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

BACKGROUND

The reparative process after myocardial infarction is related to active collagen synthesis. Previous experimental studies demonstrated that cardiac fibrosis is mediated by angiotensin II and aldosterone; this mechanism is not clearly confirmed in patients who have had a myocardial infarction. The aim of this study was to evaluate whether the suppression of aldosterone may be helpful in reducing postinfarction collagen synthesis (and progressive left ventricular dilation) in patients treated with an angiotensin-converting enzyme inhibitor for a recent myocardial infarction.

METHODS

We enrolled 46 patients (ages 60+/-11 years, 34 males) with a first episode of anterior transmural thrombolized myocardial infarction. At hospital discharge patients were randomized to receive potassium canrenoate, an oral aldosterone inhibitor, 50 mg once daily (group 1, n = 24) or placebo (group 2, n = 22). All enrolled patients were on angiotensin-converting enzyme inhibitor therapy. The serum concentration of the aminoterminal propeptide of type III procollagen was used to measure the collagen synthesis rate; dosage was obtained before enrollment, at hospital discharge, and after 3, 6, and 12 months of follow-up.

RESULTS

After 3, 6, and 12 months of treatment, the aminoterminal propeptide of type III procollagen serum levels was significantly higher in the placebo group compared with the aldosterone inhibitor group; after 6 and 12 months we observed significantly smaller left ventricular volumes in the active treatment group.

CONCLUSION

Potassium canrenoate, combined with an angiotensin-converting enzyme inhibitor, may reduce postinfarction collagen synthesis and progressive left ventricular dilation.