NITRIC OXIDE-MEDIATED FLOW-DEPENDENT DILATION IS IMPAIRED IN CORONARY-ARTERIES IN PATIENTS WITH CORONARY SPASTIC ANGINA

Objectives. This study sought to examine whether flow dependent dilati on is impaired at the site of coronary artery spasm in patients with c oronary spastic angina. Background. Physiologic stimuli such as exerci se and exposure to cold have been shown to cause an increase in corona ry blood flow, leading to flow-dependent dilation of coronary arteries in normal subjects, but cause coronary constriction in patients with coronary spastic angina. Methods. A maximal increase in blood flow was induced selectively in the left anterior descending coronary artery ( LAD) by infusion of adenosine through a Doppler flow catheter tip in t he midportion of the LAD in 10 patients with coronary spastic angina, all with angiographically demonstrated spasm of the LAD, and in 11 con trol patients. Coronary artery diameter at the proximal site of the LA D (exposed to increased flow but not to adenosine) was measured by qua ntitative angiography. Results. Flow-dependent dilation of the proxima l LAD was found to be less in spasm arteries than in control arteries. Infusion of N-G monomethyl-L arginine (L-NMMA) in the proximal LAD su ppressed flow dependent dilation in control arteries but had no signif icant effect on spasm arteries. The dilator response to nitroglycerin was not impaired in spasm coronary arteries. Conclusions Our results i ndicate that flow dependent coronary dilation is impaired in spasm art eries, partly due to a deficiency in endothelial nitric oxide bioactiv ity, which in turn may contribute to the increase in coronary tone dur ing physiologic stimuli in patients with coronary spastic angina. (C) 1997 by the American College of Cardiology.