Recent insights into the mechanisms of vasospastic angina.

Coronary artery spasm plays an important role in the pathogenesis of many types of ischemic heart disease, not only in vasospastic angina but also in myocardial infarction and sudden death, particularly in the asian population. Patients with vasospastic angina are known to have defective endothelial function due to reduced nitric oxide bioavailability. Moreover, markers of oxidative stress and plasma levels of C-reactive protein are elevated. Smoking, polymorphysms of endothelial nitric oxide synthetase (eNOS), and low-grade inflammation have been regarded as the most important risk factors for vasospastic angina. The recent body of evidence indicates that RhoA and its down stream effector, ROCK/Rho-kinase, are associated with hypercontraction of vascular smooth muscle of the coronary artery and regulation of eNOS activity. Thus, endothelial dysfunction through abnormalities of eNOS and enhanced contractility of vascular smooth muscle in coronary artery segments are considered major mechanisms in vasospastic angina. However, the precise mechanisms for coronary vasospasm are not well understood. This article will review current understanding of the mechanism of coronary artery spasm.