The American journal of cardiology · 1999
Reduced vasodilator capacity in syndrome X related to structure and function of resistance arteries.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Buus N H, Bøttcher M, Bøttker H E, Sørensen K E, Nielsen T T, Mulvany M J
Аннотация
The combination of angina pectoris, angiographically normal epicardial coronary arteries, and a positive exercise test is referred to as syndrome X. Previous studies have demonstrated an impaired coronary flow reserve and a peripheral vascular dysfunction, suggesting that vascular abnormalities in syndrome X may not be confined to the heart. The aim of this study was to investigate whether any vascular disorder of syndrome X is due to intrinsic structural or functional disturbances in resistance arteries. We compared 16 patients with syndrome X (56.6+/-1.2 years, 3 men) with 15 matched control subjects. Myocardial blood flow was measured with 13N-ammonia positron emission tomography. Forearm blood flow was measured in the brachial artery with high-resolution ultrasound. Gluteal subcutaneous resistance arteries were dissected and mounted on a myograph for measurement of active tension development, lumen diameter, and media thickness. Baseline myocardial blood flow was similar in patients and controls, but dipyridamole-induced hyperemia was decreased in patients (1.67+/-0.13 vs 2.31+/-0.12 ml/ min/g, p <0.01). Patients and controls had similar baseline forearm blood flow, but hyperemic flow after transient occlusion of the brachial artery was impaired in patients (198+/-20 vs 273+/-32 ml/min, p <0.05). Isolated resistance arteries showed no differences in constriction to noradrenaline, or relaxation to acetylcholine, dipyridamole, or nitroglycerin. Furthermore, the ratio between media thickness and lumen diameter were similar in syndrome X patients and controls. Our data show that when compared with a well-matched control group, syndrome X patients have a decreased coronary and peripheral vasodilator capacity. However, this is not reflected by functional abnormalities or structural changes as evaluated in subcutaneous resistance arteries. We conclude that syndrome X is not a generalized intrinsic abnormality of the resistance circulation.