Coronary vasospasm is currently considered to be an exaggerated contractile nonspecific response of the vascular smooth muscle in the large coronary artery to various agonists or stimulation, that is established after the process of
inflammation and fibrocellular proliferation. Endothelial dysfunction with reduced
nitric oxide bioavailability has been reported in angiographically normal coronary arteries in Japanese patients with coronary
spastic angina. Recently, several interesting findings concerning the exact mechanism of
calcium hypersensitivity of
spastic vascular smooth muscle have been reported. In animal models with coronary
spasm Rho-kinase is upregulated at the
spastic site and plays a key role in inducing vascular smooth muscle hypercontraction by inhibiting
myosin light chain phosphatase, resulting in enhancement of its phosphorylation. Also, oxidative stress has been given attention as an important mediator of the
spastic conversion of vascular smooth muscle cell "phenotype." The incidence of coronary
spastic angina in the Japanese population is reported to be remarkably high compared with that in Caucasians. Clinical and pathophysiological differences between Japanese and Caucasian patients with respect to
coronary vasospasm are characterized by a lower prevalence of fixed
coronary artery stenoses and diffuse coronary hyperreactivity in the Japanese patients. Recently, several distinct characteristics have been recognized to be associated with
coronary vasospasm in studies analyzing data obtained from Japanese patients. In the present review, we will discuss our point of view on the mechanisms and predisposing factors in
coronary vasospasm. Predisposing factors include smoking,
lipid metabolic disorders, and gene expression, all of which may be interrelated issues.