Gunther S, Green L, Muller J E, Mudge G H, Grossman W
Am J Cardiol. 1979 Oct 22;44(5):793-7. doi: 10.1016/0002-9149(79)90199-1.
Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.
冠状动脉血管收缩在变异型心绞痛（Prinzmetal 心绞痛）中已得到充分认识，它也可能参与典型心绞痛的发病机制。最近对冠状动脉阻塞性疾病患者的多项研究表明，冠状动脉血流量明显的自发性减少可导致心肌缺血甚至梗死。本文综述了支持α肾上腺素能神经系统作为此类冠状动脉血管收缩病因的证据，尤其是冷加压刺激激发试验的结果。当皮肤暴露于寒冷环境时，冠心病患者会表现出不适当的冠状动脉血管收缩反应，这种反应通常足以引发心绞痛。相比之下，正常患者的冠状动脉血管阻力没有变化。在患有疾病的冠状动脉循环中，不适当的血管收缩会进一步限制心肌灌注，而且通常剂量的β肾上腺素能阻滞剂或硝酸盐对此几乎没有影响。硝苯地平已被证明可有效预防变异型心绞痛患者的冠状动脉痉挛。目前正在进行的研究表明，它对阻止典型心绞痛患者不适当的冠状动脉血管收缩也有效。因此，硝苯地平可能是缺血性心脏病治疗中的一种有用药物。
