[Effects of ramipril and spironolactone on ventricular remodeling after acute myocardial infarction: randomized and double-blind study].
BACKGROUND
Studies have shown that angiotensin converting enzyme (ACE) inhibition prevents left ventricular remodeling and cardiovascular events after an acute myocardial infarction. The role of aldosterone in ventricular remodeling after a myocardial infarction has not been addressed.


OBJECTIVE
To compare the effects of an ACE inhibitor, an aldosterone receptor antagonist and placebo on left ventricular remodeling after a first episode of transmural acute myocardial infarction.


METHODS
Patients hospitalized for a first episode of acute myocardial 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 months of treatment.


RESULTS
Twenty four patients were assigned to placebo, 31 to ramipril and 23 to spironolactone. Age, gender, Killip class, treatment with thrombolytics, revascularization procedures and use of additional medications were similar in the three groups. After six months 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 systolic volume was similar in all three groups, increased from 43.4 +/- 3.4 to 61.4 +/- 6.0 ml/m2 in patients on placebo and did not change in patients on spironolactone or ramipril (ANOVA p < 0.05). End diastolic volume was also similar in the three groups, increased from 70.6 +/- 4.3 to 92.8 +/- 6.4 ml/m2 in patients on placebo and did not change with the other treatments.


CONCLUSIONS
Ramipril and spironolactone had similar effects on ventricular remodeling after acute myocardial infarction, suggesting that aldosterone contributes to this phenomenon and that inhibition of its receptor may be as effective as ACE inhibition in its prevention.
Rodríguez
J A
JA
Departamento de Enfermedades Cardiovasculares, Pontificia Universidad Católica de Chile.
Godoy
I
I
Castro
P
P
Quintana
J C
JC
Chávez
E
E
Yovanovich
J
J
Corbalán
R
R
Chávez
A
A
D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D018572:Disease-Free Survival; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D017257:Ramipril / Q000494:pharmacology*; D013148:Spironolactone / Q000494:pharmacology*; D013318:Stroke Volume / Q000187:drug effects; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D016277:Ventricular Function, Left / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D017257:Ramipril
Ramipril vs espironolactona en el remodelamiento ventricular izquierdo post-infarto: estudio randomizado y doble ciego.