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JACC : Heart Failure
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     ISSN (Online) 2213-1779
     Published by American College of Cardiology Foundation Homepage  [1 journal]
  • Inside This Issue
    • PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Factors Influencing the Predictive Power of Models for
           Predicting Mortality and/or Heart Failure Hospitalization in Patients
           With Heart Failure
    • Authors: Ouwerkerk W; Voors AA, Zwinderman AH.
      Abstract: The present paper systematically reviews and compares existing prediction models in order to establish the strongest variables, models, and model characteristics in patients with heart failure predicting outcome. To improve decision making accurately predicting mortality and heart-failure hospitalization in patients with heart failure can be important for selecting patients with a poorer prognosis or nonresponders to current therapy, to improve decision making. MEDLINE/PubMed was searched for papers dealing with heart failure prediction models. To identify similar models on the basis of their variables hierarchical cluster analysis was performed. Meta-analysis was used to estimate the mean predictive value of the variables and models; meta-regression was used to find characteristics that explain variation in discriminating values between models. We identified 117 models in 55 papers. These models used 249 different variables. The strongest predictors were blood urea nitrogen and sodium. Four subgroups of models were identified. Mortality was most accurately predicted by prospective registry-type studies using a large number of clinical predictor variables. Mean C-statistic of all models was 0.66 ± 0.0005, with 0.71 ± 0.001, 0.68 ± 0.001 and 0.63 ± 0.001 for models predicting mortality, heart failure hospitalization, or both, respectively. There was no significant difference in discriminating value of models between patients with chronic and acute heart failure. Prediction of mortality and in particular heart failure hospitalization in patients with heart failure remains only moderately successful. The strongest predictors were blood urea nitrogen and sodium. The highest C-statistic values were achieved in a clinical setting, predicting short-term mortality with the use of models derived from prospective cohort/registry studies with a large number of predictor variables.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Heart Failure Risk Prediction Models What Have We Learned? ∗
    • Authors: Levy WC; Anand IS.
      Abstract: Physicians are becoming enamored of risk prediction models. Cox proportional hazards, logistic regression, and classification and regression tree methods are being widely used to create a wide variety of prediction models. We should be cognizant of the following quote:“Prediction is very difficult, especially about the future.”—Niels Bohr (1)
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • “Triple Therapy” of Heart Failure
           With Angiotensin-Converting Enzyme Inhibitor, Beta-Blocker, and
           Aldosterone Antagonist May Triple Survival Time Shouldn’t We
           Tell Patients?
    • Authors: Cole GD; Patel SJ, Zaman N, et al.
      Abstract: Prescription and adherence to medical therapy for heart failure are disappointing despite convincing randomized controlled trial (RCT) evidence for angiotensin-converting enzyme inhibition, beta-blockade, and aldosterone antagonism. In this study, we report an imbalanced approach amongst clinicians, who describe focusing during patient consultations on perceived risks of therapy rather than survival benefits. Only one-half of clinicians mention increased lifespan, and very few suggest to the patient how large this gain might be. We calculate from the available RCT data that, for patients whose lifespan is limited by heart failure, triple therapy triples lifespan.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Correction
    • Abstract: McKeag NA, McKinley MC, Harbinson MT, Noad RL, Dixon LH, McGinty A, Neville CE, Woodside JV, McKeown PP
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • What Is Normal in HFNEF? The Case for HFpEF
    • Authors: Lam CP.
      Abstract: We have come a long way in the diastolic heart failure (HF)—HF with normal systolic function—HF with normal ejection fraction (EF)—HF with preserved EF world (1). Just 2 decades ago, we couldn’t agree whether this syndrome existed. This skepticism has been replaced by general recognition that it not only exists, but that it constitutes a sizeable proportion of the HF population and is a deadly disease. However, this is where the consensus seems to end—we can’t agree on what to call it, nor if it is a distinct syndrome or part of the same continuous spectrum as HF with reduced EF (HFrEF).
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Reply What Is Normal in HFNEF? The Case for HFpEF
    • Authors: Sanderson JE.
