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Background: Heart failure (HF) is a major global health problem. Clinical trials test efficacy, effectiveness, and safety of novel and emerging therapies in HF. We sought to determine the salient features of ongoing interventional clinical trials in HF.Methods and Results: We accessed the ClinicalTrials.gov registry of the National Institutes of Health (NIH) and the International Clinical Trials Registry Platform of the World Health Organization on January 1, 2017, and extracted pertinent information on current HF clinical trials for systematic review. Of 794 HF trials that met our inclusion criteria, almost one-half (49.1%) evaluated clinical end points and one-third (32.8%) examined imaging end points as primary outcomes. One-fourth (24.8%) were industry sponsored and one-third (35.6%) were university sponsored. The NIH and other United States federal agencies funded only 14 trials (1.8% of all trials; 10.7% of trials in the US). Among 536 HF trials with specified left ventricular ejection fraction status, 434 (81.0%) focused on HF with reduced ejection fraction (HFrEF) and only 102 (19.0%) trials targeted HF with preserved ejection fraction (HFpEF).Conclusions: Ongoing HF trials are predominantly sponsored by nongovernmental funding agencies. Although HFpEF occurs as commonly as HFrEF in the community, the number of clinical trials targeting HFpEF is substantially lower compared with HFrEF. [ABSTRACT FROM AUTHOR]

Background: Myocardial rupture is a relatively rare and usually fatal complication of myocardial infarction (MI). Early recognition of patients at greatest risk of myocardial rupture provides an opportunity for early intervention. Methods: VALIANT was a double-blind, randomized, controlled trial comparing valsartan, captopril, and their combination in high-risk patients post-MI. Myocardial rupture was identified by autopsy (available in 138/589 patients dying within 30 days of index MI), echocardiography, direct surgical visualization, or presence of hemopericardium. An independent clinical end points committee reviewed medical records for all deaths or suspected nonfatal cardiovascular events. Results: Rupture was identified in 45 (0.31%) patients enrolled in VALIANT, occurring 9.8 ± 6.0 days after the qualifying MI. Rupture accounted for 7.6% (45/589) of all deaths occurring in the first 30 days of follow-up and 24% (33/138) of deaths in which autopsies were obtained. Compared with survivors, rupture was associated with increased age, hypertension, increased Killip class, lower estimated glomerular filtration rate, and Q wave MI, and inversely related to β-blocker and diuretic use. Compared with patients who died of other causes within 30 days, patients with myocardial rupture were more likely to have had an inferior MI, Q wave MI, or hypertension; to have used oral anticoagulants; or to have received thrombolytic therapy. Conclusions: Although rare, myocardial rupture accounted for nearly one fourth of all deaths within the first 30 days after high-risk MI, suggesting an estimated incidence of approximately 1% within the first 30 days. A number of clinical characteristics may identify post-MI patients at higher risk of myocardial rupture. [Copyright &y& Elsevier]

Background: It is understood that coronary heart disease (CHD) is one cause of heart failure, and many risk factors are common to both entities. Hypercholesterolemia, however, being a well-recognized risk factor for CHD, has an unclear association with incident heart failure.Methods: We evaluated the relations of total and high-density lipoprotein (HDL) cholesterol to incident heart failure and CHD in 10,813 US male physicians (mean age, 68 years). Total and HDL cholesterol were analyzed both as continuous and as categorical (in quartiles) variables.Results: There were 222 incident heart failure cases on follow-up (mean, 6 years). In Cox models, after adjusting for traditional coronary risk factors, 1-SD increase in total cholesterol (36.7 mg/dL) and HDL cholesterol (15.3 mg/dL) was not related to incident heart failure with a hazard ratio and 95% CI of 0.91 (0.79-1.05) for total cholesterol and 0.95 (0.82-1.11) for HDL cholesterol. In categorical models, heart failure risk in second, third, and fourth quartiles of total and HDL cholesterol was statistically not different from those in the lowest quartile; hazard ratios with 95% CI were 0.72 (0.49-1.05), 0.76 (0.52-1.11), 0.73 (0.50-1.09) for total cholesterol, and 0.78 (0.53-1.15), 0.66 (0.43-1.00), and 1.03 (0.69-1.54), for HDL cholesterol. Further adjustment for CHD on follow-up or exclusion of individuals with CHD at baseline did not alter the results. In contrast, high total cholesterol and low HDL cholesterol increased the risk of incident CHD (P < .001).Conclusion: In healthy males, total and HDL cholesterol levels were not related to incident heart failure. [ABSTRACT FROM AUTHOR]

