Cimmino Giovanni, Conte Stefano, Morello Alberto, D'Elia Saverio, Marchese Valeria, Golino Paolo
Department of Cardio-Thoracic and Respiratory Sciences, Section of Cardiology, Second University of Naples, Naples, Italy.
Expert Rev Cardiovasc Ther. 2012 Dec;10(12):1533-43. doi: 10.1586/erc.12.157.
Acute coronary syndromes (ACS) still represent a major cause of death in Western countries; in the vast majority of cases, coronary atherosclerosis represents the common pathological lesion to all forms of ACS. It is currently believed that plaque complication (rupture, fissuration, and so on), with the consequent superimposed thrombosis, is a key factor ultimately leading to the clinical occurrence of ACS. Over the last two decades, our understanding of the basic mechanisms involved in the pathophysiology of ACS has progressed significantly and the crucial role of inflammation in this phenomenon is now widely recognized. The sequence of events is represented by plaque complication (i.e., rupture, fissuration or erosion), exposure of tissue factor and other prothrombotic substances, such as von Willebrand factor and collagen, to the blood flow, activation of platelets and of the coagulation cascade and thrombus formation within the coronary artery. However, not all complicated plaques cause the clinical occurrence of ACS and similar complicated plaques may cause different clinical manifestations. A complex interaction between different factors, such as arterial vessel wall substrates, degree of inflammation of the culprit lesion, local rheological characteristics of blood flow, as well as factors present in the circulating blood, will determine the severity (complete vs incomplete occlusion) and the persistence of coronary blood flow cessation, which, in turn, will be largely responsible for the clinical picture. Targeting tissue factor, the key player in the activation of the coagulation cascade, may represent an important therapeutic strategy to prevent the clinical manifestation of ACS.
急性冠状动脉综合征（ACS）在西方国家仍然是主要的死亡原因；在绝大多数情况下，冠状动脉粥样硬化是所有形式的ACS共同的病理病变。目前认为，斑块并发症（破裂、裂隙形成等）以及随之而来的血栓形成是最终导致ACS临床发病的关键因素。在过去的二十年里，我们对ACS病理生理学所涉及的基本机制的理解有了显著进展，炎症在这一现象中的关键作用现在已得到广泛认可。事件的顺序表现为斑块并发症（即破裂、裂隙形成或糜烂），组织因子和其他促血栓形成物质（如血管性血友病因子和胶原蛋白）暴露于血流中，血小板和凝血级联反应的激活以及冠状动脉内血栓形成。然而，并非所有复杂斑块都会导致ACS的临床发病，类似的复杂斑块可能会导致不同的临床表现。不同因素之间的复杂相互作用，如动脉血管壁基质、罪犯病变的炎症程度、局部血流流变学特征以及循环血液中存在的因素，将决定冠状动脉血流停止的严重程度（完全阻塞与不完全阻塞）和持续时间，而这反过来又在很大程度上决定了临床表现。针对凝血级联反应激活中的关键因素组织因子，可能是预防ACS临床表现的一种重要治疗策略。
