Clinical effects of early angiotensin-converting enzyme inhibitor treatment for acute myocardial infarction are similar in the presence and absence of aspirin - Systematic overview of individual data from 96,712 randomized patients

OBJECTIVES We sought to determine whether the clinical effects of early ang iotensin-converting enzyme (ACE) inhibitor (ACEi) treatment for acute myoca rdial infarction (MI) are influenced by the concomitant use of aspirin (ASA ). BACKGROUND Aspirin and ACEi both reduce mortality when given early after MI . Aspirin inhibits the synthesis of vasodilating prostaglandins, and, in pr inciple, this inhibition might antagonize some of the effects of ACEi. But it is uncertain whether, in practice, this influences the effects of ACEi o n mortality and major morbidity after MI. METHODS This overview sought individual patient data from all trials involv ing more than 1,000 patients randomly allocated to receive ACEi or control starting in the acute phase of MI (0-36 h from onset) and continuing for fo ur to six weeks. Data on concomitant ASA use were available for 96,712 of 9 8,496 patients in four eligible trials (and for none of 1,556 patients in t he one other eligible trial). RESULTS Overall 30-day mortality was 7.1% among patients allocated to ACEi and 7.6% among those allocated to control, corresponding to a 7% (standard deviation [SD], 2%) proportional reduction (95% confidence interval 2% to 1 1%, p = 0.004). Angiotensin-converting enzyme inhibitor was associated with similar proportional reductions in 30-day mortality among the 86,484 patie nts who were taking ASA (6% [SD, 3%] reduction) and among the 10,228 patien ts who were not (10% [SD, 5%] reduction: chi-squared test of heterogeneity between these reductions = 0.4; p = 0.5). Angiotensin-converting enzyme inh ibitor produced definite increases in the incidence of persistent hypotensi on (17.9% ACEi vs. 9.4% control) and of renal dysfunction (1.3% ACEi vs. 0. 6% control), but there was no good evidence that these effects were differe nt in the presence or absence of ASA (chi-squared for heterogeneity = 0.4 a nd 0.0, respectively; both not significant). Nor was there good evidence th at the effects of ACEi on other clinical outcomes were changed by concomita nt ASA use. CONCLUSIONS Both ASA and ACEi are beneficial in acute MI. The present resul ts support the early use of ACEi in acute MI, irrespective of whether or no t ASA is being given. (J Am Coll Cardiol 2000;35:1801-7) (C) 2000 by the Am erican College of Cardiology.