      Abstract: Dr. Lam makes many sensible and reasonable comments in response to my viewpoint, and it appears we are in agreement on most aspects. Of course, one can quibble about the definition of what is a truly “normal” ejection fraction (above 45%, 50%, or 55%), but it is curious that this objection is never raised when discussing the definition of heart failure with a “reduced” ejection fraction, although it can have equally important implications (1). Presumably, if one can define a reduced ejection fraction, then everything above that is fairly acceptable, and the generally recognized cutoff would appear to be 50%. However, “preserved” is definitely not the correct word to use because it is clear that in the condition some call “HFNEF,” the ejection fraction is not unchanging, but rather gradually falls; and whatever else is debatable, the definition of the word preserved is not arguable: it is generally accepted to mean something that is unchanged or “maintain (something) in its original or existing state” (OED) (2). It may appear to be nitpicking, but precision in the use of words is important, especially in science as well as politics (as George Orwell said if “thought corrupts language, language can also corrupt thought” [3]).
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Pseudobendopnea?
    • Authors: RuDusky BM.
      Abstract: The well-performed and presented study on the characterization of bendopnea in patients with advanced heart failure by Thibodeau et al. (1) merits additional clinical commentary. It is unclear as to why the patients were referred for right heart catheterization. Was this performed in concert with a left heart catheterization? It would appear that it was not. Equally so, it would appear that it was not done solely for the purpose of the study but as a secondary foundation for pathophysiological characterization of the symptom of dyspnea on bending. As a diagnostic tool, the data indicate a low sensitivity for that purpose because all patients with bendopnea (100%) had dyspnea on exertion, and of those without bendopnea, 80% had dyspnea on exertion, whereas bendopnea was present in only 29% of the patients studied.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Characterization of a Novel Symptom of Advanced Heart Failure: Bendopnea
    • Authors: Brandon N.
      Abstract: The article by Thibodeau et al. (1) characterizing the invasive hemodynamics of heart failure patients complaining of shortness of breath while bending corroborates a similar observation that I have recently published (2). Using Doppler echocardiography, I also demonstrated an increase in estimates of pulmonary capillary wedge pressure beyond baseline while bending forward, in normal patients as well as in those with known chronic heart failure (CHF). The present study adds to our knowledge of this phenomenon by examining a larger number of patients and measuring hemodynamics invasively.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Reply Bendopnea and Pseudobendopnea
    • Authors: Thibodeau JT; Levine BD, Drazner MH.
      Abstract: We appreciate the interest of Drs. RuDusky and Brandon in our study (1). Patients had been referred for diagnostic right heart catheterizations for clinical indications. A minority (19%) had a concomitant left heart catheterization. The current study was not able to address the diagnostic utility of bendopnea versus dyspnea on exertion because, as detailed in the limitations section, symptoms besides bendopnea were ascertained by patient recall over the preceding week, whereas bendopnea was assessed on the day of the right heart catheterization. We agree that it will be important to determine the prevalence and significance of bendopnea in other patient populations including those who do not have heart failure. However, we do not concur that the nomenclature “pseudobendopnea” should be used for this symptom in patients without heart failure. As a rationale for our opinion, we give the example of an obese patient without heart failure who gets short of breath in the supine position. In such a setting, the symptom would still be termed orthopnea rather than pseudo-orthopnea. In terms of where to go from here, we hope future studies will determine whether ascertainment of bendopnea can improve clinical decision making.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Are Models Better Than Cardiologists? An Analysis of Risk Prediction
           in Heart Failure
    • Authors: O’Connor C.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Colchicine in Stable Chronic Heart Failure
    • Authors: Van Tassell B; Canada J, Arena R, et al.
      Abstract: We read with interest the study of colchicine in stable heart failure by Deftereos et al. (1). Colchicine used at a dose of 0.5 mg twice daily was safe in patients with heart failure and, at least in part, effective in reducing systemic inflammation. However, the study failed to show a significant improvement in New York Heart Association functional class or functional capacity with colchicine treatment. When considering why colchicine inhibited inflammation, yet had no significant clinical advantage (2), we put forth the following considerations and questions:
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Reply Colchicine in Stable Chronic Heart Failure
    • Authors: Giannopoulos G; Deftereos S.
