Is the Tissue Affinity of ACE Inhibitors of Relevance for the Remodeling of the Left Ventricular Wall following Myocardial Infarction?

BACKGROUND: 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. AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.