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The development of heart failure and/or left ventricular systolic dysfunction (LVSD) in the setting of acute myocardial infarction (AMI) results in significant risk far above that of AMI independently. In patients admitted to the hospital for AMI, concomitant heart failure and/or LVSD on hospital admission or development of either or both of these conditions during admission are among the strongest predictors of inhospital death and are associated with significant increases in inhospital, 30-day, and long-term mortality and rehospitalization rates. Given the high risks in this population, aggressive treatment, comprising early initiation and sustained use of evidence-based treatments, is essential for improving prognosis. [Copyright &y& Elsevier]

Renal dysfunction is an independent risk factor for cardiovascular (cv) disease and its associated complications. diabetes mellitus (dm) is a common cause of renal dysfunction. whether the presence or absence of dm modifies the relation between renal dysfunction and cv disease is unclear. the valiant trial identified 14,527 patients with acute myocardial infarction complicated by either clinical or radiologic signs of heart failure and/or left ventricular dysfunction for whom baseline creatinine was measured. patients were randomly assigned to receive captopril, valsartan, or both. glomerular filtration rate (gfr) was estimated using the 4-component modification of diet in renal disease equation. using multivariable cox proportional modeling, the relation of overall mortality and composite cardiovascular events with estimated gfr (egfr) between patients with and without dm was compared. mean egfrs were 66.8 ± 22.0 and 71.2 ± 21.0 ml/min/1.73 m2 for patients with (n = 3,358) and without dm (n = 11,169), respectively. the likelihood of experiencing death or the composite end point was higher in patients with than without dm for each level of renal function. the augmentation in risk of cv events based on reduced renal function was similar between groups. each decrease in egfr by 10 units was associated with hazards of 1.09 (95% confidence interval 1.06 to 1.12, p <0.001) in patients with dm and 1.08 (95% confidence interval 1.06 to 1.10, p <0.001) in patients without dm for risk of fatal and nonfatal cv outcomes independent of treatment assignment. in conclusion, although dm is associated with higher risk of renal dysfunction and adverse cv outcomes, patients without dm had a relation between renal function and cv risk similar to that for patients with dm after high-risk acute myocardial infarction. [Copyright &y& Elsevier]

In the light of the recent randomized controlled trials in chronic heart failure, it is now commonly assumed that treatment with an angiotensin-receptor blocker (ARB) is equivalent to treatment with an angiotensin-converting enzyme (ACE) inhibitor. We performed an imputed placebo analysis using previous placebo-ACE inhibitor trials and the current ACE inhibitor-ARB comparison studies, which shows that ARBs may not even be superior to placebos, let alone an ACE inhibitor. [ABSTRACT FROM AUTHOR]

Concern has been raised about combining β blockers with angiotensin-receptor blockers in patients with heart failure. The VALsartan In Acute myocardial infarction (VALIANT) trial enrolled 14,703 patients with myocardial infarction complicated by heart failure or documented left ventricular systolic dysfunction. These patients were randomly allocated to treatment with valsartan, captopril, or both. Physicians were also encouraged to prescribe β blockers because of previous evidence of benefit. The baseline characteristics, treatments, and outcomes were compared among 4 groups: patients taking β blockers at admission only, at discharge only, at both admission and discharge, and neither. Patients treated with β blockers were at lower risk than those not treated at any period. Those treated with β blockers at both intervals had a lower 3-year mortality rate (17.7%) than those treated only at randomization (30.7%) or only at discharge (25.9%). The greatest mortality (35.1%) occurred in patients not treated at either point. No statistically significant interaction with prognosis was observed between β-blocker use and treatment with valsartan or valsartan plus captopril. Patients discharged with a β blocker had a significant survival advantage after adjustment for differences in baseline characteristics and intervening complications (hazard ratio 0.89, 95% confidence interval 0.81 to 0.98, p = 0.02). This association was most pronounced in patients prescribed consistent β blockers at randomization and discharge and was present in both patients with impaired and those with preserved systolic left ventricular function. These results have further confirmed that β blockers reduce the risk of death and nonfatal cardiovascular events in patients with heart failure or systolic left ventricular dysfunction after myocardial infarction. In conclusion, no evidence was found of adverse interactions between the angiotensin-receptor blocker valsartan and β blockers or of a negative effect of the combination of valsartan, captopril, and β blockers. [Copyright &y& Elsevier]

Severe right ventricular dysfunction independent of left ventricular ejection fraction increased the risk of heart failure (HF) and death after myocardial infarction (MI). The association between right ventricular function and other clinical outcomes after MI was less clear. Two-dimensional echocardiograms were obtained in 605 patients with left ventricular dysfunction and/or clinical/radiologic evidence of HF from the VALIANT echocardiographic substudy (mean 5.0 ± 2.5 days after MI). Clinical outcomes included all-cause mortality, cardiovascular (CV) death, sudden death, HF, and stroke. Baseline right ventricular function was measured in 522 patients using right ventricular fractional area change (RVFAC) and was related to clinical outcomes. Mean RVFAC was 41.9 ± 4.3% (range 19.2% to 53.1%). The incidence of clinical events increased with decreasing RVFAC. After adjusting for 11 covariates, including age, ejection fraction, and Killip’s classification, decreased RVFAC was independently associated with increased risk of all-cause mortality (hazard ratio [HR] 1.61, 95% confidence interval [CI] 1.31 to 1.98), CV death (HR 1.62, 95% CI 1.30 to 2.01), sudden death (HR 1.79, 95% CI 1.26 to 2.54), HF (HR 1.48, 95% CI 1.17 to 1.86), and stroke (HR 2.95, 95% CI 1.76 to 4.95), but not recurrent MI. Each 5% decrease in baseline RVFAC was associated with a 1.53 (95% CI 1.24 to 1.88) increased risk of fatal and nonfatal CV outcomes. In conclusion, decreased right ventricular systolic function is a major risk factor for death, sudden death, HF, and stroke after MI. [Copyright &y& Elsevier]