      Abstract: We would like to thank Dr. Van Tassel and colleagues for their interest in our paper (1). On a general note, we would like to point out that having tried colchicine in other settings of cardiovascular disease (namely post-ablation atrial fibrillation recurrence and post-percutaneous coronary intervention diabetic patients [2–5]) with positive results, we anticipated that we would observe some kind of beneficial effect in patients with heart failure too. The endpoint we chose for this study (improvement in New York Heart Association functional class) was rather a soft one, believing that the least clinicians should expect from any such treatment is an improvement in symptoms. In this line of thought, although we can see the rationale behind the comments put forth by Dr. Van Tassel and colleagues in their letter to the editor, we feel that some of them miss the point—namely the primary endpoint (pun intended) of the study: colchicine was not associated with any improvement in symptom severity. Having said that, we find it hard to believe that using cardiopulmonary stress testing would change the essence of the study results in any meaningful way. In regard to the degree of inflammation abatement, we agree that the levels of on-treatment C-reactive protein indicate significant residual inflammation; however, more potent anti-inflammatory action would probably require higher colchicine doses, which would entail higher frequency of adverse effects (from our experience, doses higher than 0.5 mg twice daily are associated with markedly increased—mostly gastrointestinal—side effects, which lead to significant declines in patient compliance). Whether other anti-inflammatory agents can offer full inhibition of inflammatory processes, without significant toxicity, is a matter of future research—but, again, any such effect must be accompanied by significant improvements in symptoms or, even better, in hard endpoints, including heart failure–related hospitalizations and mortality (unfortunately, clinical study results have been less than compelling in that respect).
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Chronic Counterpulsation Devices for Heart Failure ∗
    • Authors: Milano CA.
      Abstract: The C-Pulse System (Sunshine Heart, Inc., Eden Prairie, Minnesota) is a novel implanted counterpulsation heart assist pump that is positioned around the ascending aorta. It is non–blood contacting and may be turned off intermittently or weaned off in cases of ventricular recovery. In this issue of JACC: Heart Failure, Abraham et al. (1) describe a safety assessment study in which 20 heart failure patients received the device. The most encouraging outcome was that none of the 20 patients experienced a stroke. Importantly, patients were pre-screened and those with ascending aortic disease were excluded. Unfortunately, 1 patient experienced a procedure- and device-related death from a mediastinal infection. Furthermore, disappointingly 40% of patients experienced drive line exit site infection. Patients who survived with the device to a 12-month follow-up time point did experience a modest increase in 6-min walk distances, although clinical improvement of heart failure was not the primary focus of this pilot study.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Heart Failure and Peripheral Artery Disease An Unappreciated Association
    • Authors: Hiatt WR.
      Abstract: In this issue of JACC: Heart Failure, Gupta et al. (1) report on the association of the ankle-brachial index (ABI) with incident heart failure in the ARIC (Atherosclerosis Risk in Communities) study. Although this is not the first report, the association extends our knowledge of the clinical value of the ABI and provides intriguing insights into additional pathophysiologic links between occlusive arterial disease in the peripheral circulation and a variety of cardiovascular disease manifestations.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Rationale and Design of the GUIDE-IT Study Guiding Evidence
           Based Therapy Using Biomarker Intensified Treatment in Heart
    • Authors: Felker G; Ahmad T, Anstrom KJ, et al.
      Abstract: ObjectivesThe GUIDE-IT (Guiding Evidence Based Therapy Using Biomarker Intensified Treatment in Heart Failure) study is designed to determine the safety, efficacy, and cost-effectiveness of a strategy of adjusting therapy with the goal of achieving and maintaining a target N-terminal pro–B-type natriuretic peptide (NT-proBNP) level of 
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Left Ventricular Size, Mass, and Shape Is the Sum Greater Than the
           Parts? ∗
    • Authors: Shah AM; Pfeffer MA.
