Endogenous modulators of platelet aggregability and vascular tone may play a part in coronary-artery disease. We therefore measured the release of prostaglandins and thromboxane into the coronary circulation in patients with various kinds of cardiac disease. Simultaneous coronary-sinus (CS) and ascending-aortic (AO) blood samples were obtained from 60 patients for measurement of 6-keto-prostaglandin F1α (6-keto-PGF1α, a prostaglandin l2 metabolite) and of thromboxane B2 (T×B2). Samples from 45 of these patients were also tested for prostaglandin E2 (PGE2) and lactate. Patients with unstable angina pectoris who reported chest pain within 24 hours of study had higher T×B2 CS/AO ratios (5.8±2.8, mean ±S.D.) than patients whose most recent anginal pain was more than 96 hours before study (1.3±0.6; P<0.05), than those with nonischemic chest pain (1.2±0.4; P<0.05), or with valvular or congenital nonischemic heart disease (1.2±0.6; P<0.05). Those whose most recent anginal pain occurred 24 to 96 hours before study were distributed bimodally: the majority had low T×B2 CS/AO ratios (range, 0.5 to 2.1) like the patients in the three aforementioned groups, whereas a few had markedly elevated values (range, 10.5 to 46.6). The 6-keto-PGF1α and PGE2 CS/AO ratios and myocardial lactate extraction were not significantly different among the five groups. These data suggest that local thromboxane release is associated with recent episodes of angina in patients with unstable angina pectoris, but whether this release is a cause or an effect is not yet known. (N Engl J Med. 1981; 304:685–91.) THERE has been recent speculation about the role of prostaglandins and thromboxanes in ischemic heart disease.1,2 These naturally occurring compounds are potent modulators of vascular smooth-muscle tone and platelet aggregability.3 Prostaglandin I2 (PGI2) — a powerful vasodilator and inhibitor of platelet aggregation — is the predominant prostaglandin synthesized by the heart.4,5 Prostaglandin E2 (PGE2), also synthesized in the heart, dilates the coronary-vascular smooth muscle in vivo but at the same time promotes platelet aggregation.6 In contrast, thromboxane A2 (T×A2) is a potent vaso-constrictor released by platelets that in turn causes further.
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