Konermann M, Altmann C, Laschewski F, Josephs W, Odenthal H J, Horstmann E, Sanner B
Medical Department, Ruhr University of Bochum, Marienhospital Herne, Kasse, Germany.
Clin Cardiol. 1998 Apr;21(4):277-85. doi: 10.1002/clc.4960210409.
The demonstration of local renin-angiotension systems has raised the question of whether angiotensin-converting enzyme (ACE) inhibitors with different tissue affinities differ with regard to their effects on postinfarction remodeling.
The study was undertaken to investigate the influence of ACE inhibitors with different tissue affinity on morphology and function of the infarcted left ventricle.
In all, 52 patients (17 women, 35 men, 38-73 years) with large acute myocardial infarction were randomized to receive either 25-75 mg/day captopril or 10-20 mg/day fosinopril beginning on the Day 7 after infarction. Of these, 28 had anterior and 24 had posterior wall infarctions. Infarct size was determined by the creatine kinase integral method. Fifty patients were examined by cinemagnetic resonance imaging (CMRI) 1 and 26 weeks after infarction. The following parameters were determined: left ventricular end-diastolic and end-systolic volume index (LVEDVI, LVESVI), ejection fraction (LVEF), infarct weight, and muscle mass (LVMM). The volume-to-mass ratio (VMR) was calculated and the clinical status according to the guidelines of the New York Heart Association (NYHA) was documented at each examination time. The results were compared with those of a historical sample without ACE-inhibitor therapy examined in an identical manner (n = 31, 10 women, 21 men, 36-75 years).
LVEDVI and LVESVI increased in the first 6 months after infarction by 24.9 and 36.6%, respectively, in the historical sample; by 11.0 and 7.8%, respectively, under captopril; and by 13.1 and 10.7%, respectively, under fosinopril. LVEF decreased by 14.9% in the untreated sample, by 3.7% under captopril and by 5.0% under fosinopril. Infarct weight and LVMM increased by 12.7 and 15.3%, respectively, without ACE inhibition, by 5.7 and 10.1%, respectively, in patients treated with captopril, and by 6.1 and 9.3%, respectively, in patients treated with fosinopril. The VMR increased by 7.4% in the historical sample, by 3.5% in the captopril group, and by 1.8% in the fosinopril group. The NYHA clinical status improved by 18.2% without ACE inhibition, by 42.9% in the captopril group, and by 26.3% in the fosinopril group. The differences between the two ACE-inhibitor groups and the reference group were all significant, while the differences between the captopril group and the fosinopril group were significant only for VMR (p < 0.01) and NYHA class (p < 0.05).
Both captopril and fosinopril have a comparable positive influence on postinfarction remodeling and on clinical status. Lipophilicity and tissue affinity do not seem to play a clinically important role in ACE-inhibitor therapy after infarction.
局部肾素 - 血管紧张素系统的证实引发了一个问题，即具有不同组织亲和力的血管紧张素转换酶（ACE）抑制剂在对梗死后重塑的影响方面是否存在差异。
本研究旨在调查具有不同组织亲和力的ACE抑制剂对梗死左心室形态和功能的影响。
总共52例（17例女性，35例男性，38 - 73岁）大面积急性心肌梗死患者在梗死后第7天开始随机接受25 - 75毫克/天的卡托普利或10 - 20毫克/天的福辛普利治疗。其中，28例为前壁梗死，24例为后壁梗死。梗死面积通过肌酸激酶积分法测定。50例患者在梗死后1周和26周接受电影磁共振成像（CMRI）检查。测定以下参数：左心室舒张末期和收缩末期容积指数（LVEDVI、LVESVI）､射血分数（LVEF）､梗死重量和肌肉质量（LVMM）。计算容积与质量比（VMR），并在每次检查时记录根据纽约心脏协会（NYHA）指南确定的临床状态。将结果与以相同方式检查的未接受ACE抑制剂治疗的历史样本（n = 31，10例女性，21例男性，36 - 7５岁）的结果进行比较。
在历史样本中，梗死后前6个月LVEDVI和LVESVI分别增加24.9%和36.6%；在卡托普利治疗组中分别增加11.0%和7.8%；在福辛普利治疗组中分别增加13.1%和10.7%。在未治疗样本中LVEF下降14.9%，在卡托普利治疗组下降3.7%，在福辛普利治疗组下降5.0%。在未进行ACE抑制的情况下，梗死重量和LVMM分别增加12.7%和15.3%，在接受卡托普利治疗的患者中分别增加5.7%和10.1%，在接受福辛普利治疗的患者中分别增加6.1%和9.3%。VMR在历史样本中增加7.4%，在卡托普利组增加3.5%，在福辛普利组增加1.8%。NYHA临床状态在未进行ACE抑制时改善18.2%，在卡托普利组改善42.9%，在福辛普利组改善26.3%。两个ACE抑制剂组与参照组之间的差异均具有统计学意义，而卡托普利组与福辛普利组之间的差异仅在VMR（p < 0.01）和NYHA分级（p < 0.05）方面具有统计学意义。
卡托普利和福辛普利对梗死后重塑和临床状态均有类似的积极影响。亲脂性和组织亲和力在梗死后ACE抑制剂治疗中似乎不发挥重要的临床作用。
