Aldosterone inhibition limits collagen synthesis and progressive left ventricular enlargement after anterior myocardial infarction

Background The reparative process after myocardia[ infarction is related to active collagen synthesis. Previous experimental studies demonstrated that cardiac fibrosis is mediated by angiotensin II and aldosterone; this mecha nism is not clearly confirmed in patients who have had a myocardial infarct ion. The aim of this study was to evaluate whether the suppression of aldos terone may be helpful in reducing postinfarction collagen synthesis land pr ogressive left ventricular dilation) in patients treated with an angiotensi n-converting enzyme inhibitor for a recent myocardial infarction. Methods We enrolled 46 patients (ages 60 +/- 11 years, 34 males) with a fir st episode of anterior transmural thrombolized myocardial infarction. At ho spital discharge patients were randomized to receive potassium canrenoate, an oral aldosterone inhibitor, 50 mg once daily (group 1, n = 24) or placeb o (group 2, n = 22). All enrolled patients were on angiotensin-converting e nzyme inhibitor therapy. The serum concentration of the aminoterminal prope ptide of type III procollagen was used to measure the collagen synthesis ra te; dosage was obtained before enrollment, at hospital discharge, and after 3, 6, and 12 months of follow-up. Results After 3, 6, and 1 2 months of treatment, the aminoterminal propepti de of type III procollagen serum levels was significantly higher in the pla cebo group compared with the aldosterone inhibitor group; after 6 and 12 mo nths we observed significantly smaller left ventricular volumes in the acti ve treatment group. Conclusion Potassium canrenoate, combined with an angiotensin-converting en zyme inhibitor, may reduce postinfarction collagen synthesis and progressiv e left ventricular dilation.