No-Reflow Phenomenon: Maintaining Vascular Integrity
No-Reflow Phenomenon: Maintaining Vascular Integrity
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DOI：
10.1177/1074248411405990
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发表时间：
2011-09-01
影响因子：
2.6
通讯作者：
Kloner, Robert A.
中科院分区：
文献类型：
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作者：
Kloner, Robert A.
无再流现象与心肌缺血后无法再灌注区域有关，尽管切除了大的心外膜冠状动脉闭塞。其机制与微血管阻塞有关。在实验研究中，使用血流标志物（硫黄素S、炭黑、微球），灌注缺陷与非血流相关，超微结构证据表明，局部内皮肿胀和气泡似乎阻碍了血流。在人类中，由于动脉粥样硬化碎片的微栓塞和经皮冠状动脉介入治疗产生的血栓，无血流更复杂。无回流区在再灌注的最初几个小时内扩大，提示有再灌注损伤的因素。在动物模型中，广泛的无血流循环与更严重的梗死扩张相关。磁共振成像、回声造影剂、铊、锝-99m标记白蛋白微球、心肌梗死溶栓（TIMI）评分和心肌红肿分级证实了人类心肌梗死再灌注治疗后无再流现象。心肌梗死再灌注治疗后出现无回流的患者有更大的左心室扩张和重构，更多的充血性心力衰竭、休克和生存率降低。某些血管扩张剂（腺苷、硝普塞、尼可地尔和钙阻滞剂）在导管实验室中被急性使用，似乎可以改善无血流倒流，但需要对无血流倒流的治疗进行系统研究。现在有临床证据表明，无血流循环是长期死亡率的一个强有力的预测指标，它独立于梗死面积，而且超出了梗死面积的预测。识别和治疗无血流可能具有重要的益处，包括增强愈合所需的营养物质和细胞的输送，减少梗死扩张和心室重塑，最终可能减少充血性心力衰竭和死亡率。
The no-reflow phenomenon relates to the inability to reperfuse regions of the myocardium after ischemia, despite removal of the large epicardial coronary artery occlusion. The mechanism involves microvascular obstruction. In experimental studies, using markers for flow (thioflavin S, carbon black, microspheres), perfusion defects associated with no-reflow demonstrated ultrastructural evidence of localized endothelial swelling and blebs that appeared to obstruct flow. In humans no-reflow is more complicated due to the microemboli of atherosclerotic debris and thrombi generated by percutaneous coronary intervention. The no-reflow zone expands during the first few hours of reperfusion suggesting an element of reperfusion injury. In animal models, extensive no-reflow was associated with worse infarct expansion. The phenomenon of no-reflow following reperfusion therapy for myocardial infarction in humans has been demonstrated by magnetic resonance imaging, echo contrast agents, thallium, technecium-99m-labeled albumin microspheres, Thrombolysis In Myocardial Infarction (TIMI) scores, and myocardial blush grade. Patients exhibiting no-reflow following reperfusion therapy for myocardial infarction have greater left ventricular dilation and remodeling, more congestive heart failure, shock, and reduced survival. Certain vasodilators (adenosine, nitroprusside, nicorandil, and calcium blockers) are used acutely in the catheterization laboratory and appear to improve no-reflow, but systematic studies on therapy for no-reflow are needed. There is now clinical evidence that no-reflow is a strong predictor of long-term mortality that is independent of and beyond that provided by infarct size. Identifying and treating no-reflow may have important benefits including enhancing delivery of nutrients and cells required for healing and reducing infarct expansion and ventricular remodeling, which ultimately may reduce congestive heart failure and mortality.