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目的:观察急性心肌梗死直接经皮冠状动脉腔内成形术(PTCA)再灌注治疗无复流患者局部冠状动脉循坏内皮细胞凋亡及凝血活性的改变,探讨无复流的形成机制。方法:收集急性心肌梗死直接PTCA再灌注治疗无复流8例及有复流患者10例,同时选取稳定型心绞痛行择期PTCA和单纯冠状动脉造影的患者作为对照。流式细胞术检测患者冠状静脉窦血液标本内皮细胞凋亡情况及组织因子、血管性血友病因子(vWF)活性的改变。结果:无复流组内皮细胞凋亡数、组织因子及vWF水平分别为(985±245)×103／L、(359±67)ng／L、(292 ±39)％,均显著高于有复流组[(228±81)×103／L、(209±74)ng／L、(192±35)％]及对照组(均P<0．01)。结论:冠状动脉内皮细胞凋亡及高凝状态参与了急性心肌梗死无复流的发病,其机制可能与内皮细胞凋亡导致弥散性微血栓阻塞冠状动脉微循环有关。
Objective: To observe the changes of apoptosis and coagulation activity of local coronary artery in patients with coronary artery bypass grafting undergoing direct percutaneous transluminal coronary angioplasty (PTCA) reperfusion in acute myocardial infarction and to explore the mechanism of no-reflow. Methods: Eight patients with no-reflow and 10 patients with recurrent flow were enrolled in the study. The patients undergoing PTCA and simple coronary angiography were selected as the control. Flow cytometry was used to detect the changes of endothelial cell apoptosis and the activity of tissue factor and von Willebrand factor (vWF) in coronary sinus blood samples. Results: The number of apoptotic endothelial cells, tissue factor and vWF were (985 ± 245) × 103 / L, (359 ± 67) ng / L, (292 ± 39)%, respectively) (228 ± 81) × 103 / L, (209 ± 74) ng / L, (192 ± 35)%] and control group (all P <0.01). CONCLUSION: Apoptosis and hypercoagulable state of coronary artery endothelial cells are involved in the pathogenesis of no-reflow in acute myocardial infarction. The mechanism may be related to the microcirculation of coronary artery occluding microvascular thrombosis caused by endothelial cell apoptosis.