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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> © 2010 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:issn>1071-9164</prism:issn><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2010</prism:publicationDate><prism:copyright> © 2010 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/PIIS1071916409011300/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409011282/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010872/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409011294/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010926/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010914/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010902/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409011270/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010458/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010896/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010380/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916409010392/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916410000126/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916410000047/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916410000059/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916410000060/abstract?rss=yes"/><rdf:li rdf:resource="http://www.onlinejcf.com/article/PIIS1071916410000072/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409011300/abstract?rss=yes"><title>Prognosis of Stage A or B Heart Failure Patients With Elevated B-type Natriuretic Peptide Levels</title><link>http://www.onlinejcf.com/article/PIIS1071916409011300/abstract?rss=yes</link><description>Abstract: Background: Heart failure (HF) patients have a poor prognosis, yet outcomes might be improved by early identification of risk. We investigated the prognostic value of B-type natriuretic peptide (BNP) in patients at risk for HF (American College of Cardiology [ACC]/American Heart Association [AHA] HF Stages A and B), and compared prognosis with Stage C/D patients.Methods and Results: Outpatients referred for echocardiogram (n=829) were stratified by ACC/AHA HF stage and BNP levels (cutpoint of 100pg/mL). Primary outcome was death or cardiac hospitalization at 1 year. BNP levels increased with increasing numbers of cardiovascular risk factors and with HF stage. Stage A/B patients with high BNP had a similar or worse prognosis than Stage C/D patients with low BNP. In fact, the prognosis of Stage C/D patients with low BNP did not significantly differ from the prognosis of Stage A/B patients with low BNP (adjusted HR 1.21, 95% CI 0.62–2.37), whereas Stage A/B patients with high BNP did have a significantly worse prognosis (adjusted HR 1.91, 95% CI 1.11–3.28).Conclusions: Individuals without any history of HF but with BNP ≥100pg/mL are at equal or higher risk than those with a HF history whose BNP is &lt;100pg/mL. BNP may be useful to identify asymptomatic individuals at high risk for future cardiovascular events.</description><dc:title>Prognosis of Stage A or B Heart Failure Patients With Elevated B-type Natriuretic Peptide Levels</dc:title><dc:creator>Lori B. Daniels, Paul Clopton, Kevin Jiang, Barry Greenberg, Alan S. Maisel</dc:creator><dc:identifier>10.1016/j.cardfail.2009.10.020</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>93</prism:startingPage><prism:endingPage>98</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409011282/abstract?rss=yes"><title>Left Ventricular Remodeling and Myocardial Recovery on Mechanical Circulatory Support</title><link>http://www.onlinejcf.com/article/PIIS1071916409011282/abstract?rss=yes</link><description>Abstract: Background: Myocardial recovery after ventricular assist devices (VAD) is rare but appears more common in nonischemic cardiomyopathies (NICM). We sought to evaluate left ventricular (LV) end diastolic diameter (LVEDD) for predicting recovery after VAD.Methods and Results: NICM patients receiving long-term mechanical support between 1996 and 2008 were reviewed. Subjects were divided into 3 groups: mild, moderate, and severe dilation (Group A: LVEDD &lt;6.0 cm [n = 22]; Group B: 6.0-7.0 cm [n = 32]; Group C: &gt;7.0 cm [n = 48], respectively). Overall, recovery (successful explant without transplantation) occurred in 14 of 102 subjects (14%). Of these, 2 died and 2 required transplantation within 1 year. Recovery was more common in patients without LV dilation (Groups A/B/C = 32%/22%/0%, P &lt; .001), as was sustained recovery (alive and transplant free 1 year after explant; A/B/C = 27%/10%/0%, P = .001). Of the recovery patients in Group A, 6/7 (86%) had sustained recovery versus 3/6 (50%) in Group B.Conclusions: Recovery occurred in 32% of NICM patients without significant LV dilation at time of VAD, the majority of whom experienced significant sustained recovery. Recovery was not evident in those with severe LV dilation. Routine echocardiography at the time of implant may assist in targeting patients for recovery after VAD.