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不稳定型人类主动脉斑块的脂质和细胞成分。

Lipid and cellular constituents of unstable human aortic plaques.

作者信息

Davies M J, Woolf N, Rowles P, Richardson P D

机构信息

British heart foundation cardiovascular pathology unit, St. George's Hospital Medical School, London.

出版信息

Basic Res Cardiol. 1994;89 Suppl 1:33-9. doi: 10.1007/978-3-642-85660-0_3.

DOI:10.1007/978-3-642-85660-0_3
PMID:7945174
Abstract

Unstable plaques are undergoing thrombosis which, in most instances, is due to fissuring and rupture of the plaque cap. This process (deep intimal injury) is a complication of plaques with a lipid-rich core. The cap tear allows blood to enter the core from the lumen, leading initially to intraplaque thrombosis and, subsequently, in some cases intraluminal thrombosis. Cap tears reflect the interplay between the force exerted on the tissue and its inherent mechanical strength. Factors which elevate and concentrate circumferential wall stress on the cap during systole include an increasing proportion of the total plaque volume occupied by the lipid core, thinning of the cap and a loss of internal collagen struts within the core. Factors which lead to an inherent reduction in the mechanical strength of cap tissue include a reduction in collagen and glycosaminoglycan concentrations, an increase in the number and density of macrophages, and a concomitant reduction in smooth muscle cells in the cap tissue. It is therefore possible to define a vulnerable plaque as one in which the lipid core is disproportionately large, the cap thin, and in which monocytes preponderate over smooth muscle cells.

摘要

不稳定斑块正在发生血栓形成,在大多数情况下,这是由于斑块帽的裂开和破裂所致。这个过程(深层内膜损伤)是富含脂质核心斑块的一种并发症。帽的撕裂使血液从管腔进入核心,最初导致斑块内血栓形成,随后在某些情况下导致管腔内血栓形成。帽的撕裂反映了作用于组织的力与其固有机械强度之间的相互作用。在收缩期增加并集中作用于帽上的周向壁应力的因素包括脂质核心占据的总斑块体积比例增加、帽变薄以及核心内内部胶原支柱的丧失。导致帽组织固有机械强度降低的因素包括胶原和糖胺聚糖浓度降低、巨噬细胞数量和密度增加以及帽组织中平滑肌细胞相应减少。因此,可以将易损斑块定义为脂质核心不成比例地大、帽薄且单核细胞多于平滑肌细胞的斑块。

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