IIIB or Not IIIB: A Previously Unanswered Question</title><link>http://www.onlinejcf.com/article/PIIS1071916412000395/abstract?rss=yes</link><description>Abstract: The term New York Heart Association (NYHA) class IIIB has been used increasingly in clinical medicine, including as an inclusion criteria for many clinical trials assessing left ventricular assist devices (LVADs). Indeed, NYHA class IIIB is incorporated in the Food and Drug Administration’s approved indication for the Heartmate II. However, on review of the medical literature, we found that there is no consensus definition of NYHA class IIIB. Until the ambiguity is resolved, we suggest that this designation not be used in clinical practice or by investigators leading clinical trials assessing therapies which convey substantial risk to patients and therefore require clarity in describing the enrolled patient population. With ongoing improvements in LVADs, this therapy will increasingly be considered in patients less sick than those who require inotropic support, providing urgency to establish a consensus system of classifying such patients who nevertheless fall within the spectrum of advanced heart failure. Herein we propose a modification of the standard NYHA classification system which can be used to fill this void.</description><dc:title>IIIB or Not IIIB: A Previously Unanswered Question</dc:title><dc:creator>Jennifer T. Thibodeau, Joseph D. Mishkin, Parag C. Patel, Pradeep P.A. Mammen, David W. Markham, Mark H. Drazner</dc:creator><dc:identifier>10.1016/j.cardfail.2012.01.016</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Perspective</prism:section><prism:startingPage>367</prism:startingPage><prism:endingPage>372</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000383/abstract?rss=yes"><title>Comparison of Cardiac Resynchronization Therapy Outcomes in Patients With New York Heart Association Functional Class I/II Versus III/IV Heart Failure</title><link>http://www.onlinejcf.com/article/PIIS1071916412000383/abstract?rss=yes</link><description>Abstract: Background: Several randomized trials have shown that cardiac resynchronization therapy (CRT) benefits New York Heart Association (NYHA) functional class I/II heart failure (HF) patients, but it is unknown if similar outcomes occur in the real-world.Methods and Results: All patients receiving CRT between 2003 and 2008 with ejection fraction (EF) ≤35% and QRS duration ≥120 ms were included. Outcomes assessed were subjective clinical response, echocardiographic response, and survival free of cardiovascular (CV) hospitalization. Baseline demographics in functional class I/II (n = 155) and functional class III/IV (n = 512) were similar, except for differences in age and several comorbidities. Clinical response was similar in both groups. The functional class I/II group had a greater decrease in left ventricular (LV) end-diastolic dimension (P = .031), and trended toward greater improvements in LV end-systolic dimension (P = .056) and EF (P = .059). The functional class I/II group had a better 5-year survival rate (79 vs 54%; P &lt; .0001) and survival free of CV hospitalization (45% vs 26%; P &lt; .0001).Conclusions: In this real-world clinical scenario, NYHA functional class I/II CRT patients improved clinical status, and LV function and size as good as or better than those in NYHA functional class III/IV patients. These observations provide further support for the use of CRT in patients with mild symptoms of HF.</description><dc:title>Comparison of Cardiac Resynchronization Therapy Outcomes in Patients With New York Heart Association Functional Class I/II Versus III/IV Heart Failure</dc:title><dc:creator>Alan J. Bank, Ariel Rischall, Ryan M. Gage, Kevin V. Burns, Spencer H. Kubo</dc:creator><dc:identifier>10.1016/j.cardfail.2012.01.015</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-05</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-05</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>373</prism:startingPage><prism:endingPage>378</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000759/abstract?rss=yes"><title>Long-Term Effect of Bosentan Therapy on Cardiac Function and Symptomatic Benefits in Adult Patients With Eisenmenger Syndrome</title><link>http://www.onlinejcf.com/article/PIIS1071916412000759/abstract?rss=yes</link><description>Abstract: Background: Bosentan improves symptoms in patients with Eisenmenger syndrome (ES). This study evaluated the effect of long-term bosentan therapy on cardiac function and its relation to symptomatic benefits in ES patients.Methods and Results: Twenty-three consecutive adult ES patients (15 with ventricular septal defect, 6 with atrial septal defect, and 2 with patent ductus arteriosus) underwent standard and tissue Doppler echocardiography before and 24 ± 9 months after bosentan therapy. Echocardiographic measurements included pulmonary arterial systolic pressure (PASP), myocardial performance index (MPI), tricuspid and lateral mitral annular pulsed-wave tissue Doppler systolic (Sa) and early diastolic (Ea) long-axis motions. Patients’ World Health Organization (WHO) functional class, 6-minute walk distance (6MWD), and systemic arterial oxygen saturations (SaO2) were also recorded. The PASP, WHO functional class, 6MWD, and SaO2 all improved (118 ± 22 to 111 ± 19 mm Hg, 3.2 ± 0.4 to 2.4 ± 0.5, 286 ± 129 m to 395 ± 120 m, and 84.6 ± 6.5% to 88.8 ± 3.9%, respectively; all P &lt; .01) after therapy. There was also significant improvement in right ventricular (RV) MPI (by 23.9%: 0.46 ± 0.15 to 0.35 ± 0.09) and biventricular long-axis function (tricuspid Sa and Ea: 6.7 ± 1.5 to 8.8 ± 1.7 cm/s and 5.7 ± 1.3 to 7.0 ± 1.2 cm/s, respectively; lateral Sa and Ea: 6.8 ± 1.3 to 8.4 ± 1.5 cm/s and 7.6 ± 2.0 to 8.5 ± 2.1 cm/s, respectively; all P &lt; .05). Posttherapy RV MPI was moderately correlated with PASP and 6MWD.Conclusions: Sustained improvement of pulmonary arterial hypertension and RV function in ES patients was evident 2 years after bosentan therapy, and this may provide insights on the symptomatic benefits gained in these patients.</description><dc:title>Long-Term Effect of Bosentan Therapy on Cardiac Function and Symptomatic Benefits in Adult Patients With Eisenmenger Syndrome</dc:title><dc:creator>Mehmet G. Kaya, Yat-Yin Lam, Betul Erer, Selim Ayhan, Mehmet A. Vatankulu, Zekeriya Nurkalem, Murat Meric, Mehmet Eren, Namik K. Eryol</dc:creator><dc:identifier>10.1016/j.cardfail.2012.02.004</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>379</prism:startingPage><prism:endingPage>384</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412001169/abstract?rss=yes"><title>Advanced Pulmonary Vascular Therapy for Adults With Congenital Heart Disease: Potential for Progress</title><link>http://www.onlinejcf.com/article/PIIS1071916412001169/abstract?rss=yes</link><description>Owing to advances in the field of congenital heart disease interventions over the past several decades, the majority of patients born with congenital heart defects are surviving well into adulthood. These successes are paralleled by new challenges, such as the increasing number of adults with congenital heart disease (CHD) with progressive heart failure and pulmonary hypertension. In a population-based study of &gt;38,000 adults with CHD, Lowe et al reported a 6% prevalence of pulmonary hypertension. Importantly, those subjects with pulmonary hypertension had a &gt;2-fold higher risk of all-cause mortality and 3-fold higher risk of heart failure and arrhythmias compared with those without pulmonary hypertension. Until recently, therapeutic options for adults with CHD and pulmonary hypertension were limited to mainly supportive measures or in rare cases consideration of transplantation. However, recent investigations of advanced therapies for pulmonary vascular disease in this unique population have offered promise for improved quality of life and survival.</description><dc:title>Advanced Pulmonary Vascular Therapy for Adults With Congenital Heart Disease: Potential for Progress</dc:title><dc:creator>Anne Marie Valente</dc:creator><dc:identifier>10.1016/j.cardfail.2012.04.001</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Editorial Comment</prism:section><prism:startingPage>385</prism:startingPage><prism:endingPage>386</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS107191641200053X/abstract?rss=yes"><title>Improved Exercise Performance and Skeletal Muscle Strength After Simulated Altitude Exposure: A Novel Approach for Patients With Chronic Heart Failure</title><link>http://www.onlinejcf.com/article/PIIS107191641200053X/abstract?rss=yes</link><description>Abstract: Background: Adaptation to altitude leads to beneficial physiologic changes that improve oxygen delivery and utilization by the periphery. Athletes have used simulated altitude enclosures as part of their training regimen to improve exercise performance. We hypothesized that changes due to acclimatization would also be beneficial for patients with heart failure (HF). We report the results of a pilot study of altitude exposure in patients with chronic HF.Methods and Results: Subjects with chronic stable HF, left ventricular ejection fraction (LVEF) ≤35%, on optimal medical therapy were enrolled and underwent simulated altitude exposure for 10 sessions, each 3–4 hours, over a period of 22 days. Starting altitude was 1,500 m and was increased by 300 m with each subsequent session to a maximum altitude of 2,700 m. Peak oxygen consumption, 6-minute walk distance (6MW), skeletal muscle strength, quality of life scores, LVEF, and hematologic parameters