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Angiotensin II may contribute to the progression of heart failure. In this trial, valsartan, an angiotensin-receptor blocker, reduced the need for hospitalization for heart failure but had no effect on overall mortality. According to a post hoc analysis, patients treated with valsartan who were also receiving both an angiotensin-converting–enzyme (ACE) inhibitor and a beta-blocker had increased mortality; patients receiving one or neither of these types of drugs had reduced mortality. Pharmacotherapy for heart failure has advanced considerably in recent years as clinical trials have demonstrated favorable long-term effects of angiotensin-converting–enzyme (ACE) inhibitors 1 – 3 and beta-blockers 4 – 6 on morbidity and mortality. Despite the use of these potent drugs, heart failure remains the leading reason for hospitalization in the Medicare population, 7 mortality among patients with heart failure is high, and the quality of life is low. Angiotensin II, a potent vasoconstrictor and growth-stimulating hormone, may contribute to the impairment of left ventricular function and the progression of heart failure through increased impedance of left ventricular emptying, 8 adverse long-term structural effects on the . . .

BackgroundHigher body mass index (BMI) is associated with better outcome compared with normal weight in patients with HF and other chronic diseases. It remains uncertain whether the apparent protective role of obesity relates to the absence of comorbidities. Therefore, we investigated the effect of BMI on outcome in younger patients without co-morbidities as compared to older patients with co-morbidities in a large heart failure (HF) population.MethodsIn an individual patient data analysis from pooled cohorts, 5,819 patients with chronic HF and data available on BMI, co-morbidities and outcome were analysed. Patients were divided into four groups based on BMI (i.e. ≤ 18.5 kg/m2, 18.5–25.0 kg/m2; 25.0–30.0 kg/m2; 30.0 kg/m2). Primary endpoints included all-cause mortality and HF hospitalization-free survival.ResultsMean age was 65 ± 12 years, with a majority of males (78%), ischaemic HF and HF with reduced ejection fraction. Frequency of all-cause mortality or HF hospitalization was significantly worse in the lowest two BMI groups as compared to the other two groups; however, this effect was only seen in patients older than 75 years or having at least one relevant co-morbidity, and not in younger patients with HF only. After including medications and N-terminal pro-B-type natriuretic peptide and high-sensitivity cardiac troponin concentrations into the model, the prognostic impact of BMI was largely absent even in the elderly group with co-morbidity.ConclusionsThe present study suggests that obesity is a marker of less advanced disease, but does not have an independent protective effect in patients with chronic HF.Graphic abstractCategories of BMI are only predictive of poor outcome in patients aged > 75 years or with at least one co-morbidity (bottom), but not in those aged < 75 years without co-morbidities (top). The prognostic effect largely disappears in multivariable analyses even for the former group. These findings question the protective effect of obesity in chronic heart failure (HF).

Large-scale trials of therapy for heart failure over the past decade have shown improvements in outcome with angiotensin-converting–enzyme (ACE) inhibitors and beta-blockers. 1 – 7 In the Studies of Left Ventricular Dysfunction (SOLVD), two concurrent trials evaluating the efficacy of enalapril in patients with left ventricular systolic dysfunction, enalapril was associated with a 16 percent reduction in the risk of death from any cause among patients with symptoms 6 and a 20 percent reduction in the risk of death from any cause or hospitalization for heart failure among patients without symptoms. 7 These results and the results of other studies 1 – 5 led to the . . .

Heart failure is a substantial public health problem among black Americans. It is more common in the black population than in other populations in the United States, affecting approximately 3 percent of all black adults in this country. 1 , 2 Symptoms of heart failure develop in blacks at an earlier age than they do in nonblacks, 3 – 5 possibly because blacks are more likely to have hypertension and diabetes and to have ventricular hypertrophy and vascular injury than nonblacks. 5 – 8 Once diagnosed, heart failure progresses more rapidly in black patients than in white patients, as evidenced by the higher risk of initial . . .

Multiple medications have proven efficacy for the primary prevention of coronary heart disease (CHD), but the appropriate patient population remains controversial. Even in the presence of multiple cardiovascular risk factors, many patients are not considered high risk and are not offered preventive medications despite proven efficacy. We analyzed a prospective cohort of 1,710 consecutive ST-elevation myocardial infarction (STEMI) patients treated in a regional STEMI system from May 2007 to July 2010 and enrolled in a comprehensive database that includes preadmission medications. Of the 1,707 patients analyzed, 1,180 (69.1%) did not have known CHD before their event; and 482 (41.7%) of those patients had premature events (men <55 years old, women <65 years old). In patients without known CHD, cardiovascular risk factors were abundant (52.1% had hypertension, 43.6% had dyslipidemia, 41.4% had a family history of CHD, 58.5% were current or former smokers, and 14.9% were diabetic). Despite the high prevalence of risk factors, only 24.1% were on aspirin, 16.1% were on a statin, and only 7.8% were taking an aspirin and statin. Use of preventive medications was even less common in patients with premature events, including aspirin (15.2% vs 30.2%, P value < .001), statins (11.1% vs 19.5%, P value < .001), and the combination (5.6% vs 9.4%, P value < .001). Approximately 70% of a contemporary STEMI population did not have known CHD before their event, and >40% of those events would be considered premature. Despite the significant burden of cardiovascular risk factors, use of preventive therapy was alarmingly low in patients presenting with STEMI.

