心外膜血流机械恢复后 ST 段抬高型心肌梗死形态发生的特殊性,心电图无再灌注迹象

G. A. Nefedova, G. A. Gazaryan, G. P. Titova
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引用次数: 0

摘要

该研究旨在探讨在机械性恢复心外膜血流后,STEMI 形态发生的特殊性,而心电图却没有再灌注的迹象。研究分析了44例STEMI患者的尸检数据,这些患者在接受PCI治疗后的12小时内(27例)或12-24小时内(17例)死亡,且介入治疗后心电图无再灌注迹象。对比组包括85例未接受再灌注治疗(RT)的死亡病例。心肌组织学检查在以下时间进行:12 小时内、13-24 小时、2-4 天、5-8 天、9-15 天和 16-22 天。最常见的死亡原因是急性左心室衰竭(ALVF),在血流恢复但无心电图再灌注迹象的组别和未接受 RT 治疗的组别中分别为 85% 和 79%。在这两组患者中,在最初 12 小时内死亡的人数均超过三分之一,半数患者在随后的 12 小时内死亡,三分之二的死亡发生在随后的 2-3 天内。两组患者的危险因素:高龄、前部和复发性心肌梗死、冠状动脉三血管病变和大面积梗死的发生率相似。从 PCI 术后最初几小时开始,梗死区就出现出血浸润、微循环床大量损伤,第 2-4 天受损血管出现血流恢复迹象,第 5-7 天出现早期修复表现。在未进行 PCI 治疗的心肌梗死组,出血分界从第 3-4 天开始,微血管床普遍出现凝固性坏死,修复迹象出现的时间较晚。微血管多处痉挛和血栓形成可能是血压下降的反应,血压下降伴随着左心室收缩功能的急剧下降,而左心室收缩功能的急剧下降是由于梗死面积过大和/或介入治疗本身引起的并发症未得到解决所致。这一机制解释了左心室功能衰竭的快速发展,这也是介入治疗后最常见的死亡原因,介入治疗实现了心外膜血流,但心电图却没有再灌注的迹象。微循环障碍反映了心肌再灌注的缺失,这比心外膜血流的恢复对预后更有意义。
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Peculiarities of the ST-segment elevation myocardial infarction morphogenesis after mechanical restoration of epicardial blood flow without ECG signs of reperfusion
The aim of the study was to investigate the peculiarities of STEMI morphogenesis after mechanical restoration of epicardial blood flow without ECG signs of reperfusion. The autopsy data of 44 patients with STEMI who died at different times after PCI performed within the first 12 hours (27 cases), or 12–24 hours (17 cases), without ECG signs of reperfusion after the intervention, were analyzed. The comparison group consisted of 85 deceased without reperfusion therapy (RT). Histological examination of the myocardium was performed at following time: within 12 hours, at 13–24 hours, 2–4 days, 5–8 days, 9–15 and 16–22 days. The most common cause of death was acute left ventricular failure (ALVF) both in the group of blood flow restoration without ECG signs of reperfusion, and in the group without RT: 85 % and 79 %, respectively. In each of the two groups the number of deaths occurred in the first 12 hours exceeded one third, half of the patients died in the subsequent 12 hours, two thirds of the deaths occurred within further 2–3 days. The rates of risk factors: older age, anterior and recurrent myocardial infarction, three-vessel lesion of the coronary artery, and a large infarction area were similar in the two groups. From the first hours after PCI, the infarction zone was characterized by hemorrhagic imbibition, numerous injuries of the microcirculatory bed, by the signs of blood flow restoration in damaged vessels appeared from days 2–4, early manifestations of repair from days 5–7. In the MI group without PCI, the hemorrhagic demarcation started on days from 3–4, coagulation necrosis prevailed in the microvascular bed, signs of repair appeared at a later date. Multiple spasms and thromboses in the microvasculature may have been a response to a blood pressure drop that accompanies an acute decrease in the left ventricle contractile function caused by a large infarction area and/or unresolved complications arising during the interventions per se. This mechanism explains the rapid progression of left ventricular failure, the most common cause of death after the interventions with achieving the epicardial blood flow without ECG signs of reperfusion. The revealed microcirculation disorders reflect the absence of myocardial reperfusion, which is more prognostically significant than the restoration of epicardial blood flow.
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