PATHOGENESIS AND CLINICAL SIGNIFICANCE OF CORONARY SPASM

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The precise mechanisms by which coronary spasm occurs and the clinical significance of coronary spasm still remain to be elucidated. The present study shows that intracoronary injection of acetylcholine, an endothelium-dependent vasodilator, dilates the epicardial coronary arteries in the subjects less then 29 years, whereas it constricts the coronary arteries in the subjects older than 30 years. Nitroglycerin, an endothelium-independent vasodilator, dilated the coronary arteries in the younger as well as the older subjects. Injury of endothelium is essential for the pathogenesis of atherosclerosis. Thus, the endothelium of the coronary arteries are injured or coronary atherosclerosis is present in most subjects older than 30 years. Almost all of the patients with coronary spasm are older than 30 years. It is therefore concluded that coronary spasm occurs on the basis of coronary atherosclerosis. However, coronary atherosclerosis alone cannot explain the pathogenesis of coronary spasm because all patients with coronary atherosclerosis do not have coronary spasm. Mg deficiency was found in 45 % of the patients with coronary spasm. Thus, Mg deficiency may play a role in the pathogenesis of coronary spasm in some patients with coronary spasm. Acetylcholine increased coronary sinus flow in patients with coronary spasm as well as in the younger subjecjts. Thus, coronaryresistance vessels retain the vasodilatatory response to acetylcholine or endothelium-dependent relaxation in patients with coronary spasm.The present study also shows that coronary spasm in-creases plasma level of fibrinopeptide A, an indicator of fibrin formation. Thus, coronary spasm may trigger coronary thrombosis and thus lead to acute myocardial infarction by activating thrombin and fibrin formation.