Background: Intramyocardial fat deposition occurs as an age-related process and in multiple pathologic processes. Objective: We evaluated the presence of left ventricular (LV) and right ventricular (RV) intramyocardial fat with 64-slice multidetector computed tomography (MDCT). Methods: One hundred persons with no history of coronary artery disease (47 women, 53 men; mean age [± SD], 53 ± 12.2 years) and 25 patients with CT findings of myocardial infarction (17 men, 8 women; mean age, 71.3 ± 9.6 years) were studied for intramyocardial fat in defined segments of the ventricles (17 LV and 10 RV segments) at 3 levels. Fat deposition was defined as density range of −30 to −190 Hounsfield units on images both before and after contrast. Results: In healthy persons, LV intramyocardial fat was primarily located in the basal segments (5% anteroseptal, 5% inferior), and RV intramyocardial fat was primarily located in the anterolateral (24% of base, 23% of mid) and inferolateral (27% base, 27% mid) segments. Older age was associated with an increased odds of RV (sex-adjusted odds ratio [OR] per decade increment, 1.61; 95% confidence interval [CI], 1.11–2.33; P = 0.012) but not LV (OR, 0.97; 95% CI, 0.67–1.40; P = 0.85) intramyocardial fat. Compared with women, men had a lower risk of LV (95% CI, 0.1–0.64; P = 0.004) but not RV (95% CI, 0.35–1.87; P = 0.62) intramyocardial fat. Patients with old myocardial infarction (>3 years) had increased percentage of fat in infarcted left ventricles at all 3 levels (P ≤ 0.004). Conclusions: Intramyocardial fat can be detected by MDCT and is common in healthy and infarcted myocardium. [Copyright &y& Elsevier]

Higher blood pressure and body mass index (BMI) are risk factors for heart failure. It is unknown whether the presence of these risk factors in midadulthood affect the future development of heart failure. In the community-based Framingham Heart Study, we examined the associations of antecedent blood pressure and BMI with heart failure incidence in later life. We studied 3362 participants (57% women; mean age: 62 years) who attended routine examinations between 1969 and 1994 and examined their systolic and diastolic blood pressure, pulse pressure, and BMI at current (baseline), recent (average of readings obtained 1 to 10 years before baseline), and remote (average of readings obtained 11 to 20 years before baseline) time periods. During 67 240 person-years of follow-up, 518 participants (280 women) developed heart failure. Current, recent, and remote systolic pressure; pulse pressure; and BMI were individually associated with incident heart failure (all P<0.001). Recent systolic pressure (hazards ratio [HR] per 1-SD increment: 1.31; 95% CI: 1.11 to 1.55), pulse pressure (HR per 1-SD increment: 1.33; 95% CI: 1.14 to 1.54), and BMI (HR per unit increase: 1.15; 95% CI: 1.08 to 1.23) were associated with heart failure risk even after adjusting for current measures. Similarly, remote systolic pressure (HR per 1 SD: 1.17; 95% CI: 1.04 to 1.31), pulse pressure (HR per 1 SD: 1.17; 95% CI: 1.06 to 1.31), and BMI (HR per unit: 1.09; 95% CI: 1.05 to 1.14) remained associated with incident heart failure after adjusting for current measurements. Higher blood pressure and BMI in midlife are harbingers of increased risk of heart failure in later life. Early risk factor modification may decrease heart failure burden. [ABSTRACT FROM AUTHOR]

Background: Left ventricular systolic dysfunction (LVSD) and heart failure (HF) are powerful predictors of poor outcome after acute myocardial infarction (MI). It is not known, however, whether the extent of coronary artery disease (CAD) independently influences cardiovascular (CV) outcomes in these high-risk patients. Methods: In the VALIANT, 14703 patients were randomly assigned to receive either captopril monotherapy, valsartan monotherapy, or a valsartan and captopril combination between 0.5 and 10 days after acute MI complicated by LVSD, HF, or both. Cox proportional hazards models were used to evaluate the relation between the extent of CAD (the number of diseased vessels as assessed by angiography) and a range of CV outcomes and all-cause mortality. Results: Coronary angiography data were available on 5742 (40%) of the 14703 randomized patients. Single-vessel disease was reported in 1955 patients (34%), 2-vessel disease in 1598 (28%), and 3-vessel disease in 2189 (38%). For all CV outcomes, the risk increased with the severity of CAD (P for trend < .002). A comparison of single-, 2-, and 3-vessel disease showed that, after adjusting for all known covariates, including revascularization and ejection fraction, 2-vessel disease was associated with a 40% increased hazard (P = .008) and 3-vessel disease was associated with an 85% increased hazard (P < .001) for all-cause mortality. The fully adjusted hazard ratios for death and other CV outcomes increased significantly with increasing extent of CAD. Conclusions: Increasing extent of CAD, as detected by angiography, is a significant and independent risk factor for adverse CV outcomes after MI complicated by HF, LVSD, or both. The observed risk was apparent even after excluding patients who had undergone revascularization. [ABSTRACT FROM AUTHOR]