Internal Medicine
Online ISSN : 1349-7235
Print ISSN : 0918-2918
ORIGINAL ARTICLES
Effects of Enalapril and Losartan in Left Ventricular Remodeling after Acute Myocardial Infarction: A Possible Mechanism of Prevention of Cardiac Events by Angiotensin-converting Enzyme Inhibitors and Angiotensin Receptor Blockers in High-risk Myocardial Infarction
Shigemasa TaniKen NagaoTakeo AnazawaHirofumi KawamataShingo FuruyaHiroshi TakahashiKiyoshi IidaMichiaki MatsumotoNarimichi KumabeMotoyuki OnikuraAtsushi Hirayama
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JOURNALS OPEN ACCESS

Volume 48 (2009) Issue 11 Pages 877-882

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Abstract

Background Angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin II receptor blockers (ARB) have been shown to have a significant cardioprotective effect in high-risk patients after myocardial infarction (MI). However, there are few data on the effects of these drugs on left-ventricular (LV) remodeling after MI in Japanese patients.
Methods and Results We randomly assigned 100 patients with anterior-wall MI who had received reperfusion therapy to treatment with either enalapril (n=50) or losartan (n=50), and calculated the LV ejection fraction (LVEF) and LV end-diastolic volume index (LVEDVI) in these patients at baseline and after 6 months of treatment. While a significant increase in the LVEF as compared with that at the baseline was observed in both groups, no significant difference was found in the rate of change of this parameter between the two groups. However, inverse correlations were observed between the baseline LVEF and LVEDVI and also the rates of change of the two parameters, suggesting that the greater the compromise of the LV function at baseline, the greater the preventive effect of both classes of drugs on LV remodeling.
Conclusion The results of this study suggest that neither enalapril nor losartan is superior to the other in terms of the effect on LV remodeling after MI in Japanese patients. In addition, the suppressive effect of both classes of drugs on LV remodeling was greater in patients with more extensive infarction and greater compromise of LV function at baseline.

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© 2009 by The Japanese Society of Internal Medicine
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