Background: Ventricular arrhythmias (VAs) are independent predictors of mortality in survivors of myocardial infarction (MI), and they are more likely to be induced in dilated hearts with increased wall stress. Angiotensin-converting enzyme (ACE) inhibitors have been shown to prevent progressive dilation of the left ventricle after MI.
Methods and results: The effects of captopril were evaluated in 58 patients with left ventricular (LV) dysfunction after MI. Patients were randomized on day 7 to either placebo or captopril (50 mg daily) in a double-blind parallel study over a period of 6 months. Patients were followed up by means of ambulatory ECG monitoring and echocardiography. There was a significant increase in VA in the placebo group (P < .05) in contrast to a significant decrease in the captopril group (P < .05). As a consequence, there was a significant between-group difference after 6 months (P < .05). Furthermore, the number of patients without VA at baseline who presented with this at the completion of the study was 6% in the captopril group versus 38% in the placebo group (P < .05). At baseline as well as at the termination of the study, LV end-diastolic volume index (LVEDVI) and LV end-systolic volume index (LVESVI) were significantly increased among patients with VA (P < .01). On day 180, both myocardial ischemia and an increase in the LVEDVI were independent predictors of VA; however, progressive dilation of the left ventricle was confined to the placebo patients with significant increases in the LVEDVI compared with the captopril group: 17% versus 0%, respectively (P < .01). Furthermore, the duration of ambulatory ST-segment depression was significantly longer in this group compared with the captopril group (P < .01).
Conclusions: Dilation of the left ventricle and myocardial ischemia predict VA during both the acute and chronic phases after MI. In post-MI patients with LV dysfunction, captopril has a beneficial effect on both the number of complex VAs as well as the number of patients who develop VA during the chronic phase. This is in all probability mediated through effects on both LV remodeling, LV function, and myocardial ischemia in patients who are exposed to an increased risk of undergoing progressive dilation of the left ventricle.