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类川崎冠状动脉血栓在不稳定型心绞痛发病中的作用。

Role of a streamer-like coronary thrombus in the genesis of unstable angina.

机构信息

Japan Foundation for Cardiovascular Research, Funabashi, Japan.

出版信息

J Interv Cardiol. 2010 Jun;23(3):216-22. doi: 10.1111/j.1540-8183.2010.00558.x.

DOI:10.1111/j.1540-8183.2010.00558.x
PMID:20636841
Abstract

INTRODUCTION

It is generally believed that the coronary occlusion occurs at the site of plaque disruption in acute coronary syndromes. An exceptional mechanism of coronary occlusion, namely a streamer-like thrombus (SLT) originating in a nonstenotic lesion extended distally to obstruct a just distal nondisrupted stenotic segment, was found by angioscopy in patients with unstable angina (UA). This study was carried out to examine the incidence of this phenomenon and its relationship to the subtypes of UA.

METHODS

The culprit coronary artery was investigated by angioscopy in successive 48 patients (mean +/- SE age, 61.0 +/- 2.3 years; 10 females and 38 males) with UA.

RESULTS

SLT originating in a nonstenotic lesion extended distally, and obstructed the just distal most stenotic segment (DMSS) by its tail in 11 patients (eight with class III and three with class II according to Braunwald's classification). Recurrent anginal attacks were observed in all. The nonstenotic lesion in which the SLT originated was a disrupted yellow plaque in most cases. The SLT was frequently red and yellow in a mosaic pattern, indicating a mixture of fresh thrombus and plaque debris. The plaques that constructed the DMSS were not disrupted. Angiographically, the SLT was not detectable and the entry of the DMSS showed a "tapering" configuration.

CONCLUSIONS

Obstruction of the DMSS by the tail of SLT originating in a nonstenotic lesion is another mechanism of UA. Therefore, treatment of both the nonstenotic lesion and DMSS is needed to prevent recurrent thrombus formation and consequent reattacks.

摘要

简介

人们普遍认为,在急性冠脉综合征中,斑块破裂部位会发生冠状动脉阻塞。在不稳定型心绞痛(UA)患者中,血管镜发现了一种异常的冠状动脉阻塞机制,即起源于非狭窄病变的线状血栓(SLT)向远端延伸,阻塞远端尚未破裂的狭窄节段。本研究旨在探讨这种现象的发生率及其与 UA 亚型的关系。

方法

连续对 48 例 UA 患者(平均年龄 +/- SE 为 61.0 +/- 2.3 岁;女性 10 例,男性 38 例)进行血管镜检查,以研究罪犯冠状动脉。

结果

SLT 起源于非狭窄病变并向远端延伸,其尾部阻塞了最近的最狭窄节段(DMSS)(根据 Braunwald 分类,8 例为 III 级,3 例为 II 级)。所有患者均出现反复发作的心绞痛。大多数情况下,SLT 起源的非狭窄病变是破裂的黄色斑块。SLT 常呈红色和黄色镶嵌模式,表明新鲜血栓和斑块碎片的混合物。构成 DMSS 的斑块没有破裂。血管造影显示,SLT 无法检测到,DMSS 的入口呈“渐细”状。

结论

起源于非狭窄病变的 SLT 尾部阻塞 DMSS 是 UA 的另一种机制。因此,需要同时治疗非狭窄病变和 DMSS,以防止再次形成血栓和随后的再次发作。

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