were measured at baseline and 48 hours and 4 weeks after the final session. Twelve subjects (median age 52.5 y, ejection fraction 31.7%) successfully completed the protocol without any adverse effects. Peak oxygen consumption significantly improved after altitude sessions from 13.5 ± 1.8 to 14.2 ± 1.9 mL kg−1 min−1 (P = .036) and remained elevated after 4 weeks. There were significant improvements in exercise time, 6MW, skeletal muscle strength, and quality of life scores and a trend toward improvement in LVEF after completion of altitude sessions, which were sustained after 1 month.Conclusions: Simulated altitude exposure up to 2,700 m is safe and well tolerated in patients with chronic stable HF and may have beneficial effects on exercise performance, muscular strength, and quality of life.</description><dc:title>Improved Exercise Performance and Skeletal Muscle Strength After Simulated Altitude Exposure: A Novel Approach for Patients With Chronic Heart Failure</dc:title><dc:creator>Omar Saeed, Vivek Bhatia, Philip Formica, Auris Browne, Thomas K. Aldrich, Jooyoung J. Shin, Simon Maybaum</dc:creator><dc:identifier>10.1016/j.cardfail.2012.02.003</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>387</prism:startingPage><prism:endingPage>391</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000437/abstract?rss=yes"><title>Young Patients With Nonischemic Cardiomyopathy Have Higher Likelihood of Left Ventricular Recovery During Left Ventricular Assist Device Support</title><link>http://www.onlinejcf.com/article/PIIS1071916412000437/abstract?rss=yes</link><description>Abstract: Background: Recovery of ventricular function during left ventricular assist device (LVAD) support allowing device explantation occurs infrequently. We explored the hypothesis that certain patient profiles are more likely to exhibit LV recovery during LVAD support.Methods and Results: A retrospective analysis of data from the HeartMate II bridge to transplant (BTT) and destination therapy (DT) trials was conducted, including 490 BTT, 600 DT, and 18 compassionate-use patients. Of the 1,108 patients, 20 (1.8%; 10 BTT, 10 DT) were explanted owing to LV recovery. The median age was 33 years, and 12 patients (60%) were &lt;40 years of age. History of heart failure was &lt;1 year for 11 patients (61%), and the primary etiology was nonischemic (90%). Of the patients with nonischemic etiologies and &lt;1-year history of heart failure, 13% were explanted. Three patients required LVAD reimplantation; of the remaining 17, 16 remain alive. At follow-up (median 510 days), the mean ejection fraction was 42% (20%–67%) and the mean left ventricular end-diastolic diameter was 55 ± 8 mm. At the 2-year follow-up (n = 13), patients were New York Heart Association functional class I or II and overall survival rate was 85 ± 11%.Conclusions: The results of this study suggest that LV recovery is most likely to occur in young patients (&lt;40 years) with nonischemic cardiomyopathy of &lt;1 year duration. Two-year postexplant survival was excellent.</description><dc:title>Young Patients With Nonischemic Cardiomyopathy Have Higher Likelihood of Left Ventricular Recovery During Left Ventricular Assist Device Support</dc:title><dc:creator>Daniel J. Goldstein, Simon Maybaum, Thomas E. MacGillivray, Stephanie A. Moore, Roberta Bogaev, David J. Farrar, O. Howard Frazier, HeartMate II Clinical Investigators</dc:creator><dc:identifier>10.1016/j.cardfail.2012.01.020</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>392</prism:startingPage><prism:endingPage>395</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000401/abstract?rss=yes"><title>Pediatric Cardiomyopathy: Importance of Genetic and Metabolic Evaluation</title><link>http://www.onlinejcf.com/article/PIIS1071916412000401/abstract?rss=yes</link><description>Abstract: Background: Cardiomyopathy is a heterogeneous disease with a strong genetic component. A research-based pediatric cardiomyopathy registry identified familial, syndromic, or metabolic causes in 30% of children. However, these results predated clinical genetic testing.Methods and Results: We determined the prevalence of familial, syndromic, or metabolic causes in 83 consecutive unrelated patients referred for genetic evaluation of cardiomyopathy from 2006 to 2009. Seventy-six percent of probands (n = 63) were categorized as familial, syndromic, or metabolic. Forty-three percent (n = 18) of hypertrophic cardiomyopathy (HCM) patients had mutations in sarcomeric genes, with MYH7 and MYBPC3 mutations predominating. Syndromic (17%; n = 7) and metabolic (26%; n = 11) causes were frequently identified in HCM patients. The metabolic subgroup was differentiated by decreased endocardial shortening fraction on echocardiography. Dilated cardiomyopathy (DCM) patients had similar rates of syndromic (20%; n = 5) and metabolic (16%; n = 4) causes, but fewer familial cases (24%; n = 6) compared with HCM patients.Conclusions: The cause of cardiomyopathy is identifiable in a majority of affected children. An underlying metabolic or syndromic cause is identified in &gt;35% of children with HCM or DCM. Identification of etiology is important for management, family-based risk assessment, and screening.