Management of vasospastic angina—Role of nicorandil

Summary

Clinical and experimental observations have confirmed that an episodic increase in the vasomotor tone of a major coronary artery may play a pathogenetic role not only in “variant angina” but also in other, more common anginal syndromes. In chronic stable angina, dynamic changes of vascular smooth muscle tone at the site of eccentric atheromatous plaques are responsible for “mixed angina.” Abnormal coronary vasomotion contributes to myocardial ischemia in acute coronary syndromes as well. Studies have shown that a “primary” reduction of coronary blood flow, usually associated with plaque fissuring and thrombus formation, causes infarction and unstable angina. Abnormal vasoconstriction associated with the release of vasoactive substances by platelets and other constituents of the thrombus can contribute to coronary flow reduction in patients with unstable angina and myocardial infarction. Better understanding of the complex interactions among atherosclerotic coronary obstructions, the vascular smooth muscle, and the vascular endothelium has resulted in novel therapeutic approaches and has stimulated the search for more efficacious and safer coronary vasodilators. Recently interest has focused on vasodilator agents such as nicorandil that influence coronary arterial tone by acting through potassium channel activation. Nicorandil appears to be effective for treatment of vasospastic angina, as suggested by studies in Japan and Europe. In addition to its “antivasospastic” properties, nicorandil dilates coronary artery stenoses in patients with stable angina pectoris. It also improves myocardial ischemia in patients with mixed angina. Thus nicorandil may be useful for treatment of patients with “variable threshold angina” in whom myocardial ischemia results from the combined effects of obstructive coronary plaques and changes of coronary vasomotor tone.