Jugdutt B I, Schwarz-Michorowski B L, Khan M I
Cardiology Division, University of Alberta, Edmonton, Canada.
J Am Coll Cardiol. 1992 Mar 1;19(3):713-21. doi: 10.1016/s0735-1097(10)80298-0.
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 and 6 weeks, captopril decreased (p less than 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 less than 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-/noninfarct-containing segment length) decreased (p less than 0.001) with captopril but increased (p less than 0.001) with placebo. Also, thinning ratio (infarct/normal wall thickness) decreased (p less than 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 less than 0.01) and global ejection fraction a greater increase (p less than 0.05) with captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
为了确定急性前壁心肌梗死后愈合期间卡托普利长期降低前负荷和后负荷是否可能减弱左心室重构并改善功能，30只通过结扎左冠状动脉前降支造成梗死且长期植入监测仪器的犬在2天后被随机分为两组，一组口服安慰剂（n = 15），另一组口服卡托普利，每日两次，每次50 mg（n = 15），持续6周。在6周内测量一系列血流动力学以及形态学和功能变量（二维超声心动图）。在6周时测量瘢痕形态（面积测量）、梗死床大小（冠状动脉造影）和胶原蛋白（羟脯氨酸）含量。在2天至6周期间，卡托普利比安慰剂更能降低（p<0.001）平均动脉压和平均左心房压，但对心率无影响。两组在6周时的梗死瘢痕质量、透壁性和胶原蛋白含量相似，但与安慰剂相比，卡托普利组瘢痕的变薄和扩张程度更小（p<0.001）。超声心动图显示两组在2天时梗死扩展和变薄情况相似，但卡托普利组在6周时动脉瘤较少。在2天至6周期间，卡托普利使扩张指数（含梗死/不含梗死节段长度）降低（p<0.001），而安慰剂使其升高（p<0.001）。此外，安慰剂使变薄率（梗死/正常壁厚）降低（p<0.001），而卡托普利组无变化（p =无显著性差异）。到6周时，卡托普利使左心室运动失调和容积有更大程度降低（p<0.01），整体射血分数有更大程度升高（p<0.05）。（摘要截短于250字）