</description><dc:title>Pediatric Cardiomyopathy: Importance of Genetic and Metabolic Evaluation</dc:title><dc:creator>Steven J. Kindel, Erin M. Miller, Resmi Gupta, Linda H. Cripe, Robert B. Hinton, Robert L. Spicer, Jeffrey A. Towbin, Stephanie M. Ware</dc:creator><dc:identifier>10.1016/j.cardfail.2012.01.017</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>396</prism:startingPage><prism:endingPage>403</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000516/abstract?rss=yes"><title>Septal Rebound Stretch is a Strong Predictor of Outcome After Cardiac Resynchronization Therapy</title><link>http://www.onlinejcf.com/article/PIIS1071916412000516/abstract?rss=yes</link><description>Abstract: Background: Septal rebound stretch (SRSsept) is a distinctive characteristic of discoordination-related mechanical inefficiency. We assessed how intermediate- and long-term outcome after cardiac resynchronization therapy (CRT) relate to baseline SRSsept.Methods and Results: A total of 101 patients (age 65 ± 11 years, 69 men, 18 New York Heart Association (NYHA) class IV, QRS 173 ± 23 ms) scheduled for CRT underwent clinical assessment, echocardiography, and brain-type natriuretic peptide (BNP) measurements before and 6.4 ± 2.3 months after CRT. Baseline SRSsept (all systolic stretch after initial shortening in the septum) was quantified by speckle tracking echocardiography. Primary composite end point was death, urgent cardiac transplantation, or left ventricular assist device implantation at the end of the study. Secondary end points were intermediate-term (6 months) response, quantified as decreases in left ventricular end-systolic volume (ΔLVESV) and BNP (ΔBNP). After a mean clinical follow-up of 15.6 ± 9.0 months; 23 patients had reached the primary end point. Baseline SRSsept (hazard ratio [HR] 0.742; 95% confidence intervals [CI] 0.601–0.916, P &lt; .01]) was independently associated with a better outcome and NYHA class (HR 5.786: 95% CI 2.341–14.299, P &lt; .001) with a worse outcome. Contrary to baseline NYHA class, baseline SRSsept was an independent predictor of both ΔLVESV (beta 0.53; P &lt; .001) and ΔBNP (beta 0.29; P &lt; .01). Intermediate-term ΔLVESV and ΔBNP were associated with a favorable long-term outcome.Conclusions: SRSsept at baseline is a strong, independent predictor of long-term prognosis after CRT and of improvements in left ventricular remodeling and neurohormonal activation at intermediate term.</description><dc:title>Septal Rebound Stretch is a Strong Predictor of Outcome After Cardiac Resynchronization Therapy</dc:title><dc:creator>Geert E. Leenders, Bart W.L. De Boeck, Arco J. Teske, Mathias Meine, Margot D. Bogaard, Frits W. Prinzen, Pieter A. Doevendans, Maarten J. Cramer</dc:creator><dc:identifier>10.1016/j.cardfail.2012.02.001</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>404</prism:startingPage><prism:endingPage>412</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000528/abstract?rss=yes"><title>Bronchodilators in Heart Failure Patients With COPD: Is It Time for a Clinical Trial?</title><link>http://www.onlinejcf.com/article/PIIS1071916412000528/abstract?rss=yes</link><description>Abstract: Chronic heart failure (HF) and chronic obstructive pulmonary disease (COPD) commonly coexist, and patients with both diseases fare worse than those with either disease alone. Several factors may contribute to worse outcomes, including an increased burden of care related to greater disease complexity, an overlap of symptoms resulting in misapplication of therapy, and the adverse effects of treatment for one disease on the symptoms and outcomes related to the other. For example, there are conflicting data about the cardiovascular risks of bronchodilators in HF patients who may experience worse outcomes with inhaled beta-2 agonists via arrhythmogenesis, ischemia, and/or attenuation of beta-blocker benefits. In contrast, the long-acting anticholinergic class of bronchodilators has a more reassuring safety profile. Anticholinergic bronchodilators may be the preferred first-line agents for COPD patients with comorbid HF, yet data supporting these recommendations are limited. Therapeutic trials in COPD patients have generally excluded patients with significant HF and vice-versa. This paper reviews bronchodilator therapy in HF and proposes a randomized trial designed to enroll patients with significant COPD and HF to determine the risks and/or benefits of adding a long-acting beta-2 agonist to patients currently taking a long-acting anticholinergic agent.