</description><dc:title>Left Ventricular Remodeling and Myocardial Recovery on Mechanical Circulatory Support</dc:title><dc:creator>Marc A. Simon, Brian A. Primack, Jeffrey Teuteberg, Robert L. Kormos, Christian Bermudez, Yoshiya Toyoda, Hemal Shah, John Gorcsan, Dennis M. McNamara</dc:creator><dc:identifier>10.1016/j.cardfail.2009.10.018</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>99</prism:startingPage><prism:endingPage>105</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010872/abstract?rss=yes"><title>Patient Expectations From Implantable Defibrillators to Prevent Death in Heart Failure</title><link>http://www.onlinejcf.com/article/PIIS1071916409010872/abstract?rss=yes</link><description>Abstract: Background: Indications for implantable cardioverter-defibrillators (ICDs) in heart failure (HF) are expanding and may include more than 1 million patients. This study examined patient expectations from ICDs for primary prevention of sudden death in HF.Methods and Results: Study participants (n = 105) had an EF &lt;35% and symptomatic HF, without history of ventricular tachycardia/fibrillation or syncope. Subjects completed a written survey about perceived ICD benefits, survival expectations, and circumstances under which they might deactivate defibrillation. Mean age was 58, LVEF 21%, 40% were New York Heart Association Class III-IV, and 65% already had a primary prevention ICD. Most patients anticipated more than10 years survival despite symptomatic HF. Nearly 54% expected an ICD to save ≥50 lives per 100 during 5 years. ICD recipients expressed more confidence that the device would save their own lives compared with those without an ICD (P &lt; .001). Despite understanding the ease of deactivation, 70% of ICD recipients indicated they would keep the ICD on even if dying of cancer, 55% even if having daily shocks, and none would inactivate defibrillation even if suffering constant dyspnea at rest.Conclusions: HF patients anticipate long survival, overestimate survival benefits conferred by ICDs, and express reluctance to deactivate their devices even for end-stage disease.</description><dc:title>Patient Expectations From Implantable Defibrillators to Prevent Death in Heart Failure</dc:title><dc:creator>Garrick C. Stewart, Joanne R. Weintraub, Parakash P. Pratibhu, Marc J. Semigran, Janice M. Camuso, Kimberly Brooks, Sui W. Tsang, Mary Susan Anello, Viviane T. Nguyen, Eldrin F. Lewis, Anju Nohria, Akshay S. Desai, Michael M. Givertz, Lynne W. Stevenson</dc:creator><dc:identifier>10.1016/j.cardfail.2009.09.003</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-05</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-05</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>106</prism:startingPage><prism:endingPage>113</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409011294/abstract?rss=yes"><title>Endothelial Function and Arterial Compliance are not Impaired in Subjects With Heart Failure of Non-Ischemic Origin</title><link>http://www.onlinejcf.com/article/PIIS1071916409011294/abstract?rss=yes</link><description>Abstract: Background: Patients with heart failure and underlying ischemic heart disease (IHD) exhibit both endothelial dysfunction and increased arterial stiffness. We investigated whether this is also the case in heart failure of nonischemic etiology.Methods and Results: Eleven patients with heart failure and IHD, 12 patients with heart failure from angiographically verified idiopathic nonischemic dilated cardiomyopathy (DCM), and 16 healthy subjects of similar age and sex were compared. Endothelium-dependent and independent function were evaluated by ultrasonic measurement of flow-mediated dilatation (FMD) and glyceryl trinitrate (GTN)-induced dilatation of the brachial artery respectively. Vascular compliance was assessed by carotid-femoral pulse wave velocity (PWV) and augmentation index (AIx). Heart failure severity was similar in IHD and DCM patients. FMD was impaired in the subjects with IHD as compared with control subjects (4.8 ± 0.3 vs. 8.0 ± 3.6 %, P &lt; .01), but not in those with DCM. GTN-induced vasodilatation was not different in patients and controls. PWV was also increased in IHD patients compared with controls (12.1 ± 3.6 vs. 8.0 ± 1.6 m/s, P &lt; .01), but not in DCM patients. AIx was similar in patients and controls.Conclusion: Heart failure of nonischemic etiology is not associated with abnormalities of endothelium-mediated dilatation or of arterial compliance. The findings of our study now need to be confirmed in larger studies.