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Recent studies suggest that statin therapy reduces hospitalizations for heart failure (HF). However, few data exist regarding the role of statins in preventing HF after acute myocardial infarction (AMI). In addition, the potential impact of left ventricular (LV) ejection fraction (EF) and coexisting functional mitral regurgitation (MR) on the efficacy of statin therapy was not considered. We prospectively studied 1,563 patients with AMI. The primary endpoint was readmission for the treatment of HF. The effect of statin therapy initiated before hospital discharge was evaluated using a Cox model, adjusting for clinical variables, a propensity score for statin therapy, LVEF, and MR grade. Patients with recurrent infarctions were censored. Statins were prescribed in 1,048 patients (67.1%) before hospital discharge. During a median follow-up of 17 months, admissions for HF were lower in patients receiving statins (6.5% vs 14.8%; unadjusted hazard ratio 0.45, 95% confidence interval 0.32 to 0.63, p <0.0001). In a multivariable Cox model, statin therapy was associated with a significant reduction of hospitalization for HF (HR 0.62, 95% confidence interval 0.43 to 0.89, p = 0.009). There was a significant interaction between MR and statin therapy (p = 0.039), such that the beneficial effect of statins on HF hospitalizations was most pronounced in patients without concomitant MR and absent in patients with hemodynamically significant MR. In conclusion, in patients with AMI statin therapy initiated before hospital discharge significantly reduces subsequent hospitalizations for HF. The effect of statins is driven largely by the reduction in events in patients without concomitant hemodynamically significant MR.

Background: The development of ischemic mitral regurgitation (MR) after myocardial infarction may impose hemodynamic load during a period of active left ventricular remodeling and promote heart failure (HF). However, few data are available on the relationship between ischemic MR and the long-term risk for HF., Methods: We prospectively studied 1190 patients admitted for acute myocardial infarction. Mitral regurgitation was assessed by echocardiography and was considered mild, moderate, and severe when the regurgitant jet area occupied less than 20%, 20% to 40%, and greater than 40% of the left atrial area, respectively. The median duration of follow-up was 24 months (range, 6-48 months)., Results: Mild and moderate or severe ischemic MR was present in 39.7% and 6.3% of patients, respectively. After adjusting for ejection fraction and clinical variables (age, sex, Killip class, previous infarction, hypertension, diabetes mellitus, anterior infarction, ST-elevation infarction, and coronary revascularization), compared with patients without MR, the hazard ratios for HF were 2.8 (95% confidence interval [CI], 1.8-4.2; P<.001) and 3.6 (95% CI, 2.0-6.4; P<.001) in patients with mild and moderate or severe ischemic MR, respectively. The adjusted hazard ratios for death were 1.2 (95% CI, 0.8-1.8; P = .43) and 2.0 (95% CI, 1.2-3.4; P = .02) in patients with mild and moderate or severe MR, respectively., Conclusions: There is a graded independent association between the severity of ischemic MR and the development of HF after myocardial infarction. Even mild ischemic MR is associated with an increase in the risk of HF.

Background: Objective evidence of elevated left ventricular (LV) filling pressures is infrequently demonstrated in clinical practice in patients with heart failure (HF) and preserved LV ejection fraction (LVEF) and the clinical diagnosis of HF is commonly questionable in these patients. The objective of this study was to examine whether elevated LV filling pressures can be demonstrated noninvasively in consecutive patients with HF and preserved (vs reduced) LVEF., Methods: Echocardiography was performed in 141 patients hospitalized with acute pulmonary edema (within 3 days of admission in 83.6%). LV filling was assessed in 116 patients without significant valve disease (median age 76 years; 51.7% men) and LV filling pressures were estimated based on mitral and pulmonary venous flow patterns and mitral annular diastolic velocities., Results: LVEF was preserved (> or =45%) in 49 patients (42.2%) and reduced (<45%) in 67 patients (57.8%). In patients with in sinus rhythm, normal LV filling pattern and abnormal relaxation, pseudonormal, and restrictive LV filling patterns (the latter two patterns associated with elevated LV filling pressures) were evident in 8, 1, 11, and 9 patients with preserved LVEF, versus 5, 11, 15, and 23 patients with reduced LVEF, respectively (P = .01) (LV filling pattern was nonconclusive in 12 patients). In patients with atrial arrhythmias, elevated LV filling pressures were evident in 4 of 14 patients with preserved LVEF and 3 of 4 patients with reduced LVEF. Overall, elevated LV filling pressures were demonstrable in 24 patients with preserved LVEF (49.0%) and in 41 patients with reduced LVEF (68.3%) (P = .26)., Conclusions: Elevated LV filling pressures are frequently evident by Doppler echocardiography in patients with HF and preserved or reduced LVEF. Thus, Doppler echocardiography can provide objective noninvasive evidence of abnormal LV filling in a large proportion of patients with HF and preserved LVEF.