Maseri A
J Am Coll Cardiol. 1987 Feb;9(2):249-62. doi: 10.1016/s0735-1097(87)80372-8.
The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). Continuous monitoring initially of patients with variant angina and subsequently of patients with unstable and stable angina proved that often painful and painless ischemic episodes are caused by a transient impairment of regional coronary blood flow rather than by an excessive increase of myocardial demand. The transient impairment of coronary flow appears to be caused by dynamic stenosis of epicardial coronary arteries. This most often occurs at the site of atherosclerotic plaques encroaching on the lumen to a variable extent. Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.
冠状动脉痉挛概念的复兴推动了对冠状动脉疾病的研究。对变异型心绞痛患者的观察极大地促进了对无痛性心肌缺血的认识。然而，缺血发作时疼痛的有无与缺血原因无关，因为在变异型心绞痛（由痉挛引起）、劳力性心绞痛（由心肌需求增加引起）和心肌梗死（由血栓形成引起）中都可观察到无痛性缺血。最初对变异型心绞痛患者，随后对不稳定型和稳定型心绞痛患者进行的连续监测证明，有痛和无痛的缺血发作通常是由局部冠状动脉血流的短暂受损引起的，而不是由心肌需求的过度增加引起的。冠状动脉血流的短暂受损似乎是由心外膜冠状动脉的动态狭窄所致。这最常发生在不同程度侵犯管腔的动脉粥样硬化斑块部位。动态狭窄可由以下原因引起：1）冠状动脉张力的“生理性”增加，如在稳定型心绞痛中；2）痉挛，如在变异型心绞痛中；3）血栓形成，通常与张力的“生理性”变化或痉挛，或两者兼而有之，如在不稳定型心绞痛中。变异型心绞痛中典型观察到的痉挛机制与张力的“生理性”增加机制不同；它们似乎与一种局部改变有关，这种改变使冠状动脉的一段对各种收缩刺激具有高反应性，而在其他冠状动脉中仅引起轻微程度的收缩。这种异常的性质可能会持续数月甚至数年保持稳定，目前尚不清楚。