</description><dc:title>Endothelial Function and Arterial Compliance are not Impaired in Subjects With Heart Failure of Non-Ischemic Origin</dc:title><dc:creator>Ashish Shah, Eugenia Gkaliagkousi, James M. Ritter, Albert Ferro</dc:creator><dc:identifier>10.1016/j.cardfail.2009.10.019</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>114</prism:startingPage><prism:endingPage>120</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010926/abstract?rss=yes"><title>Long-Term Outcomes With Ambrisentan Monotherapy in Pulmonary Arterial Hypertension</title><link>http://www.onlinejcf.com/article/PIIS1071916409010926/abstract?rss=yes</link><description>Abstract: Background: This study evaluated long-term outcomes in patients with pulmonary arterial hypertension (PAH) undergoing treatment with ambrisentan monotherapy, a selective oral endothelin-1 receptor antagonist.Methods and Results: Patients who participated in the Ambrisentan in Pulmonary Arterial Hypertension: A Phase 3, Randomized, Double-Blind, Placebo-Controlled Multicenter Efficacy Study (ARIES-1) clinical trial and extension phase at our institution were included. Cardiac catheterization, 6-minute walk distance (6MWD), and cardiac magnetic resonance (MRI) data were retrospectively reviewed. Twelve patients with PAH (11 idiopathic, 1 fenfluramine) had follow-up from 3 to 5.5 years from the initiation of ARIES-1. Patients received ambrisentan therapy throughout the study period and were on ambrisentan monotherapy for the first 2 years. At year 1, improvements in median mean pulmonary arterial pressure (PA), cardiac output, and pulmonary vascular resistance (PVR) were seen (P = .02, P = .03, P &lt; .01), and the improvement in PVR persisted at 2 years. 6MWD also improved significantly between baseline (350 m) and 1 and 2 years (397 m, P &lt; .01 and 393 m, P = .01). Cardiac MRI results were more varied, with an increase in RV ejection fraction from 29% at baseline to 46% at 2 years (P = .02), but other MRI variables did not improve.Conclusions: Ambrisentan monotherapy led to improvements in catheterization, 6MWD, and RV ejection fraction, and shows promise as a long-term treatment for pulmonary arterial hypertension.</description><dc:title>Long-Term Outcomes With Ambrisentan Monotherapy in Pulmonary Arterial Hypertension</dc:title><dc:creator>Shannon E. Blalock, Susan Matulevicius, Laura C. Mitchell, Sharon Reimold, John Warner, Ronald Peshock, Fernando Torres, Kelly M. Chin</dc:creator><dc:identifier>10.1016/j.cardfail.2009.09.008</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-23</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-23</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>121</prism:startingPage><prism:endingPage>127</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010914/abstract?rss=yes"><title>Baseline Plasma NT-proBNP and Clinical Characteristics: Results From the Irbesartan in Heart Failure With Preserved Ejection Fraction Trial</title><link>http://www.onlinejcf.com/article/PIIS1071916409010914/abstract?rss=yes</link><description>Abstract: Background: N-terminal B type natriuretic peptide (NT-proBNP) is usually elevated in heart failure (HF) patients with reduced ejection fraction (EF). Less is known about NT-proBNP in HF with preserved EF (HF-PEF). We measured baseline NT-proBNP in 3562 HF-PEF enrolled patients in the Irbesartan in Heart Failure with Preserved Ejection Fraction trial.Methods and Results: Patients with EF ≥45%, age ≥60 years, and either New York Heart Association (NYHA) II-IV symptoms with HF hospitalization (HFH) within 6 months or NYHA III-IV symptoms with corroborative evidence of HF or structural changes associated with HF-PEF. NT-proBNP (pg/mL) measured centrally using the Elecsys proBNP assay (Roche). Mean age 72 ± 7 years, 60% were women, the investigator indicated HF etiology was hypertension in 64%; the majority were in NYHA III. Medications included diuretics in 82%, angiotensin-converting enzyme inhibitor in 26%, β-blocker in 59%, and spironolactone in 15%. Median NT-proBNP was 341 pg/mL (interquartile range 135 to 974 pg/mL) and geometric mean was 354 pg/mL. In multivariate analysis, the baseline characteristics most strongly associated with higher NT-proBNP levels were atrial fibrillation (ratio of geometric mean 2.59, P &lt; .001), NYHA IV symptoms (1.52, P &lt; .001), lower estimated glomerular filtration rate (1.44, P &lt; .001), and HFH hospitalization within 6 months (1.37, P &lt; .001).Conclusions: Most HF-PEF patients have elevated NT-proBNP levels. The NT-proBNP concentrations were related to baseline characteristics generally associated with worse outcomes for HF patients.</description><dc:title>Baseline Plasma NT-proBNP and Clinical Characteristics: Results From the Irbesartan in Heart Failure With Preserved Ejection Fraction Trial</dc:title><dc:creator>Robert S. Mckelvie, Michel Komajda, John Mcmurray, Michael Zile, Agata Ptaszynska, Mark Donovan, Peter Carson, Barry M. Massie, I-Preserve Investigators</dc:creator><dc:identifier>10.1016/j.cardfail.2009.09.007</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-05</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-05</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>128</prism:startingPage><prism:endingPage>134</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010902/abstract?rss=yes"><title>The Impact of Perceived Adverse Effects on Medication Changes in Heart Failure