Heusch Gerd, Schulz Rainer, Haude Michael, Erbel Raimund
Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse 55, Essen 45122, Germany.
J Mol Cell Cardiol. 2004 Jul;37(1):23-31. doi: 10.1016/j.yjmcc.2004.04.011.
Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features--arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve--, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.
动脉粥样硬化斑块破裂是急性冠脉综合征发病机制以及冠脉介入过程中的关键事件。动脉粥样硬化斑块破裂并不总是导致整个心外膜冠状动脉完全血栓性闭塞并继而引发急性心肌梗死,而是可能以较轻的形式导致动脉粥样硬化和血栓碎片栓塞进入冠脉微循环。本综述总结了死于冠状动脉疾病(尤其是猝死)患者冠脉微栓塞的现有形态学证据。然后详细阐述了急性冠脉综合征动物模型中冠脉微栓塞的实验病理生理学。最后,本综述展示了患者冠脉微栓塞的现有临床证据,突出了其关键特征——心律失常、收缩功能障碍、微梗死和冠脉储备降低,将这些特征与实验模型的特征进行比较,并探讨通过机械保护装置和糖蛋白IIb/IIIa拮抗剂对其进行预防。