Li Jian-Jun, Nie Shao-Ping, Xu Bo, Guo Yuan-Lin, Gao Zhan, Zheng Xin
Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.
Med Hypotheses. 2007;68(3):635-40. doi: 10.1016/j.mehy.2006.05.068. Epub 2006 Oct 6.
Variant angina, defined as spontaneous angina pectoris associated with transient ST-segment elevation, has proved to be caused usually by episodic coronary spasm since Prinzmetal and his associates described a form of angina quite different from classic Heberden angina pectoris in 1959. Currently, coronary artery spasm is defined as reversible coronary stenosis, which limits coronary blood flow under resting conditions, and it plays an important role in ischemic heart disease, particularly in variant angina. Data available in respect of coronary vasospasm showed that it is closely related to atherosclerotic coronary artery disease, since intravascular ultrasound studies reveal atherosclerotic plaques in almost any spastic segment. Risk factors for coronary artery disease and coronary vasospasm, however, differ profoundly. Cigarette smoking is the only established risk factor. Although several candidates and predisposing factors, such as serotonin, histamine, thromboxane, and endothelin, have been described, the mediators and the pathogenesis of the disease remain unknown. There are abundant studies that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease. The evidence regarding the role of inflammatory pathways in different clinical entities of coronary artery disease has significantly been accumulated. And also, primary studies have showed that inflammation may be a contributor for variant angina or vasospastic coronary disease is at least partially driven by inflammation. Although much more research is obviously needed, primary evidence provide us with some direction for that research.
变异型心绞痛被定义为与短暂性ST段抬高相关的自发性心绞痛，自1959年普林兹梅尔及其同事描述了一种与经典的赫伯登心绞痛截然不同的心绞痛形式以来，已证实其通常由发作性冠状动脉痉挛引起。目前，冠状动脉痉挛被定义为可逆性冠状动脉狭窄，它在静息状态下限制冠状动脉血流，并且在缺血性心脏病中，尤其是在变异型心绞痛中起重要作用。有关冠状动脉痉挛的现有数据表明，它与动脉粥样硬化性冠状动脉疾病密切相关，因为血管内超声研究几乎在任何痉挛节段都发现了动脉粥样硬化斑块。然而，冠状动脉疾病和冠状动脉痉挛的危险因素却有很大差异。吸烟是唯一已确定的危险因素。尽管已经描述了几种候选因素和诱发因素，如血清素、组胺、血栓素和内皮素，但该疾病的介质和发病机制仍然未知。有大量研究表明炎症在动脉粥样硬化的发生、发展以及演变中起重要作用，这表明动脉粥样硬化是一种炎症性疾病。关于炎症途径在冠状动脉疾病不同临床实体中的作用的证据已大量积累。而且，初步研究表明炎症可能是变异型心绞痛的一个促成因素，或者血管痉挛性冠状动脉疾病至少部分是由炎症驱动的。尽管显然还需要更多的研究，但初步证据为该研究提供了一些方向。
