Microvascular Obstruction Underlying Pathophysiology and Clinical Diagnosis
Microvascular Obstruction Underlying Pathophysiology and Clinical Diagnosis
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DOI：
10.1016/j.jacc.2009.12.037
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发表时间：
2010-04-20
影响因子：
24
通讯作者：
Waltenberger, Johannes
中科院分区：
文献类型：
--
作者：
Bekkers, Sebastiaan C. A. M.;Yazdani, Saami K.;Waltenberger, Johannes
长期闭塞后成功恢复心外膜冠状动脉通畅可能导致微血管阻塞（MVO），这在实验和临床上都有观察。在再灌注心肌，心肌细胞出现水肿和肿胀的渗透负荷。内皮细胞的变化通常伴随着在心肌细胞中观察到的改变，但滞后于心肌细胞损伤。内皮细胞体积变大，管腔内内皮细胞突起进入血管腔，并与周围肿胀的肌细胞一起阻塞毛细血管。中性粒细胞和血小板的浸润和活化以及纤维蛋白的沉积在再灌注引起的微血管损伤和阻塞中也起重要作用。除了这些缺血再灌注相关事件外，经皮冠状动脉介入治疗后动脉粥样硬化碎片的冠状动脉微栓塞是临床观察到的MVO的主要原因。再灌注后的微血管流动在空间和时间上是复杂的。充血区域、血管舒张血流储备受损和极低血流共存，并且这些灌注模式由于再灌注损伤而随时间变化。MVO首先出现在梗死核心的中心，随着时间的推移向心外膜延伸。MVO的准确检测是至关重要的，因为它与心室重构和患者预后独立相关。临床和实验中使用了几种测量略有不同的生物和功能参数的技术（冠状动脉造影、心肌造影超声心动图、心血管磁共振成像、心电图）。目前，对于急性心肌梗死后如何以及何时评估MVO还没有达成共识。（J Am科尔心脏病学杂志2010;55：1649-60）（C）美国心脏病学会基金会2010年
Successful restoration of epicardial coronary artery patency after prolonged occlusion might result in microvascular obstruction (MVO) and is observed both experimentally as well as clinically. In reperfused myocardium, myocytes appear edematous and swollen from osmotic overload. Endothelial cell changes usually accompany the alterations seen in myocytes but lag behind myocardial cell injury. Endothelial cells become voluminous, with large intraluminal endothelial protrusions into the vascular lumen, and together with swollen surrounding myocytes occlude capillaries. The infiltration and activation of neutrophils and platelets and the deposition of fibrin also play an important role in reperfusion-induced microvascular damage and obstruction. In addition to these ischemia-reperfusion-related events, coronary microembolization of atherosclerotic debris after percutaneous coronary intervention is responsible for a substantial part of clinically observed MVO. Microvascular flow after reperfusion is spatially and temporally complex. Regions of hyperemia, impaired vasodilatory flow reserve and very low flow coexist and these perfusion patterns vary over time as a result of reperfusion injury. The MVO first appears centrally in the infarct core extending toward the epicardium over time. Accurate detection of MVO is crucial, because it is independently associated with adverse ventricular remodeling and patient prognosis. Several techniques (coronary angiography, myocardial contrast echocardiography, cardiovascular magnetic resonance imaging, electrocardiography) measuring slightly different biological and functional parameters are used clinically and experimentally. Currently there is no consensus as to how and when MVO should be evaluated after acute myocardial infarction. (J Am Coll Cardiol 2010;55:1649-60) (C) 2010 by the American College of Cardiology Foundation