[Pathophysiology of coronary spasm].

There is a deficiency in both basal and stimulated NO release in the spasm arteries of patients with coronary spastic angina. The deficient NO release may lead to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with coronary spastic angina. Flow-dependent coronary dilation of proximal LAD was found to be less in spasm arteries than in control arteries. The infusion of L-NMMA in the proximal site of LAD suppressed the flow-dependent dilation in control arteries, while L-NMMA did not have significant effect in spasm arteries. The results indicate that flow-dependent coronary dialtion is impaired in spasm arteries partly due to deficiency in endothelial NO bioactivity, which in turn may possibly contribute to increase in coronary tone during the physiological stress in patients with coronary spastic angina.