      Abstract: Alterations in cardiac structure and function have long been recognized as markers of heightened risk for cardiovascular events. Indeed, even before the advent of noninvasive imaging, electrocardiographic left ventricular hypertrophy (LVH) was identified as one of the earliest “factors of risk” for cardiovascular morbidity and mortality by the Framingham Heart Study investigators, alongside hypertension, hyperlipidemia, smoking, and obesity (1,2). Concurrently, Linzbach (3) used pathology samples to describe 2 distinct patterns of LVH, reflecting the impact of volume and pressure loading on LV muscle mass and chamber size: eccentric (volume) hypertrophy, characterized by increased chamber size and residual volume; and concentric (pressure) hypertrophy, with preserved chamber size and residual volume. Hammermeister et al. used left ventriculography to demonstrate the prognostic importance of LV volumes (4) and ejection fraction (5) for survival in patients with valvular and coronary diseases, respectively.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Ambulatory Extra-Aortic Counterpulsation in Patients With Moderate to
           Severe Chronic Heart Failure
    • Authors: Abraham WT; Aggarwal S, Prabhu SD, et al.
      Abstract: ObjectivesThe study sought to assess feasibility, safety, and potential efficacy of a novel implantable extra-aortic counterpulsation system (C-Pulse) in functional class III and ambulatory functional class IV heart failure (HF) patients.Background30% to 40% of HF patients suffer from poor functional status and quality of life (QoL) but are not in need of end-stage treatments. We undertook a multicenter single-arm study to assess the C-Pulse System in such patients.MethodsNew York Heart Association (NYHA) functional class III or ambulatory functional class IV HF patients were eligible. Safety was assessed continuously through 12 months. Efficacy measurements included changes from baseline to 6 and 12 months in NYHA functional class, Minnesota Living with Heart Failure (MLWHF) and Kansas City Cardiomyopathy Questionnaire (KCCQ) scores, 6-min walk distance (6MWD), and exercise peak oxygen consumption (pVO2; 6 months only).ResultsTwelve men and 8 women (56.7 ± 7 years, 34 to 71 years of age) with ischemic (n = 7) or nonischemic (n = 13) cardiomyopathy were implanted. There was no 30-day mortality and no neurological events or myocardial infarctions through 12 months. At 6 months, there were 3 deaths (1 device-related). One-year survival was 85%. At 6 months, C-Pulse produced improvements in NYHA functional class (3.1 ± 0.3 to 1.9 ± 0.7, p = 0.0005), MLWHF (63.6 ± 19.9 to 40.2 ± 23.2, p = 0.0005), and KCCQ scores (43.6 ± 21.1 to 65.6 ± 21.5, p = 0.0002), but not 6MWD (275.5 ± 64.0 to 296.4 ± 104.9, p = NS) or pVO2 (14.5 ± 3.6 to 13.1 ± 4.4, p = NS). Improvements continued at 12 months, with 6MWD change becoming statistically significant (336.5 ± 91.8, p = 0.0425).ConclusionsUse of C-Pulse in this population is feasible, appears safe, and improves functional status and QoL. A prospective, multicenter, randomized controlled trial is underway. (C-Pulse IDE Feasability Study-A Heart Assist System; NCT00815880)
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Risk Prediction in Patients With Heart Failure A Systematic
           Review and Analysis
    • Authors: Rahimi K; Bennett D, Conrad N, et al.
      Abstract: ObjectivesThis study sought to review the literature for risk prediction models in patients with heart failure and to identify the most consistently reported independent predictors of risk across models.BackgroundRisk assessment provides information about patient prognosis, guides decision making about the type and intensity of care, and enables better understanding of provider performance.MethodsMEDLINE and EMBASE were searched from January 1995 to March 2013, followed by hand searches of the retrieved reference lists. Studies were eligible if they reported at least 1 multivariable model for risk prediction of death, hospitalization, or both in patients with heart failure and reported model performance. We ranked reported individual risk predictors by their strength of association with the outcome and assessed the association of model performance with study characteristics.ResultsSixty-four main models and 50 modifications from 48 studies met the inclusion criteria. Of the 64 main models, 43 models predicted death, 10 hospitalization, and 11 death or hospitalization. The discriminatory ability of the models for prediction of death appeared to be higher than that for prediction of death or hospitalization or prediction of hospitalization alone (p = 0.0003). A wide variation between studies in clinical settings, population characteristics, sample size, and variables used for model development was observed, but these features were not significantly associated with the discriminatory performance of the models. A few strong predictors emerged for prediction of death; the most consistently reported predictors were age, renal function, blood pressure, blood sodium level, left ventricular ejection fraction, sex, brain natriuretic peptide level, New York Heart Association functional class, diabetes, weight or body mass index, and exercise capacity.ConclusionsThere are several clinically useful and well-validated death prediction models in patients with heart failure. Although the studies differed in many respects, the models largely included a few common markers of risk.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Heart Failure Risk Across the Spectrum of Ankle-Brachial Index
           The ARIC Study (Atherosclerosis Risk In Communities)
    • Authors: Gupta DK; Skali H, Claggett B, et al.
