Dakak N, Quyyumi A A, Eisenhofer G, Goldstein D S, Cannon R O
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1650.
Am J Cardiol. 1995 Jul 15;76(3):125-30. doi: 10.1016/s0002-9149(99)80043-5.
Mental stress often causes myocardial ischemia in patients with coronary artery disease (CAD). There is increasing evidence that the coronary microcirculation of patients with atherosclerosis may be dysfunctional, with the potential of contributing to myocardial ischemia. This study investigated sympathetically mediated coronary microcirculatory and regional noradrenergic effects of mental stress. We measured left anterior descending coronary artery blood flow and norepinephrine kinetics at rest and during a 10-minute video game in 10 CAD patients with nonsignificant atherosclerosis of this artery and in 5 patients with normal coronary angiograms (NCA). The 2 groups did not differ in their responses of systemic and cardiac norepinephrine spillovers, heart rate, and blood pressure during mental stress. Patients with NCA had microvascular dilation during mental stress (26 +/- 9% [mean +/- SD] decline in coronary vascular resistance from baseline, p < 0.01), whereas patients with CAD did not (9 +/- 20% decline, p = 0.11). Six patients with CAD then received intracoronary phentolamine (1.7 micrograms/kg/min for 5 minutes, followed by 0.17 micrograms/kg/min) and played the video game again. In contrast to nonsignificant changes in coronary resistance during the initial video game (6 +/- 15% decline, p = 0.20), coronary vascular resistance decreased significantly during the repeat video game (25 +/- 19% decline, p = 0.02). Vasomotor responses of epicardial coronary artery segments did not differ between the 2 video game studies. Five other patients (4 with CAD, 1 with NCA) repeated the video game during intracoronary administration of 5% dextrose, with systemic and coronary hemodynamic and noradrenergic responses unchanged from those during the initial video game.(ABSTRACT TRUNCATED AT 250 WORDS)
精神压力常导致冠心病（CAD）患者发生心肌缺血。越来越多的证据表明，动脉粥样硬化患者的冠状动脉微循环可能功能失调，这有可能导致心肌缺血。本研究调查了精神压力下交感神经介导的冠状动脉微循环及局部去甲肾上腺素能效应。我们测量了10例该动脉粥样硬化不显著的CAD患者和5例冠状动脉造影正常（NCA）患者在静息状态及进行10分钟电子游戏期间左前降支冠状动脉血流量和去甲肾上腺素动力学。两组在精神压力期间全身和心脏去甲肾上腺素溢出、心率及血压的反应方面无差异。NCA患者在精神压力期间出现微血管扩张（冠状动脉血管阻力较基线下降26±9%[平均值±标准差]，p<0.01），而CAD患者则未出现（下降9±20%，p = 0.11）。6例CAD患者随后接受冠状动脉内酚妥拉明治疗（1.7微克/千克/分钟，持续5分钟，随后为0.17微克/千克/分钟），并再次进行电子游戏。与初次电子游戏期间冠状动脉阻力无显著变化（下降6±15%，p = 0.20）不同，重复电子游戏期间冠状动脉血管阻力显著下降（下降25±19%，p = 0.02）。两次电子游戏研究中心外膜冠状动脉节段的血管舒缩反应无差异。另外5例患者（4例CAD患者，1例NCA患者）在冠状动脉内输注5%葡萄糖期间重复进行电子游戏，全身和冠状动脉血流动力学及去甲肾上腺素能反应与初次电子游戏期间无变化。（摘要截断于250字）
