Effects of Aspirin on Angiotensin-Converting Enzyme Inhibition and Left Ventricular Dilation One Year After Acute Myocardial Infarction

There are conflicting reports on the interaction of aspirin with angiotensin-converting enzyme inhibitors in heart failure and systemic hypertension. A post hoc analysis of the Captopril and Thrombolysis Study (CATS) study was conducted. At randomization, 94 patients (31.5%) took aspirin. In patients who took aspirin, the cumulative α-hydroxy butyrate dehydrogenase release was 1,151 ± 132 IU/L in patients randomized to captopril compared with 1,401 ± 136 IU/L in patients randomized to placebo (difference −250 ± 189 [95% confidence interval (CI) −620 to 120]). This difference was comparable to the difference in patients who did not use aspirin (−199 ± 147 [95% CI −488 to 897]). One year after acute myocardial infarction, an increase in left ventricular end-diastolic volume index of 2.2 ± 3.0 ml/m2 in captopril-treated and 1.9 ± 2.9 ml/m2 in placebo-treated patients was observed in patients who took aspirin (difference 0.4 ± 4.2 [95% CI −8.2 to 8.9]). This difference was also comparable to the difference in patients who did not take aspirin (2.2 ± 3.8 [95% CI − 5.2 to 9.7]). One year after acute myocardial infarction, patients who did take aspirin had a mean change in LV end-diastolic volume index of 2.1 ± 2.1 ml/m2 compared with 8.4 ± 1.9 ml/m2 in patients who did not use aspirin (p = 0.02). Thus, aspirin does not attenuate the acute and long-term effects of angiotensin-converting enzyme inhibition after acute myocardial infarction, but independently reduces LV dilation after myocardial infarction.