      Abstract: ObjectivesThe aim of this study was to describe the relationship between ankle brachial index (ABI) and the risk for heart failure (HF).BackgroundThe ABI is a simple, noninvasive measure associated with atherosclerotic cardiovascular disease and death; however, the relationship between ABI and risk for HF is less well characterized.MethodsBetween 1987 and 1989 in the ARIC (Atherosclerosis Risk In Communities) study, an oscillometric device was used to measure blood pressure in a single upper and randomly chosen lower extremity to determine the ABI. Incident HF events were defined by the first hospitalization with an International Classification of Diseases, Ninth Revision, code of 428.x through 2008. The risk for HF was assessed across the ABI range using restricted cubic splines and Cox proportional hazards models.ResultsABI was available in 13,150 participants free from prevalent HF. Over a mean 17.7 years of follow-up, 1,809 incident HF events occurred. After adjustment for traditional HF risk factors, prevalent coronary heart disease, subclinical carotid atherosclerosis, and interim myocardial infarction, compared with an ABI of 1.01 to 1.40, participants with ABIs ≤0.90 were at increased risk for HF (hazard ratio: 1.40; 95% confidence interval: 1.12 to 1.74), as were participants with ABIs of 0.91 to 1.00 (hazard ratio: 1.36; 95% confidence interval: 1.17 to 1.59).ConclusionsIn a middle-age community cohort, an ABI ≤1.00 was significantly associated with an increased risk for HF, independent of traditional HF risk factors, prevalent coronary heart disease, carotid atherosclerosis, and interim myocardial infarction. Low ABI may reflect not only overt atherosclerosis but also pathologic processes in the development of HF beyond epicardial atherosclerotic disease and myocardial infarction alone. A low ABI, as a simple, noninvasive measure, may be a risk marker for HF.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Effects of Obesity and Weight Changes on Cardiac and Vascular Structure
           and Function Does the Clinical Impact Carry Any Weight? ∗
    • Authors: Lavie CJ; Milani RV, Ventura HO.
      Abstract: Overweight and obesity have increased in the United States and most of the Westernized world over recent decades, reaching a prevalence in the United States of well over 70% (1). Clearly, overweight and obese patients have increased cardiovascular (CV) risk factors, including hypertension, dyslipidemia, glucose abnormalities (impaired fasting glucose, metabolic syndrome, type II diabetes), and inflammation (1,2). Although a lack of physical activity is the primary cause of obesity (3–5), once obesity is manifest, physical activity and cardiorespiratory fitness progressively decline with weight gain. Therefore, it is not surprising that obesity is associated with a marked increased risk for most CV diseases.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Adverse Left Ventricular Remodeling in Community-Dwelling Older
           Adults Predicts Incident Heart Failure and Mortality
    • Authors: Zile MR; Gaasch WH, Patel K, et al.
