Transcardiac 5-hydroxytryptamine release and impaired coronary endothelialfunction in patients with vasospastic angina

1. The present study was designed to test the hypotheses whether platelet d egranulation across the coronary bed is detectable during non-ischaemic per iods in patients with vasospastic angina (VSA) and whether the exogenous ni tric oxide (NO) donor nitroglycerin (GTN) is able to modify platelet degran ulation, reflecting an impaired endothelial production of NO. 2. We studied 13 patients with VSA and 10 controls. The time course of coro nary sinus (CS) plasma 5-hydroxytryptamime (5-HT) levels was evaluated ever y 4 h before and after intravenous infusion of GTN over a period of 40 h. C oronary sinus plasma 5-HT levels were significantly higher at any measured time point in patients with VSA compared with control and were significantl y decreased in patients with VSA following treatment with GTN, but not in c ontrols. Femoral artery plasma 5-HT levels remained almost constant through out the study. The ratio of CS:aorta 6-keto-prostaglandin F-1 alpha was sig nificantly and inversely correlated with the transcardiac plasma 5-HT diffe rence only in patients with VSA (r = -0.68; P < 0.02; n = 13). 3. The time course of CS 5-HT levels confirmed significant platelet degranu lation across the coronary bed supplied by the spasming artery in patients with VSA and this was modified by GTN. The present data suggest that platel et degranulation occurs during non-ischaemic periods in patients with VSA a nd that prostacyclin biosynthesis may be a compensatory response to an impa ired endothelial release of NO, limiting the degree of the effects of plate let degranulation.