Patients</title><link>http://www.onlinejcf.com/article/PIIS1071916409010902/abstract?rss=yes</link><description>Abstract: Background: Given the importance of patient safety and well-being, we quantified the likelihood and type of medication changes observed after 5 possible adverse effects (AE) perceived by heart failure (HF) patients.Methods and Results: We conducted a retrospective cohort study using 18 months follow-up data from the Coordinating study evaluating Outcomes of Advising and Counseling in HF study on 754 patients previously hospitalized for HF (NYHA II-IV, mean age 70 years). Data used for this secondary analysis included problem checklists that patients had completed at 3 points in time, and medication data collected from chart review. Changes in potential causal cardiovascular medication and relevant alleviating medication were classified. Within group and relative risks (RR) for medication changes were calculated. Of the 754 patients, 50% reported dizziness, 44% dry cough, 19% nausea, 19% diarrhea, and 12% gout on the first checklist. Overall, the likelihood of a medication change was increased by 38% after a perceived AE. Dry cough had the highest increased likelihood of an associated cardiovascular medication change (RR 1.83, CI 1.35-2.49). Patients reporting gout had a four fold higher likelihood of alleviating medication started or intensified.Conclusions: A considerable number of HF patients perceived possible AE. However, the likelihood of medication being changed after a possible AE was rather low. There seems to be room for improving the management of AE.</description><dc:title>The Impact of Perceived Adverse Effects on Medication Changes in Heart Failure Patients</dc:title><dc:creator>Ruth H.E. De Smedt, Tiny Jaarsma, Flora M. Haaijer-Ruskamp, Petra Denig</dc:creator><dc:identifier>10.1016/j.cardfail.2009.09.006</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-09</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-09</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>135</prism:startingPage><prism:endingPage>141.e2</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409011270/abstract?rss=yes"><title>Medication Adherence is a Mediator of the Relationship Between Ethnicity and Event-Free Survival in Patients With Heart Failure</title><link>http://www.onlinejcf.com/article/PIIS1071916409011270/abstract?rss=yes</link><description>Abstract: Background: Rehospitalization rates are higher in African American than Caucasian patients with heart failure (HF). The reasons for the disparity in outcomes between African Americans and Caucasians may relate to differences in medication adherence. To determine whether medication adherence is a mediator of the relationship between ethnicity and event-free survival in patients with HF.Methods and Results: Medication adherence was monitored longitudinally in 135 HF patients using the Medication Event Monitoring System. Events (emergency department visits for HF exacerbation, HF and cardiac rehospitalization, and all-cause mortality) were obtained by interview and hospital data base review. A series of regression models and survival analyses was conducted to determine whether medication adherence mediated the relationship between ethnicity and event-free survival. Event-free survival was significantly worse in African Americans than Caucasians. Ethnicity was a predictor of medication adherence (P=.011). African Americans were 2.57 times more likely to experience an event than Caucasians (P=.026). Ethnicity was not a predictor of event-free survival after entering medication adherence in the model (P=.06).Conclusions: Medication adherence was a mediator of the relationship between ethnicity and event-free survival in this sample. Interventions designed to reduce barriers to medication adherence may decrease the disparity in outcomes.</description><dc:title>Medication Adherence is a Mediator of the Relationship Between Ethnicity and Event-Free Survival in Patients With Heart Failure</dc:title><dc:creator>Jia-Rong Wu, Terry A. Lennie, Marla J. De Jong, Susan K. Frazier, Seongkum Heo, Misook L. Chung, Debra K. Moser</dc:creator><dc:identifier>10.1016/j.cardfail.2009.10.017</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-12-11</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-12-11</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>142</prism:startingPage><prism:endingPage>149</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010458/abstract?rss=yes"><title>Patients' Self-Assessed Functional Status in Heart Failure by New York Heart Association Class: A Prognostic Predictor of Hospitalizations, Quality of Life and Death</title><link>http://www.onlinejcf.com/article/PIIS1071916409010458/abstract?rss=yes</link><description>Abstract: Background: Clinician-assigned New York Heart Association (NYHA) class is an established predictor of outcomes in heart failure. This study aims to test whether patients' self-assessment of functional status by NYHA class predicts hospital