      Abstract: ObjectivesThis study sought to determine whether specific patterns of adverse left ventricular (LV) structural remodeling are associated with differential rates of cardiovascular (CV) outcomes.BackgroundIt is not known whether a stepwise combinatorial assessment of LV volume, mass, and geometry done to define specific remodeling patterns provides incremental prognostic information.MethodsA total of 3,181 Cardiovascular Health Study participants (mean age, 73 years of age; 60% women, 5% African American) were categorized by LV remodeling patterns and related to a multivariate-adjusted (age, sex, race, ejection fraction, hypertension, myocardial infarction, diabetes mellitus, chronic kidney disease) analysis of CV outcomes (incident heart failure [HF], all-cause mortality, and a combined endpoint of HF and mortality) over a 13-year follow-up period.ResultsExamined independently, either left ventricular enlargement (LVE) or left ventricular hypertrophy (LVH) was associated with a higher risk of HF (32%, 34%, respectively) than with normal geometry (17%; p < 0.001). When LV volume and mass were used in combination, important incremental prognostic information was achieved. In the absence of LVE, HF was more common in those with LVH than in those with normal mass (32% vs. 16%, respectively; p < 0.001). In the presence of LVE, HF was more common in those with LVH than in those with normal mass (37% vs. 29%, respectively; p = 0.021). The subgroup with normal volume and mass but relative wall thickness (RWT) >0.42 carried a higher risk of HF (21%) than those with normal geometry (15%; p = 0.011). Once LVH or LVE was present, the addition of RWT to this analysis did not affect HF rate. Similar results were obtained for the other CV outcomes.ConclusionsStepwise combinatorial assessment of LV volume, mass, and geometry provides incremental prognostic information regarding CV outcomes.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Association of Obesity in Early Adulthood and Middle Age With
           Incipient Left Ventricular Dysfunction and Structural Remodeling
           The CARDIA Study (Coronary Artery Risk Development in Young Adults)
    • Authors: Kishi S; Armstrong AC, Gidding SS, et al.
      Abstract: ObjectivesThe goal of this study was to investigate the relationship of body mass index (BMI) and its 25-year change to left ventricular (LV) structure and function.BackgroundLongstanding obesity may be associated with clinical cardiac dysfunction and heart failure. Whether obesity relates to cardiac dysfunction during young adulthood and middle age has not been investigated.MethodsThe CARDIA (Coronary Artery Risk Development in Young Adult) study enrolled white and black adults ages 18 to 30 years in 1985 to 1986 (Year-0). At Year-25, cardiac function was assessed by conventional echocardiography, tissue Doppler imaging (TDI), and speckle tracking echocardiography (STE). Twenty-five–year change in BMI (classified as low: 
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Impact of General and Central Adiposity on Ventricular-Arterial Aging
           in Women and Men
    • Authors: Wohlfahrt P; Redfield MM, Lopez-Jimenez F, et al.
      Abstract: ObjectivesThe aim of this study was to assess the effects of central and general obesity measures on long-term longitudinal changes in ventricular-arterial mechanics.BackgroundObesity, female sex, and ventricular-arterial stiffening are associated with the development of heart failure with preserved ejection fraction. Fat distribution and chronic changes in body composition may affect longitudinal changes in LV properties, independent of arterial load.MethodsIn 1,402 subjects from a randomly selected, community-based population, comprehensive echo-Doppler echocardiography was performed at two examinations separated by 4 years. From this population, 788 subjects had paired data adequate for determining left ventricular end-systolic elastance (Ees), end-diastolic elastance (Eed), and effective arterial elastance (Ea).ResultsOver 4 years, Ea was decreased by 3% in tandem with improved blood pressure control, whereas Ees and Eed were increased by 14% and 8% (all, p < 0.001). Greater weight loss over 4 years was associated with progressively greater decreases in Ea in men and women. After adjustment for Ea change, weight gain was correlated with increases in Eed in both women and men. Central obesity was associated with greater age-related increases in Ees in women but not in men, independent of arterial load, but central obesity did not predict changes in Eed or Ea.ConclusionsIn these subjects, weight gain was associated with increases in LV diastolic stiffness, even after adjustment for changes in arterial afterload, whereas weight loss was associated with reductions in arterial stiffness. Age-related LV systolic stiffening was increased in women, but not in men, with central obesity. Strategies for promoting weight loss and reducing central adiposity may be effective in preventing heart failure with preserved ejection fraction, particularly in women.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Charting a Roadmap for Heart Failure Biomarker Studies
    • Authors: Ahmad T; Fiuzat M, Pencina MJ, et al.
