The Changes in Arachidonic Acid Metabolism in Ischemic Heart Disease — Their Pathophysiological Consequences

The interest in studying arachidonic acid (AA) metabolism in ischemic heart disease (IHD) comes from the awareness that prostacyclin (PGI2) and thromboxane A2 (TXA2) are powerful modulators of vascular tone and platelet aggregability, and that they may be involved in the occurrence of various clinical manifestations of IHD. Platelets from IHD patients when stimulated produced a larger amount of TXB2 in comparison with control platelets, and TXB2 plasma levels in IHD patients were higher than the ones inhibited by ASA pretreatment (10 mg/kg i.V.). In contrast, plasma PGI2-like activity and PGI2-like activity produced by vessel wall after three-minute ischemia were significantly reduced in IHD patients (Neri Serneri et al., 1982). Moreover, in these patients an increase of TXB2 plasma levels during ischemic attacks, symptomatic or asymptomatic, could be found even when TXB2 formation by platelets was completely inhibited.