Bellamy M F, Goodfellow J, Tweddel A C, Dunstan F D, Lewis M J, Henderson A H
Department of Cardiology, University of Wales College of Medicine, Cardiff, UK.
Cardiovasc Res. 1998 Nov;40(2):410-7. doi: 10.1016/s0008-6363(98)00184-9.
Syndrome X (angina, normal coronary arteriogram and positive exercise test) remains an enigma with unexplained features and apparent conflicts of evidence. The present study addressed whether (i) the Syndrome is characterised by generalised flow-related endothelial dysfunction, (ii) myocardial thallium201 defects reflect myocardial or microvascular dysfunction, (iii) endothelial dysfunction and its consequences can be improved by oral L-arginine.
Flow-mediated brachial artery dilatation was measured by ultrasonic 'wall-tracking' in 7 Syndrome X patients, further characterised as having thallium201 defects and no known cause of endothelial dysfunction, and a normal control group. Syndrome X patients entered a 4-week randomised double-blind placebo-controlled cross-over trial of oral L-arginine (7 g twice daily), with brachial artery studies, exercise tests and technetium99 tetrafosmin scans.
Flow-mediated dilatation was absent in Syndrome X vs. normal. Stress technetium99 tetrafosmin and thallium201 scans showed similar defects. Flow-mediated dilatation, symptom-limited exercise duration and peak oxygen consumption (VO2max) were increased but rate-pressure-product (RPP) and radionuclide defects were unchanged after L-arginine vs. placebo.
The study supports coronary microvascular rather than myocardial dysfunction and shows loss of flow-mediated dilatation in systemic arteries. Oral L-arginine improved flow-mediated dilatation, exercise capacity and VO2max (by ca. 17%) despite unchanged RPP. The findings support generalised endothelial dysfunction. The arginine effects imply NO-mediated improvement of skeletal muscle perfusion suggesting improved homogeneity of microvascular distribution.
X综合征（心绞痛、冠状动脉造影正常及运动试验阳性）仍是一个谜团，具有无法解释的特征且证据明显相互矛盾。本研究探讨了以下问题：（i）该综合征是否以全身性血流相关内皮功能障碍为特征；（ii）心肌铊201缺损反映的是心肌功能障碍还是微血管功能障碍；（iii）口服L-精氨酸能否改善内皮功能障碍及其后果。
通过超声“壁跟踪”测量7例X综合征患者（进一步分为有铊201缺损且无已知内皮功能障碍病因者）和一个正常对照组的血流介导的肱动脉扩张。X综合征患者进入一项为期4周的口服L-精氨酸（每日两次，每次7 g）的随机双盲安慰剂对照交叉试验，同时进行肱动脉研究、运动试验和锝99四膦酸盐扫描。
与正常情况相比，X综合征患者不存在血流介导的扩张。应激锝99四膦酸盐和铊201扫描显示出类似的缺损。与安慰剂相比，L-精氨酸治疗后血流介导的扩张、症状限制运动持续时间和峰值耗氧量（VO2max）增加，但心率血压乘积（RPP）和放射性核素缺损未改变。
该研究支持冠状动脉微血管功能障碍而非心肌功能障碍，并表明全身动脉存在血流介导的扩张功能丧失。口服L-精氨酸尽管RPP未改变，但改善了血流介导的扩张、运动能力和VO2max（约提高17%）。这些发现支持全身性内皮功能障碍。精氨酸的作用意味着一氧化氮介导的骨骼肌灌注改善，提示微血管分布均匀性提高。
