Prostaglandins in myocardial infarction: With emphasis on myocardial preservation

Various therapies during early hours of acute myocardial infarction (AMI) have been suggested to protect ischemic myocardium and reduce infarct size. Despite reports that prostaglandins (PGs) are released during myocardial ischemia, and that prostacyclin (PGI2) and thromboxane A₂ (TXA₂) have opposing effects on vasomotion and platelet aggregation, the physiologic roles of PGs, PGI2 and TXA₂ in AMI have not been clearly defined. However, in pharmacologic doses, experimental evidence suggests that vasodilator PGs might be beneficial, and vasoconstrictor PGs might be deleterious, in AMI. Recent recognition that coronary spasm is frequent in AMI has led to the notion that an increased PGI₂/TXA₂ ratio might be desirable. Thus, exogenous PGEl, exogenous PGI2 or its more stable analogs, drugs that stimulate PGI2 release, and inhibitors of TXA₂ and harmful PGs are potential agents for protective therapy in AMI.