Aizawa T, Ogasawara K, Kato K
Cardiovascular Institute Hospital, Tokyo, Japan.
J Cardiovasc Pharmacol. 1987;10 Suppl 8:S123-9.
In cases where fixed stenosis of coronary arteries plays a predominant role in the pathogenesis of angina pectoris, antianginal drugs can be expected to produce therapeutic effects. By decreasing myocardial oxygen consumption, these drugs improve or even reestablish the normal balance between the myocardial demand for oxygen and the supply of oxygen to myocardial tissues. On the other hand, there is another conceptually important pathophysiologic mechanism of causation of angina pectoris, i.e., dynamic coronary obstruction. Where such a lesion underlies a clinical disease, dilatation of large coronary arteries and relief of coronary spasm account for the main mechanism of action of antianginal drugs. In the present study, the acute coronary hemodynamic and vasodilating effects of nicorandil, a newly developed antianginal drug, were assessed in comparison with nitroglycerin in two groups of ischemic heart disease patients: those with and those without coronary spasm. The results indicate that nicorandil decreased both preload and afterload, though to a lesser extent than nitroglycerin, and also, in striking contrast to nitroglycerin, reduced coronary vascular resistance. The vasodilatory action of nicorandil on the epicardial coronary artery was especially pronounced in cases with increased coronary vascular tonus. Furthermore, the drug strongly potentiated on spontaneous coronary spasm. Nicorandil was thus considered to produce its antianginal effect primarily by redistribution of coronary blood flow as a result of dilatation of vascular beds and by its antispasmodic action.
