EFFECTS OF CAPTOPRIL ON ISCHEMIC EVENTS AFTER MYOCARDIAL-INFARCTION -RESULTS OF THE SURVIVAL AND VENTRICULAR ENLARGEMENT TRIAL

Citation
Jd. Rutherford et al., EFFECTS OF CAPTOPRIL ON ISCHEMIC EVENTS AFTER MYOCARDIAL-INFARCTION -RESULTS OF THE SURVIVAL AND VENTRICULAR ENLARGEMENT TRIAL, Circulation, 90(4), 1994, pp. 1731-1738
Citations number
42
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
0009-7322
Volume
90
Issue
4
Year of publication
1994
Pages
1731 - 1738
Database
ISI
SICI code
0009-7322(1994)90:4<1731:EOCOIE>2.0.ZU;2-C
Abstract
Background In the Survival and Ventricular Enlargement (SAVE) trial, r ecurrent myocardial infarction (MI) was the most important predictor o f a poor outcome and conferred a sevenfold increase in risk of death. The purpose of this study was to determine the predictors of recurrent MI in study participants and to examine the influence of the angioten sin-converting enzyme inhibitor captopril on this and other myocardial ischemic events. Methods and Results The 2231 patients had survived t he acute phase of MI (3 to 16 days) and had a radionuclide ventricular ejection fraction less than or equal to 40%. Patients were randomly a ssigned to receive double-blind treatment with either placebo or capto pril and were followed for an average of 42 months. The influence of c aptopril on recurrent MI, cardiac revascularization procedures, and ho spitalization with unstable angina was examined. The likelihood of rec urrent MI was greater in patients with an MI or functional disability before the index infarction and higher systolic pressure (all P<.001) but was not influenced by baseline left ventricular ejection fraction. Therapy with captopril reduced the risk of development of recurrent M I by 25% (95% confidence intervals, 5% to 40%; P=.015) and the risk of death after recurrent MI by 32% (95% confidence intervals, 4% to 51%; P=.029). Captopril-assigned patients were also less likely to require cardiac revascularization procedures (P=.010), but hospitalization fo r unstable angina was unaltered. When all three of these major coronar y ischemic events were considered together, captopril therapy reduced the risk (14% risk reduction; 95% confidence intervals, 0% to 26%; P=. 047). Conclusions In post-MI patients with asymptomatic left ventricul ar dysfunction, long-term administration of captopril reduced recurren ce of MI and the need for cardiac revascularization but had no influen ce on the rate of hospitalization with a discharge diagnosis of unstab le angina. The finding that the recurrence of MI was independent of le ft ventricular ejection fraction suggests that captopril could be usef ul in preventing recurrent MI in patients with more preserved left ven tricular function. The need for cardiac revascularization was reduced in patients receiving long-term captopril therapy, suggesting either a n anti-ischemic effect or the ability of the angiotensin-converting en zyme inhibitor to modify the atherosclerotic process in survivors of M I.