This clinical trial, in which the study group was made up of black patients with heart failure, showed that the combination of isosorbide dinitrate and hydralazine significantly improves survival when added to standard therapy for heart failure. In this clinical trial of black patients with heart failure, the combination of isosorbide dinitrate and hydralazine significantly improved survival when added to standard therapy. Neurohormonal inhibitors alone or in combination slow the progression of left ventricular dysfunction, retarding the structural remodeling of the left ventricle that characterizes chronic heart failure and reducing the rates of death and complications among patients with heart failure. 1 – 10 Endothelial dysfunction, impaired bioavailability of nitric oxide, and increased oxidant stress also occur in patients with congestive heart failure and contribute to the remodeling process in experimental and clinical models of heart failure. 11 – 27 Augmentation of nitric oxide may therefore be an alternative or supplemental approach to slow or reverse progressive heart failure. The first Vasodilator Heart Failure Trial (V-HeFT . . .

In 2013, clinical trials in heart failure focused on drugs and devices that might improve treatment of symptomatic patients beyond standard therapy. None achieved this aim. Therefore, future efforts should emphasize increased adherence to current, evidence-based therapy, and trials might better address efforts to prevent, rather than treat, heart failure.

The B-type or brain natriuretic peptides (BNP) and the amino-terminal probrain natriuretic peptide (NT-proBNP) are good markers of prognosis and diagnosis in chronic heart failure (HF). It is unclear, however, whether differences in their biological characteristics modify their clinical correlates and prognostic performance in HF. This work aimed to provide a direct comparison of the prognostic value of BNP and NT-proBNP in patients with chronic and stable HF. We measured BNP and NT-proBNP at baseline in 3916 patients enrolled in the Valsartan Heart Failure Trial. To identify the variables associated with both peptides, we conducted simple and multivariable linear regression analyses. We used Cox multivariable regression models to evaluate the independent prognostic value for all-cause mortality, mortality and morbidity, and hospitalization for HF. Prognostic performance was assessed by pairwise comparisons of the area under the curve of receiver-operator characteristic curves. NT-proBNP and BNP had similar relationships with age, left ventrical ejection fraction, and internal diameter and creatinine clearance. Either peptide ranked as the first independent predictor of outcome after adjustment for major confounding clinical characteristics. ROC curves were almost superimposable for all-cause mortality (area under the curve (SE): BNP 0.665 (0.011) vs NT-proBNP 0.679 (0.011); P=0.0734), but NT-proBNP was superior to BNP for predicting mortality and morbidity (P=0.032) or hospitalization for HF (P=0.0143). Overall sensitivity and specificity ranged from 0.590 to 0.696. The natriuretic peptides BNP and NT-proBNP showed subtle differences in their relation to clinical characteristics and prognostic performance in a large population of patients with chronic and stable HF. They were the most powerful independent markers of outcome in HF.

Atrial fibrillation (AF) in heart failure (HF) is generally considered a negative prognostic factor. Recent studies indicate that the incidence of AF might be decreased by renin angiotensin aldosterone system inhibitors. The identification of a treatment to prevent its occurrence is likely to improve patients outcome. The aims of these subanalyses of Val-HeFT were to assess ( a) the effects of valsartan in the prevention of AF, ( b) the independent predictors of this event, and ( c) the prognostic role of AF occurrence. The occurrence of AF was evaluated based on adverse event reports in the patients with HF enrolled in Val-HeFT. Patients were randomized to valsartan or placebo on top of their prescribed treatments for HF. During the mean 23 months of follow-up, AF was reported in 287/4395 patients (6.53%) in sinus rhythm at baseline, of whom 113/2205 (5.12%) were allocated to valsartan and 174/2190 (7.95%) to placebo ( P = .0002). Multivariable analysis showed that brain natriuretic peptide (BNP) levels at baseline above the median value (HR 2.28, 95% CI 1.75-2.98), age over 70 years (HR 1.51, 95% CI 1.17-1.95), male sex (HR 1.53, 95% CI 1.07-2.18), and the valsartan treatment (HR 0.63, 95% CI 0.49-0.81) were independently associated with AF occurrence. Cox multivariable regression analysis showed that occurrence of AF was independently associated with a worse prognosis, with the adjusted hazard risks for all-cause mortality and combined mortality/morbidity of 1.40 (95% CI 1.16-1.58) and 1.38 (95% CI 1.12-1.70), respectively. The results of the present study demonstrate that ( a) adding valsartan to prescribed therapy for HF significantly reduces the incidence of AF by 37%; ( b) BNP level and advanced age were the strongest independent predictors for AF occurrence; and ( c) AF occurrence further worsens the outcome in patients with HF.