      Abstract: Heart failure is a syndrome with a pathophysiological basis that can be traced to dysfunction in several interconnected molecular pathways. Identification of biomarkers of heart failure that allow measurement of the disease on a molecular level has resulted in enthusiasm for their use in prognostication and selection of appropriate therapies. However, despite considerable amounts of information available on numerous biomarkers, inconsistent research methodologies and lack of clinical correlations have made bench-to-bedside translations rare and left the literature with countless publications of varied quality. There is a need for a systematic and collaborative approach aimed at definitively studying the clinical benefits of novel biomarkers. In this review, on the basis of input from academia, industry, and governmental agencies, we propose a systematized approach based on adherence to specific quality measures for studies looking to augment current prediction model or use biomarkers to tailor therapeutics. We suggest that study quality, rather than results, should determine publication and propose a system for grading biomarker studies. We outline the need for collaboration between clinical investigators and statisticians to introduce more advanced statistical methodologies into the field of biomarkers that would allow for data from a large number of variables to be distilled into clinically actionable information. Lastly, we propose the creation of a heart failure biomarker consortium that would allow for a comprehensive list of biomarkers to be concomitantly analyzed in a pooled sample of randomized clinical trials and hypotheses to be generated for testing in biomarker-guided trials. Such a consortium could collaborate in sharing samples to identify biomarkers, undertake meta-analyses on completed trials, and spearhead clinical trials to test the clinical utility of new biomarkers.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Can We Now Find the Needle in the Haystack? ∗
    • Authors: Russell SD.
      Abstract: Endomyocardial biopsy (EMB) is rarely performed today to determine the etiology of cardiomyopathies or to guide the therapy of patients who present with cardiomyopathies of unknown etiology. There are a number of reasons for this, including a lack of specific therapies for most cardiomyopathies, a low incidence of actually finding abnormal tissue with biopsy, and the advancement of other imaging technologies such as magnetic resonance imaging that although not diagnostic, can assist in ruling in or out specific disease processes. The Myocarditis Treatment Trial, which evaluated the use of immunosuppressive therapy in patients with biopsy-proven myocarditis, was one of the first steps in this resultant decrease (1). Patients with acute or chronic myocarditis were randomized to immunosuppressive therapy with prednisone plus either azathioprine or cyclosporine versus usual care. After 24 weeks of therapy, there was no difference in ejection fraction or survival between the 2 groups. However, many have reported differences in the prognosis of patients based on the specific etiology found on EMB, some of which might determine different therapeutic approaches. McCarthy et al. (2) identified differences in outcome in patients with fulminant myocarditis compared with those with acute myocarditis. One could argue that patients with fulminant myocarditis requiring acute ventricular assist device support should undergo placement of a temporary device instead of a long-term device because their chances of recovery appear to be higher, knowledge only gained by biopsy. Additionally, specific diagnoses may help guide therapy based on prognosis. Felker et al. (3) reported the outcomes of 1,230 patients that underwent an extensive evaluation (history, cardiac catheterization, and EMB) to determine the etiology of patients with unexplained heart failure. They found significant differences in outcome based on etiology. However, despite this extensive evaluation, they were able to determine the etiology in 50% of the patients and EMB provided a specific histological diagnosis in only 15%.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
  • Electrogram Guidance A Method to Increase the Precision and
           Diagnostic Yield of Endomyocardial Biopsy for
           Suspected Cardiac Sarcoidosis and Myocarditis
    • Authors: Liang JJ; Hebl VB, DeSimone CV, et al.
      Abstract: ObjectivesThe aim of this study was to describe the method used to perform electrogram-guided EMB and correlate electrogram characteristics with pathological and clinical outcomes.BackgroundEndomyocardial biopsy (EMB) is valuable in determining the underlying etiology of a cardiomyopathy. The sensitivity, however, for focal disorders, such as lymphocytic myocarditis and cardiac sarcoidosis (CS), is low. The sensitivity of routine fluoroscopically guided EMB is low. Abnormal intracardiac electrograms are seen at sites of myocardial disease. However, the exact value of electrogram-guided EMB is unknown.MethodsWe report 11 patients who underwent electrogram-guided EMB for evaluation of myocarditis and CS.ResultsOf 40 total biopsy specimens taken from 11 patients, 19 had electrogram voltage 5 mV signified normal myocardium with no significant diagnostic yield. Biopsy results guided therapy in all patients, including 5 with active myocarditis or CS, all of whom subsequently received immunosuppressive therapy. There were no procedural complications.ConclusionsIn patients with suspected myocarditis or CS, electrogram-guided EMB targeting sites with abnormal or low-amplitude electrograms may increase the diagnostic yield for detecting abnormal pathological findings.
      PubDate: Wed, 01 Oct 2014 00:00:00 GMT
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