Atherosclerotic plaque rupture in symptomatic carotid artery stenosis
Atherosclerotic plaque rupture in symptomatic carotid artery stenosis
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DOI：
10.1016/s0741-5214(96)70237-9
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发表时间：
1996-05-01
影响因子：
4.3
通讯作者：
Yao, JST
中科院分区：
文献类型：
--
作者：
Carr, S;Farb, A;Yao, JST
目的：斑块破裂是急性冠状动脉综合征的重要诱因。我们假设在与缺血性神经症状相关的狭窄颈动脉斑块中也发生了类似的过程。我们的目的是研究狭窄的颈动脉斑块的几个形态学特征，并确定哪些特征是更常见的相关斑块从患者有症状的颈动脉疾病比从患者无症状的颈动脉diseases.Methods：44颈动脉内膜切除术标本（25无症状和19有症状的患者）进行了分析与五色染色和光学显微镜。无症状患者和有症状患者的平均狭窄百分比相似（77% vs 74%）。其他危险因素，包括高血压、糖尿病、冠状动脉疾病、吸烟史、血清胆固醇和甘油三酯水平，两组之间相似。结果：与无症状组相比，有症状的颈动脉疾病患者更容易发生斑块破裂、纤维帽变薄和纤维帽泡沫细胞浸润。斑块破裂见于74%的症状性斑块，而无症状患者仅32%的斑块（p = 0.004）。95%的有症状斑块和48%的无症状斑块中观察到纤维帽变薄（p = 0.003）。泡沫细胞纤维帽浸润在有症状斑块中也明显更常见（84% vs 44%无症状斑块; P = 0.006）。此外，斑块内纤维蛋白在症状性斑块中比在无症状斑块中更常见（100% vs 68%; p = 0.008）。两组之间没有显着差异被发现斑块出血，存在的坏死核心，管腔血栓，平滑肌细胞浸润，偏心形状，斑块类型（纤维，坏死，或钙化）。结论：在冠状动脉系统，动脉粥样硬化斑块破裂可能发挥重要作用，在颈动脉狭窄引起的缺血性中风的发病机制。炎症过程，包括纤维帽的泡沫细胞浸润，可能导致动脉粥样硬化斑块破裂。
Purpose: Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid plaques and to determine which characteristics are more commonly associated with plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease.Methods: Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups.Results: Patients with symptomatic carotid artery disease were found to have more frequent plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic plaques and in only 32% of plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic plaques and in 48% of asymptomatic plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic plaques (84% vs 44% of asymptomatic plaques; P = 0.006). In addition, intraplaque fibrin was more common in symptomatic plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and plaque type (fibrous, necrotic, or calcified).Conclusions: As in the coronary artery system, rupture of the atherosclerotic plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the atherosclerotic plaque.