admissions, quality of life, and mortality.Methods and Results: This was an observational study within a randomized controlled trial. A total of 293 adult patients diagnosed with heart failure were recruited after an emergency admission at 3 acute hospitals in Norfolk, UK. Outcome measures included number of emergency admissions over 6 months, self-assessed quality of life measured with the Minnesota Living with Heart Failure questionnaire (MLHFQ) and EQ-5D at 6 months, and deaths up to 20 months' follow-up. Patients were grouped into 3 NYHA groups (I/II, III, and IV) based on patients' self-assigned NYHA class (SA-NYHA). A Poisson model indicated an increased readmission rate associated with higher SA-NYHA class (adjusted rate ratio 1.21; 95% CI 1.04–1.41; P=.02). Higher SA-NYHA class at baseline predicted worse quality of life at 6 months' follow-up (P=.002 for MLHFQ; P=.047 for EQ-5D), and was associated with higher mortality rate (adjusted hazard ratio 1.84; 95% CI 1.10–3.06; P=.02).Conclusions: SA-NYHA class is predictive of hospitalization, quality of life, and mortality among patients with heart failure.</description><dc:title>Patients' Self-Assessed Functional Status in Heart Failure by New York Heart Association Class: A Prognostic Predictor of Hospitalizations, Quality of Life and Death</dc:title><dc:creator>Richard Holland, Boika Rechel, Karolina Stepien, Ian Harvey, Iain Brooksby</dc:creator><dc:identifier>10.1016/j.cardfail.2009.08.010</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-10-23</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-10-23</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>150</prism:startingPage><prism:endingPage>156</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010896/abstract?rss=yes"><title>Plasma ACE2 Activity is an Independent Prognostic Marker in Chagas' Disease and Equally Potent as BNP</title><link>http://www.onlinejcf.com/article/PIIS1071916409010896/abstract?rss=yes</link><description>Abstract: Background: Angiotensin-converting enzyme (ACE) 2 is a novel homologue of ACE. It metabolizes angiotensin (Ang)II to Ang-(1-7). This study aims to investigate the diagnostic and prognostic potency of circulating ACE2 activity in patients with heart failure (HF) from Chagas' disease (CD).Methods and Results: Blood samples were obtained from 111 CD patients and 40 age- and gender-matched healthy subjects. The CD patients were further subdivided according to their New York Heart Association classification. ACE2 activity was significantly increased in CD patients with HF, but not in patients without systolic dysfunction. Moreover, plasma ACE2 activity was significantly correlated with their clinical severity and echocardiographic parameters. Importantly, the potency of circulating ACE2 activity in CD patients was equally potent as that of B-type natriuretic peptide to predict cardiac death and heart transplant. Most importantly, patients with both parameters elevated were on a 5-fold higher risk to reach an endpoint than patients with increase in only 1 of the 2 parameters.Conclusions: Determination of ACE2 activity may provide a new and important diagnostic and prognostic marker for patients with CD. ACE2 activity and BNP concentration have additive predictive value and may be used in combination to offer a new dimension of prediction in HF.</description><dc:title>Plasma ACE2 Activity is an Independent Prognostic Marker in Chagas' Disease and Equally Potent as BNP</dc:title><dc:creator>Yong Wang, Maria da Consolação V. Moreira, Silvia Heringer-Walther, Linda Ebermann, Heinz-Peter Schultheiss, Niels Wessel, Wolf-Eberhard Siems, Thomas Walther</dc:creator><dc:identifier>10.1016/j.cardfail.2009.09.005</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-11-05</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-11-05</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Clinical Investigations</prism:section><prism:startingPage>157</prism:startingPage><prism:endingPage>163</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010380/abstract?rss=yes"><title>Sleep-Disordered Breathing and Heart Failure: Focus on Obstructive Sleep Apnea and Treatment With Continuous Positive Airway Pressure</title><link>http://www.onlinejcf.com/article/PIIS1071916409010380/abstract?rss=yes</link><description>Abstract: Background: Among patients with heart failure, sleep-disordered breathing is a common problem, with a prevalence ranging from 24% to 76%. Encompassed within the general category of sleep-disordered breathing are 2 types of sleep apnea: obstructive sleep apnea (OSA) occurs when the oropharyngeal musculature relaxes, causing a collapse of the upper airway, and central sleep apnea occurs when the brain stem fails to stimulate breathing.Methods and Results: This article focuses on the relationship between heart failure and OSA, the treatment of OSA with continuous positive airway pressure (CPAP), and the role of CPAP in improving such effects of heart failure as ejection fraction, blood pressure, sympathetic activity, sleepiness, heart rate, and mortality.Conclusions: It is important to distinguish the type of sleep-disordered breathing a patient may have. Further studies are needed to elucidate the effects of CPAP and other therapies.