Mechanisms of progression in native coronary artery disease: role of healed plaque disruption
Mechanisms of progression in native coronary artery disease: role of healed plaque disruption
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DOI：
10.1136/hrt.82.3.265
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发表时间：
1999-09-01
期刊：
影响因子：
5.7
通讯作者：
Davies, MJ
中科院分区：
文献类型：
--
作者：
Mann, J;Davies, MJ
目的：探讨斑块愈合破裂在慢性高级别冠状动脉狭窄发生中的作用。方法：取尸检冠状动脉，用生理盐水100 mg Bg灌注固定24小时。以最近的组织学正常节段的管腔大小为参考点，测量每个含有斑块的3mm节段的管腔直径狭窄百分比。对每段进行组织学检查，用天狼星红和免疫组化染色检测平滑肌肌动蛋白。当在偏振光下，帽上的黄白色致密胶原蛋白被更松散排列的绿色胶原蛋白填充时，被认为存在愈合破坏。需要增加绿色染色区域的平滑肌密度。每一部分由两名观察员独立阅读；任何观点不一致的部分都被认为是负面的。31名51-69岁男性突然死于缺血性心脏病。排除陈旧性全闭塞、急性罪魁祸首血栓性病变、无正常动脉段的弥漫性疾病和与陈旧性心肌瘢痕相关的冠状动脉后，研究了包含256个独立斑块的39条冠状动脉。结果：99个斑块中有16个狭窄直径小于20%，有先前的破裂。在21-50%狭窄范围内，86个斑块中有16个出现愈合破裂。71个斑块狭窄大于或等于直径的51%，其中52个斑块表现为愈合破坏模式。狭窄度< 50%与狭窄度大于或等于51%之间的差异通过chi(2)检验具有显著性（p < 0.001）。结论：亚临床斑块破裂后愈合是突然发生的斑块生长的刺激因素，是导致慢性高级别冠状动脉狭窄的主要因素。这一机制可以解释慢性缺血性心脏病患者每年进行的血管造影中观察到的冠状动脉疾病的阶段性进展而不是线性进展。
Objective-To determine the role of healed plaque disruption in the generation of chronic high grade coronary stenosis.Methods-Coronary arteries obtained at necropsy were perfuse fixed with formal saline for 24 hours at 100 mg Bg. The percentage lumen diameter stenosis was measured in each 3 mm segment containing a plaque, using the lumen size at the nearest histologically normal segment as the reference point. Each segment was prepared for histological examination and stained with Sirius red and immunohistochemistry for smooth muscle actin. Healed disruption was considered to be present when under polarised light there was a break in the yellow-white dense collagen of the cap filled in by more loosely arranged green collagen. Increased smooth muscle density in the green staining areas was required. Each section was read independently by two observers; any segment with discordant views was considered negative.Material-31 men aged 51-69 dying suddenly of ischaemic heart disease. 39 coronary arteries were studied containing 256 separate plaques, after excluding coronary arteries with old total occlusions, an acute culprit thrombotic lesion, diffuse disease without normal arterial segments, and arteries related to old myocardial scars.Results-16 of 99 plaques causing < 20% diameter stenosis had prior disruption. In the 21-50% stenosis range 16 of 86 plaques showed healed disruption. Stenosis greater than or equal to 51% by diameter was present in 71 plaques, 52 of which showed a healed disruption pattern. The difference between stenosis < 50% and stenosis greater than or equal to 51% was significant by the chi(2) test (p < 0.001).Conclusions-Subclinical episodes of plaque disruption followed by healing are a stimulus to plaque growth that occurs suddenly and is a major factor in causing chronic high grade coronary stenosis. This mechanism would explain the phasic rather than linear progression of coronary disease observed in angiograms carried out annually in patients with chronic ischaemic heart disease.