Prostaglandin inhibition and myocardial infarct size

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Abstract
In parallel with experimental research into methods for salvage of ischemic myocardium after acute myocardial infarction (AMI) over the last decade, there has been a growing interest in prostaglandins (PG) and their inhibition by aspirin‐like drugs or nonsteroidal anti‐inflammatory drugs (NSAID). The finding of enhanced PG release during myocardial ischemia and its blockade by the NSAID indomethacin led to the hypothesis that PG might influence the infarction process. Because PG differ in vasoactive, cellular, and metabolic properties, and PG inhibitors also differ in their ability to inhibit synthesis of different PG and their metabolites, some PG inhibitors might be expected to reduce myocardial ischemic injury and infarct size. In addition, the NSAID may directly modify cellular events during infarction. Experiments with NSAID in the anesthetized and conscious animals have demonstrated a reduction of myocardial infarct size with ibuprofen, but an increase in infarct size with indomethacin. The opposite effects of these agents on infarct size might have been related to the different doses used, different degrees of inhibition of PG and their metabolites, and different effects on factors influencing myocardial oxygen supply and demand, metabolic and cellular events during infarction. It has recently been suggested that some of these agents might also influence the healing process after AMI and, therefore, late complications. Thus, further critical studies are needed before embarking on clinical trials of these agents during AMI in humans

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