</description><dc:title>Sleep-Disordered Breathing and Heart Failure: Focus on Obstructive Sleep Apnea and Treatment With Continuous Positive Airway Pressure</dc:title><dc:creator>Mahdi Chowdhury, Suzanne Adams, David J. Whellan</dc:creator><dc:identifier>10.1016/j.cardfail.2009.08.006</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-10-29</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-10-29</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Review Article</prism:section><prism:startingPage>164</prism:startingPage><prism:endingPage>174</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916409010392/abstract?rss=yes"><title>Influence of Rapid Fluid Loading on Airway Structure and Function in Healthy Humans</title><link>http://www.onlinejcf.com/article/PIIS1071916409010392/abstract?rss=yes</link><description>Abstract: Background: The present study examined the influence of rapid intravenous fluid loading (RFL) on airway structure and pulmonary vascular volumes using computed tomography imaging and the subsequent impact on pulmonary function in healthy adults (n = 16).Methods and Results: Total lung capacity (ΔTLC = −6%), forced vital capacity (ΔFVC = −14%), and peak expiratory flow (ΔPEF = −19%) decreased, and residual volume (ΔRV = +38%) increased post-RFL (P &lt; .05). Airway luminal cross-sectional area (CSA) decreased at the trachea, and at airway generation 3 (P &lt; .05), wall thickness changed minimally with a tendency for increasing in generation five (P = .13). Baseline pulmonary function was positively associated with airway luminal CSA; however, this relationship deteriorated after RFL. Lung tissue volume and pulmonary vascular volumes increased 28% (P &lt; .001) post-RFL, but did not fully account for the decline in TLC.Conclusions: These data suggest that RFL results in obstructive/restrictive PF changes that are most likely related to structural changes in smaller airways or changes in extrapulmonary vascular beds.</description><dc:title>Influence of Rapid Fluid Loading on Airway Structure and Function in Healthy Humans</dc:title><dc:creator>Maile L. Ceridon, Eric M. Snyder, Nicholas A. Strom, Juerg Tschirren, Bruce D. Johnson</dc:creator><dc:identifier>10.1016/j.cardfail.2009.08.005</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2009-10-23</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2009-10-23</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Basic Science and Experimental Studies</prism:section><prism:startingPage>175</prism:startingPage><prism:endingPage>185</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916410000126/abstract?rss=yes"><title>Calendar of Events</title><link>http://www.onlinejcf.com/article/PIIS1071916410000126/abstract?rss=yes</link><description></description><dc:title>Calendar of Events</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(10)00012-6</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>186</prism:startingPage><prism:endingPage>186</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916410000047/abstract?rss=yes"><title>Editorial Board</title><link>http://www.onlinejcf.com/article/PIIS1071916410000047/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(10)00004-7</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</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/PIIS1071916410000059/abstract?rss=yes"><title>Masthead</title><link>http://www.onlinejcf.com/article/PIIS1071916410000059/abstract?rss=yes</link><description></description><dc:title>Masthead</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(10)00005-9</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A7</prism:startingPage><prism:endingPage>A7</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916410000060/abstract?rss=yes"><title>Table of Contents</title><link>http://www.onlinejcf.com/article/PIIS1071916410000060/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(10)00006-0</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A9</prism:startingPage><prism:endingPage>A10</prism:endingPage></item><item rdf:about="http://www.onlinejcf.com/article/PIIS1071916410000072/abstract?rss=yes"><title>Information for Authors</title><link>http://www.onlinejcf.com/article/PIIS1071916410000072/abstract?rss=yes</link><description></description><dc:title>Information for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1071-9164(10)00007-2</dc:identifier><dc:source>Journal of Cardiac Failure 16, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Journal of Cardiac Failure</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>16</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1071-9164(10)X0002-1</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A11</prism:startingPage><prism:endingPage>A12</prism:endingPage></item></rdf:RDF>