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40年前已证明尸检所观察到的冠状动脉粥样硬化与心绞痛临床综合征之间的密切联系,从此认为心绞痛系由于固定性的阻塞,它限制冠状动脉在代谢需求增进时增加血流的能力,当达到氧的释放不能再增加的阈值时则发生心绞痛。然而,在过去的10年,2个重要的发展已有效地驳斥了这种认为固定性狭窄能完全解释以心绞痛为特征的不同临床综合征的概念。第一个主要异议是:大的冠状动脉痉挛经证示是 Prinzmetal’s 或变异型心绞痛的主要原因。它彻底改变了作者对形成心绞痛的病理生理的了解,并引出这样的概念,即大的冠状动脉的动力性阻塞的增加可诱发缺血症状。第二个异议是:晚近证明,小冠状动脉的收缩可诱发静息和劳力型心绞
The close link between coronary atherosclerosis and the clinical syndrome of angina observed autopsy 40 years ago proved that angina is due to a fixed obstruction that limits the ability of the coronary arteries to increase blood flow as metabolic needs increase, Angina pectoris occurs when the threshold for the release of oxygen can not be increased. However, in the past 10 years, two important developments have effectively refuted the notion that fixed stenosis completely explains the different clinical syndromes characterized by angina. The first major objection is that large coronary spasms have been shown to be the main cause of Prinzmetal’s or variant angina. It completely changed the author’s understanding of the pathophysiology of angina pectoris and led to the concept that an increase in motorized obstruction of large coronary arteries can induce ischemic symptoms. The second objection is: Recently proved that the contraction of small coronary arteries can induce resting and labor heart