Is the tissue affinity of ACE inhibitors of relevance for the remodeling of the left ventricular wall following myocardial infarction? Estimations with cine magnetic resonance imaging

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 advan tages 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 inhib itors with differing tissue affinities on the remodeling of the left ventri cular wall in patients recovering from myocardial infarction. Methods: 52 p atients (17 women, aged 38-73 years) suffering their first acute myocardial infarction were randomized to receive a daily dose of either 25-75 mg capt opril or 10-20 mg fosinopril, beginning on the 7th postinfarction day. 28 p atients had an anterior wall infarction and 24 patients an inferior wail in farction. The size of the infarct was determined using the creatine kinase integral method. 50 patients were investigated by cine magnetic resonance i maging 1 and 26 weeks after the infarction. The following parameters were d etermined: infarct weight and diastolic diameter of the infarcted zone, sys tolic 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 fosin opril by 6.1% (p < 0.05). The diastolic diameter of the infarcted zone decr eased 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 m uscle mass by 12.7% (p < 0.001) under captopril and by 15.4% (p < 0.001) an d 9.6% (p < 0.01), respectively, under fosinopril. Under captopril, the dia stolic diameter increased by 2.3% (p < 0.05) and the systolic diameter by 1 7.8% (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 captopr il (p < 0.001) and by 129.4% under fosinopril (p < 0.001). The motility dec reased by 13.8% (p < 0.05) under captopril and by 6.0% (n.s.) under fosinop ril. For all parameters, the results seen in anterior wall infarction were appreciably poorer than those seen in inferior wall infarction. All the dif ferences between captopril and fosinopril were not significant. Conclusions : Captopril and fosinopril show no major differences in their influence on left ventricular wail remodeling following myocardial infarction. On the ba sis of the present results, the tissue affinity of an ACE inhibitor does no t appear to be of a significant relevance for postinfarction treatment. Cop yright (C) 2001 S. Karger AG, Basel.