Mann J, Davies M J
St George's Hospital Medical School, British Heart Foundation Cardiovascular Pathology Unit, Cranmer Terrace, London SW17 ORE, UK.
Heart. 1999 Sep;82(3):265-8. doi: 10.1136/hrt.82.3.265.
To determine the role of healed plaque disruption in the generation of chronic high grade coronary stenosis.
Coronary arteries obtained at necropsy were perfuse fixed with formal saline for 24 hours at 100 mg Hg. 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.
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.
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 >/= 51% by diameter was present in 71 plaques, 52 of which showed a healed disruption pattern. The difference between stenosis < 50% and stenosis >/= 51% was significant by the chi(2) test (p < 0.001).
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.
确定愈合的斑块破裂在慢性重度冠状动脉狭窄形成中的作用。
尸检获取的冠状动脉用含100毫克汞的甲醛盐水在100毫米汞柱压力下灌注固定24小时。以最接近组织学正常节段的管腔大小为参考点，测量每个含斑块的3毫米节段的管腔直径狭窄百分比。每个节段均制备用于组织学检查，并用天狼星红染色及平滑肌肌动蛋白免疫组织化学染色。当在偏振光下帽部的黄白色致密胶原出现断裂，且被排列较疏松的绿色胶原填充时，认为存在愈合的破裂。绿色染色区域需有平滑肌密度增加。每个切片由两名观察者独立阅片；意见不一致的任何节段均视为阴性。
31名年龄在51 - 69岁之间因缺血性心脏病突然死亡的男性。在排除有陈旧性完全闭塞、急性罪犯血栓性病变、无正常动脉节段的弥漫性病变以及与陈旧性心肌瘢痕相关的动脉后，对39条冠状动脉进行研究，其中包含256个独立斑块。
导致直径狭窄<20%的99个斑块中，16个有先前的破裂。在狭窄范围为21% - 50%时，86个斑块中有16个显示有愈合的破裂。直径狭窄≥51%的有71个斑块，其中52个显示有愈合的破裂模式。通过卡方检验，狭窄<50%和狭窄≥51%之间的差异具有显著性（p < 0.001）。
斑块破裂后愈合的亚临床事件是斑块突然生长的刺激因素，是导致慢性重度冠状动脉狭窄的主要因素。这一机制可以解释在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心病阶段性而非线性进展。
