RANDOMIZED CONTROLLED TRIAL ON THE EFFECT S OF RAMIPRIL AND SPIRONOLACTONE ON VENTRICULAR REMODELING AFTER AN ACUTE MYOCARDIAL-INFARCTION

Background: Studies have shown that angiotensin converting enzyme (ACE ) Inhibition prevents left ventricular remodeling and cardiovascular e vents after an acute myocardial infarction. The role of aldosterone in ventricular remodeling after a myocardial infarction has not been add ressed. Aim: To compare the effects of an ACE inhibitor an aldosterone receptor antagonist and placebo or? left ventricular remodeling after a first episode of transmural acute myocardial infartion. Patients an d methods: Patients hospitalized for a first episode of acute myocardi al infarction were blindly and randomly assigned to receive ramipril ( 2.5 mg bid), spironolactone (25 mg tid) or placebo. Ejection fraction, left ventricular end diastolic and end systolic volumes were measured by multigated radionuclide angiography, at baseline and after six mon ths of treatment. Results: Twenty four patients were assigned to place bo, 31 to ramipril and 23 to spironolactone. Age, gender, Killip class , treatment with thrombolytics, revascularization procedures and use o f additional medications were similar in the three groups. After six m onths of treatment ejection fraction increased from 34,5 +/- 2,3 to 40 ,2 +/- 2,4 % in patients on ramipril, from 32,6 +/- 2,9 to 36,6 +/- 2, 7 % in patients on spironolactone, and decreased from 37+/-3 to 31+/-3 % in patients on placebo (ANOVA between groups p<0.05). Basal end sys tolic volume was similar in all three groups, increased from 43,4 +/- 3,4 to 61,4 +/- 6,0 ml/m(2) in patients on placebo and did not change in patients on spironolactone or ramipril (ANOVA p<0.05). End diastoli c volume was also similar in the three groups, increased from 70,6 +/- 4,3 to 92,8 +/- 6,4 ml/m(2) in patients on placebo and did no change with the other treatments. Conclusions: Ramipril and spironolactone ha d similar effects on ventricular remodeling after acute myocardial inf arction, suggesting that aldosterone contributes to this phenomenon an d that inhibition of its receptor may be as effective as ACE inhibitio n in its prevention.