Konermann M, Sanner B M, Altmann C, Laschewski F, Rawert B, Trappe H J
Medizinische Klinik, Marienkrankenhaus, Marburger Strasse 85, D-34127 Kassel, Germany.
Cardiology. 2000;94(3):179-87. doi: 10.1159/000047314.
Angiotensin-converting enzyme (ACE) inhibitors have been shown to be of value in the treatment of postinfarction remodeling. The question whether substances with a greater tissue affinity are associated with advantages for the acute and the chronic course is, however, still unclear.
The aim of the present study was to investigate the influence of ACE inhibitors with differing tissue affinities on the remodeling of the left ventricular wall in patients recovering from myocardial infarction.
52 patients (17 women, aged 38-73 years) suffering their first acute myocardial infarction were randomized to receive a daily dose of either 25-75 mg captopril or 10-20 mg fosinopril, beginning on the 7th postinfarction day. 28 patients had an anterior wall infarction and 24 patients an inferior wall infarction. The size of the infarct was determined using the creatine kinase integral method. 50 patients were investigated by cine magnetic resonance imaging 1 and 26 weeks after the infarction. The following parameters were determined: infarct weight and diastolic diameter of the infarcted zone, systolic wall stress, muscle mass, diastolic and systolic diameters, systolic wall thickening, and motility of the noninfarcted myocardium.
The infarct weight increased under captopril by 5.7% (p < 0.05) and under fosinopril by 6.1% (p < 0.05). The diastolic diameter of the infarcted zone decreased by 12% under captopril (p < 0.001) and by 11% under fosinopril (p < 0.001). The systolic wall thickness increased by 12.1% (p < 0.001) and the muscle mass by 12.7% (p < 0.001) under captopril and by 15.4% (p < 0.001) and 9.6% (p < 0.01), respectively, under fosinopril. Under captopril, the diastolic diameter increased by 2.3% (p < 0.05) and the systolic diameter by 17.8% (p < 0.01) and under fosinopril by 2.8% (n.s.) and 17.5% (p < 0.001), respectively. The systolic wall thickening increased by 73.9% under captopril (p < 0.001) and by 129.4% under fosinopril (p < 0.001). The motility decreased by 13.8% (p < 0.05) under captopril and by 6.0% (n.s.) under fosinopril. For all parameters, the results seen in anterior wall infarction were appreciably poorer than those seen in inferior wall infarction. All the differences between captopril and fosinopril were not significant.
Captopril and fosinopril show no major differences in their influence on left ventricular wall remodeling following myocardial infarction. On the basis of the present results, the tissue affinity of an ACE inhibitor does not appear to be of a significant relevance for postinfarction treatment.
血管紧张素转换酶（ACE）抑制剂已被证明在心肌梗死后重塑的治疗中具有价值。然而，具有更高组织亲和力的物质是否对急性和慢性病程具有优势，这一问题仍不清楚。
本研究的目的是调查具有不同组织亲和力的ACE抑制剂对心肌梗死恢复患者左心室壁重塑的影响。
52例首次发生急性心肌梗死的患者（17例女性，年龄38 - 73岁），从心肌梗死后第7天开始随机接受每日剂量25 - 75 mg卡托普利或10 - 20 mg福辛普利治疗。28例患者为前壁梗死，24例患者为下壁梗死。使用肌酸激酶积分法确定梗死面积。50例患者在梗死后1周和26周接受心脏磁共振成像检查。测定以下参数：梗死重量、梗死区舒张直径、收缩期壁应力、肌肉质量、舒张期和收缩期直径、收缩期壁增厚以及非梗死心肌的运动。
卡托普利治疗下梗死重量增加5.7%（p < 0.05），福辛普利治疗下增加6.1%（p < 0.05）。卡托普利治疗下梗死区舒张直径减少12%（p < 0.001），福辛普利治疗下减少11%（p < 0.001）。卡托普利治疗下收缩期壁厚度增加12.1%（p < 0.001），肌肉质量增加12.7%（p < 0.001），福辛普利治疗下分别增加15.4%（p < 0.001）和9.6%（p < 0.01）。卡托普利治疗下舒张期直径增加2.3%（p < 0.05），收缩期直径增加17.8%（p < 0.01），福辛普利治疗下分别增加2.8%（无显著性差异）和17.5%（p < 0.001）。卡托普利治疗下收缩期壁增厚增加73.9%（p < 0.001），福辛普利治疗下增加129.4%（p < 0.001）。卡托普利治疗下运动减少13.8%（p < 0.05），福辛普利治疗下减少6.0%（无显著性差异）。对于所有参数，前壁梗死患者的结果明显比下壁梗死患者差。卡托普利和福辛普利之间的所有差异均无显著性。
卡托普利和福辛普利在对心肌梗死后左心室壁重塑的影响方面无重大差异。基于目前的结果，ACE抑制剂的组织亲和力似乎与心肌梗死后治疗无显著相关性。
