Effect of long-term captopril therapy on left ventricular remodeling and function during healing of canine myocardial infarction

To determine whether the long-term reduction of preload and afterload by Captopril during healing after acute anterior myocardial infarction might attenuate left ventricular remodeling and improve function, 30 chronically instrumented dogs with infarction produced by left anterior descending coronary artery ligation were randomized 2 days later to oral therapy with placebo (n = 15) or Captopril, 50 mg twice daily (n = 15), for 6 weeks. Serial hemodynamic as well as topographic and functional variables (two-dimensional echocardiography) were measured over 6 weeks. Scar topography (planimetry), occluded bed size (coronary arteriography) and collagen (hydroxyproline) content were measured at 6 weeks.Between 2 days are 6 weeks, Captopril decreased (p < 0.001) mean arterial pressure and mean left atrial pressure more than did placebo, but it did not influence heart rate. Infarct scar mass, transmurality and collagen content at 6 weeks were similar in the two groups but scars showed less (p < 0.001) thinning and expansion with Captopril than with placebo. Echocardiograms showed similar infarct expansion and thinning in the two groups at 2 days but less aneurysm with Captopril at 6 weeks. Between 2 days and 6 weeks, expansion index (infarct-Moninfarct-containing segment length) decreased (p < 0.001) with Captopril but increased (p < 0.001) with placebo. Also, thinning ratio (infarct/normal wall thickness) decreased (p < 0.001) with placebo but did not change (p = NS) with Captopril.By 6 weeks, left ventricular asynergy and volumes showed a greater decrease (p < 0.01) and global ejection fraction a greater increase (p < 0.05) with Captopril. Thus, Captopril therapy during healing after canine anterior infarction limits left ventricular remodeling and improves left ventricular function