</description><dc:title>Bronchodilators in Heart Failure Patients With COPD: Is It Time for a Clinical Trial?</dc:title><dc:creator>Robert J. Mentz, Mona Fiuzat, Monica Kraft, Joann Lindenfeld, Christopher M. O’Connor</dc:creator><dc:identifier>10.1016/j.cardfail.2012.02.002</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-12</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-12</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Review Article</prism:section><prism:startingPage>413</prism:startingPage><prism:endingPage>422</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412000784/abstract?rss=yes"><title>Ventricular Arrhythmias are Related to the Presence of Autoantibodies With Adrenergic Activity in Chronic Chagasic Patients With Preserved Left Ventricular Function</title><link>http://www.onlinejcf.com/article/PIIS1071916412000784/abstract?rss=yes</link><description>Abstract: Background: The presence of G-type immunoglobulins with functional activity was previously demonstrated in chronic chagasic patients (CChP) with heart failure. Here we evaluated the profile and the arrhythmogenic effects of sera from CChP with preserved ventricular function.Methods: Electrocardiography (ECG), Holter monitoring, exercise testing, and left ventricular ejection fraction of 40 CChP were measured. Serum from each patient was characterized in isolated rabbit hearts where ECG parameters were analyzed.Results: From the total sera of the 40 CChP tested in rabbit hearts, 42.5% activated β-adrenergic receptors (Ab-β), 5% activated muscarinic receptors (Ab-M), and 30% activated both muscarinic and β-receptors (Ab-Mβ). In addition, 22.5% of the sera were not reactive (Ab-NR). Ab-β patients presented more cases of arrhythmias in exercise testing (P &lt; .001). In Holter, ventricular arrhythmias appeared more than twice as often in the Ab-β group than in the Ab-NR group and in numbers similar to the Ab-Mβ group (Ab-NR: 2; Ab-β: 5; Ab-Mβ: 3). Arrhythmias were induced by Ab-Mβ in isolated rabbit hearts. Sera from patients with Ab-Mβ, who had longer PR intervals, were able to reversibly prolong PR when perfused in isolated rabbit heart (r² = 0.74; P = .02).Conclusions: High prevalence of Ab-β in CChP with preserved left ventricular function led to a greater incidence of ventricular arrhythmias in the patients.</description><dc:title>Ventricular Arrhythmias are Related to the Presence of Autoantibodies With Adrenergic Activity in Chronic Chagasic Patients With Preserved Left Ventricular Function</dc:title><dc:creator>Leonardo Maciel, Roberto C. Pedrosa, Antonio Carlos Campos De Carvalho, Jose H.M. Nascimento, Emiliano Medei</dc:creator><dc:identifier>10.1016/j.cardfail.2012.02.007</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-03-29</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-03-29</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Basic Science and Experimental Study</prism:section><prism:startingPage>423</prism:startingPage><prism:endingPage>431</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412001248/abstract?rss=yes"><title>Editorial Board</title><link>http://www.onlinejcf.com/article/PIIS1071916412001248/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(12)00124-8</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A3</prism:startingPage><prism:endingPage>A3</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS107191641200125X/abstract?rss=yes"><title>Masthead</title><link>http://www.onlinejcf.com/article/PIIS107191641200125X/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(12)00125-X</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A5</prism:startingPage><prism:endingPage>A5</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412001261/abstract?rss=yes"><title>Table of Contents</title><link>http://www.onlinejcf.com/article/PIIS1071916412001261/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(12)00126-1</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A6</prism:startingPage><prism:endingPage>A7</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916412001273/abstract?rss=yes"><title>Information for Authors</title><link>http://www.onlinejcf.com/article/PIIS1071916412001273/abstract?rss=yes</link><description></description><dc:title>Information for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(12)00127-3</dc:identifier><dc:source>Journal of Cardiac Failure 18, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>18</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1071-9164(12)X0005-8</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A9</prism:startingPage><prism:endingPage>A10</prism:endingPage></item></rdf:RDF>
