Abstract
Administration of aspirin in patients with evolving acute myocardial infarction (AMI) has been associated with reduced short and long term mortality. Neither the mechanism of the beneficial effect of aspirin nor the kinetics of its absorption in these patients have been determined. We studied the pharmacokinetics of rapid release aspirin (100mg) in 20 patients with evolving AMI. The peak creatine kinase (CK) level was 2452 ±416 (SEM) IU/L. Thrombolytic therapy was utilised in 16 patients. Aspirin was administered 5.8 ±0.8 hours after onset of pain (range 1.5 to 11 hours). The peak aspirin concentration was 939 ±137 μg/L, occurring 0.71 ±0.11 hours (range 0.3 to 2.0 hours) after aspirin ingestion. There was considerable interindividual variability in aspirin absorption, which was not significantly correlated with age, sex, bodyweight, time after onset of pain, thrombolytic therapy, infarct site or peak CK level. However, the maximal aspirin concentration was lower and time to peak concentration greater than that observed in a previous analogous study in normal subjects.
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