ROLE OF NITRIC-OXIDE IN CORONARY ARTERIAL VASOMOTION AND THE INFLUENCE OF CORONARY ATHEROSCLEROSIS AND ITS RISKS

Healthy coronary vascular endothelium releases nitric oxide to modulat e resting and dynamic coronary arterial cone. We studied the impact of atherosclerosis and/or ifs risks on endothelial nitric oxide release in response to metabolic stimuli by evaluating coronary vasomotor resp onses to atrial pacing before and after the inhibition of nitric oxide production by intracoronary NG-monomethyl-L-arginine (L-NMMA) (20 mu mol/min) infusion. The study includes 34 patients (15 with coronary di sease, 11 with normal coronary arteries and greater than or equal to 1 risk factor, and 8 with normal coronary arteries and no risks). Coron ary blood flow was derived from Doppler flow velocity (0.018-inch Dopp ler wire) and coronary diameter. L-NMMA infusion reduced coronary bloo d flow by 18 +/- 16% and coronary diameter by 10 +/- 9%. Responses wer e identical in all subgroups. Coronary blood flow responses to pacing were similar in all subgroups and were unaffected by L-NMMA (11 +/- 11 vs 13 +/- 9 ml/min; p = 0.26). Epicardial coronary vasodilation to co ntrol pacing occurred in patients with normal coronary arteries with ( 4.0 9 +/- 5.2%, p = 0.01) or without (8.0 +/- 5.2%, p = 0.03) risks, b ut not in patients with coronary disease (2.8 +/- 5.9%). L-NMMA abolis hed pacing-induced epicardial vasodilation in patients without coronar y artery disease, producing a 1.8 +/- 5.1% response, which was similar in all subgroups, We conclude that microvascular responses to rapid a trial pacing are not mediated by nitric oxide. Flow-mediated epicardia l coronary arterial responses may be nitric oxide dependent. (C)1998 b y Excerpta Medico, Inc.