Effects of early Captopril administration on infarct expansion, left ventricular remodelling and exercise capacity after acute myocardial infarction

In a double-blind study, 99 patients (82 men, age range 40 to 75 years) with acute myocardial infarction (AMI) were randomly assigned to receive captopril or placebo. Treatment began within 24 hours of admission. Serial echocardiographic measurements of endocardial segment lengths and left ventricular (LV) volumes, and ejection fractions were obtained. The 2 groups were matched at baseline except for an excess of previous AMI in the placebo group (13 of 50 vs 2 of 49 patients, p = 0.002). The increase in anterior segment length, from baseline to 2 months, was significantly less in the captopril than in the placebo group (2.8 ± 1.6 vs 10.4 ± 2.4mm, 95% confidence interval [CI] −13.5 to −1.7, p = 0.01). The increase in posterior segment length was also less in the captopril group, but the difference was not significant (3.2 ± 1.2 vs 7.0 ± 1.8mm, 95% CI −8.0 to 0.5, p = 0.08). Fewer patients in the captopril group demonstrated increases in segment length >2 standard deviations of the measurement error (14 of 70 [20%] vs 29 of 72 [40%] patients, p = 0.009). In patients with anterior AMI, the infarct-containing anterior segment length increased by 4.5 ± 2.3 mm in the captopril versus 12.4 ± 3.1 mm in the placebo group (95% CI −15.7 to −0.2, p = 0.046), and fewer patients in the captopril group demonstrated infarct expansion (6 of 20 [30%] vs 13 of 21 [62%] patients, p = 0.04). In patients with inferoposterior AMI, the infarct-containing posterior segment length increased by 3.1 ± 1.6 mm in the captopril versus 9.8 ± 2.4 mm in the placebo group (95% CI −13.3 to −0.1, p = 0.046). No significant treatment effects were seen in LV volumes or maximal exercise performance. This study suggests that early treatment with captopril after AMI can attenuate infarct expansion and favorably influence early LV remodeling