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[Effects of ramipril and spironolactone on ventricular remodeling after acute myocardial infarction: randomized and
J A Rodríguez1, I Godoy, P Castro
1Departamento de Enfermedades Cardiovasculares, Pontificia Universidad Católica de Chile.
Insights
Ramipril and spironolactone similarly prevented adverse left ventricular remodeling after myocardial infarction. Aldosterone receptor blockade may be as effective as ACE inhibition in preventing post-MI cardiac changes.
Area of Science:
- Cardiology
- Pharmacology
- Internal Medicine
Background:
- Angiotensin converting enzyme (ACE) inhibition is known to prevent left ventricular remodeling and cardiovascular events post-myocardial infarction.
- The specific role of aldosterone in ventricular remodeling following myocardial infarction has remained largely unaddressed.
Purpose of the Study:
- To compare the efficacy of an ACE inhibitor (ramipril), an aldosterone receptor antagonist (spironolactone), and placebo in mitigating left ventricular remodeling after a first acute myocardial infarction.
Main Methods:
- A double-blind, randomized trial involving patients hospitalized for their first transmural acute myocardial infarction.
- Participants were assigned to receive either ramipril, spironolactone, or placebo for six months.
- Left ventricular remodeling was assessed using multigated radionuclide angiography to measure ejection fraction, end-diastolic volume, and end-systolic volume.
Main Results:
- Both ramipril and spironolactone groups showed improved ejection fraction compared to placebo.
- Ramipril and spironolactone prevented the increase in left ventricular end-systolic and end-diastolic volumes observed in the placebo group.
- No significant differences in baseline characteristics or concomitant medications were noted between the groups.
Conclusions:
- Ramipril and spironolactone demonstrated comparable effects in preventing left ventricular remodeling post-myocardial infarction.
- These findings suggest aldosterone plays a significant role in post-myocardial infarction ventricular remodeling.
- Aldosterone receptor inhibition may offer a therapeutic strategy comparable to ACE inhibition for preventing adverse cardiac remodeling.
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.
Aim:
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.
Patients And 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.