FLOW-MEDIATED, ENDOTHELIUM-DEPENDENT DILATATION OF THE BRACHIAL ARTERIES IS IMPAIRED IN PATIENTS WITH CORONARY SPASTIC ANGINA

Coronary spasm is induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is int act, and is promptly relieved by nitroglycerin, which vasodilates thro ugh the direct action on ;smooth muscle. Endothelial dysfunction is th erefore possibly involved in the pathogenesis of coronary artery spasm . The aim of this study was to determine whether endothelium-dependent vasodilation is impaired in the peripheral arteries of patients with coronary spastic angina. Flow-dependent vasodilation of the brachial a rteries during reactive hyperemia after the transient arterial occlusi on was examined by using the high-resolution ultrasound technique in 3 5 patients with coronary spastic angina and 35 controls. Flow-dependen t vasodilation of the brachial arteries was impaired in patients with coronary spastic angina compared with controls (5.9% +/- 4.2% vs 9.6% +/- 3.4%, p < 0.001) although the percent increase in blood flow durin g reactive hyperemia was not different between the two groups. The dil ator response to nitroglycerin was preserved in patients with coronary spastic angina compared with controls (18.6% +/- 5.1% vs 16.2% +/- 3. 9%, p < 0.04). The results indicate that endothelium-dependent vasodil ation of the brachial arteries is impaired in patients with coronary s pastic angina. Thus endothelial vasomotor dysregulation may also be pr esent in the systemic arteries as well as coronary arteries in patient s with coronary spastic angina.