The question whether patients with posterior infarctions (PMI) have a comparable benefit of an ACE-inhibitor therapy to those with anterior infarction (AMI) is still open. The study was undertaken to investigate the different influence of ACE inhibitors on the remodeling of the left ventricle after AMI or PMI. 52 patients (Pt.) (17 female, 38-73 years) were randomized to receive either 25-75 mg/day captopril (C) or 5-20 mg/day fosinopril (F) beginning on day 7 after acute myocardial infarction. 28 Pt. had AMI, 24 Pt. PMI. Infarct size was determined by the creatine kinase integral method. 50 Pt. were examined by cine magnetic resonance imaging 1 and 26 weeks after infarction. We determined: left ventricular end-diastolic (LVEDVI) and end-systolic (LVESVI) volume index, ejection fraction (EF), infarction weight (IW), left ventricular muscle mass (MM), systolic wall thickening (SWT) and motility (MOT) of the vital myocardium, and clinical behavior according to the guidelines of the New York Heart Association (NYHA). The results were compared with those of a sample (V) without ACE inhibitor therapy (10 females, 21 males, 36-75 years, 19 AMI, 12 PMI). There were no significant differences between C and F. Without ACE-inhibition therapy LVEDVI increased by 28.2% in AMI, by 18.4% in PMI (p < 0.001), with ACE-inhibition by 13.7% in AMI and by 9.9% in PMI (p < 0.001). LVESVI increased in V by 40.1% in AMI, by 28.5% in PMI (p < 0.001). With ACE-inhibitor we found an increase of 11.2% in AMI and 5.3% in PMI (p < 0.001). EF decreased without ACE-inhibitor by 18.7% in AMI and by 10.2% in PMI (p < 0.001), with ACE-inhibition increased by 4.3% in AMI and PMI, respectively (n. s.). NYHA got better in all groups, by 17.4% in AMI and 20.8% in PMI without ACE-inhibitor (n.s.), by 45.5% in AMI and 31.6% in PMI with ACE-inhibitor (p < 0.001). IG increased by 15.5% in AMI and 8.8% in PMI in V (p < 0.001), by 11.2% in AMI and 5.3% in PMI with C or F (p < 0.001). MM got bigger in V by 16.6% in AMI and 12.7% in PMI (p < 0.05), with ACE-inhibitor by 11.7% in AMI and 8.0% in PMI (p < 0.05). sWD increased by 12.9% in AMI and by 6.7% in PMI in V (p < 0.01), by 37.1% in AMI and 88.0% in PMI with C or F (p < 0.001). MOT decreased by 39.6% in AMI and 14.9% in PMI without ACE-inhibition (p < 0.001) and increased by 4.3% in AMI and by 5.0% in PMI with ACE-inhibitor (n. s.). All differences between V and the ACE-inhibitor groups were significant. Even patients with PMI clearly benefit from ACE-inhibitor therapy, but less than those with AMI. Captopril and fosinopril show no different effects after myocardial infarction.