Thromboxane A2 and Prostaglandin I2 as Precipitating Factors of Vasospastic and Thrombotic Events in Coronary Artery Disease
Recent clinical evidence has indicated that during the active phase of coronary artery disease, coronary thrombosis and/or vasospasm could initiate the pathological events associated with angina pectoris and acute myocardial infarction (1). Platelet aggregates within the coronary circulation may exert their effects directly through machanical obstruction to blood flow, resulting in myocardial ischemic injury. In addition they may release thromboxane A2 (TXA2), a potent vasoconstrictor and platelet aggregating agent (2), thereby causing coronary vasospasm and myocardial ischemia. We have already shown that transcardiac TXA2 release is associated with the induction of myocardial ischemia in patients with angina pectoris (3).
KeywordsAngina Pectoris Coronary Sinus Anginal Attack Coronary Vasospasm Variant Angina
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- 12.Kuzuya T, Tada M, Ohmori M, Inui M, Inoue M, Abe H, Yamagishi M, Kodama K: Altered metabolism of thromboxane A2 and prostaglandin I2 in patients with angina pectoris. (abstr) Circulation (64):IV–143, 1981.Google Scholar
- 17.Tada M, Esumi K, Yamagishi M, Kuzuya T, Matsuda H, Abe H, Uchida Y, Murao S: Reduction of prostacyclin synthesis as a possible cause of transient flow reduction in a partially constricted canine coronary artery. J Mol Cell Cardiol 1984, in press.Google Scholar
- 20.Ohmori M, Tada M, Kuzuya T, Yamagishi M, Matsuda H, Inoue M, Abe H, Kodama K: Thromboxane A2 as a precipitating factor in coronary arterial spasm of variant angina, (abstr) Circulation (68):111–22, 1983.Google Scholar
- 24.Kuzuya T, Tada M, Hoshida S, Ohmori M, Matsuda H, Inoue M, Abe H, Minamino T: Excessive thromboxane A2 generation could be a possible aggravating factor in unstable angina, (abstr) Circulation (68): III–398, 1983.Google Scholar
- 25.Tada M, Hoshida S, Kuzuya T, Inoue M, Minamino T, Abe H: Augmented thromboxane A2 generation and efficacy of its blockade in acute myocardial infarction. Br Heart J 1984, in press.Google Scholar