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首页> 外文期刊>The American Journal of the Medical Sciences >The role of carotid plaque vulnerability and inflammation in the pathogenesis of acute ischemic stroke.
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The role of carotid plaque vulnerability and inflammation in the pathogenesis of acute ischemic stroke.

机译：颈动脉斑块易损性和炎症在急性缺血性卒中发病中的作用。

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BACKGROUND:: Increasing evidences show that disruption of carotid plaque followed by arterio-arterial thromboembolism is an important mechanism in the generation of ischemic stroke. Inflammatory mechanisms play a key role in transforming structurally vulnerable plaques into functionally unstable ones. The purpose of the present study is to evaluate the roles of carotid plaque vulnerability and inflammation in the pathogenesis of acute ischemic stroke. METHODS:: Fifty-two patients with acute ischemic stroke affecting the anterior circulation (stroke group) and 44 with asymptomatic carotid stenosis (asymptomatic group) were investigated. Duplex ultrasonography was used to evaluate the characteristics of carotid plaque and grading the degree of carotid stenosis. Plaque echogenicity was assessed as echolucent, predominantly echolucent, predominantly echogenic, or echogenic. Plaque surface was classified as smooth, irregular, or ulcerated. All subjects had duplex-determined 50% to 99% carotid stenosis. Serum levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitors of metalloproteinases (TIMP-1), soluble CD40 ligand (sCD40L) and high-sensitivity C-reactive protein (hsCRP) were measured. RESULTS:: Plaques in the stroke group were echolucent or predominantly echolucent, whereas those of the asymptomatic group were predominantly echogenic or echogenic plaques (P 0.05). Irregular and ulcerated plaques were frequently found in stroke patients, while smooth plaques were frequently detected in asymptomatic patients (P 0.05). Serum levels of MMP-9, sCD40L, hsCRP were higher in stroke than in asymptomatic patients. By contrast, serum TIMP-1 levels were significantly higher in the asymptomatic than in the stroke group. CONCLUSIONS:: The results suggest that inflammation plays a crucial role in carotid plaque vulnerability and, together with carotid plaque morphology, in the pathogenesis of acute ischemic stroke.
机译：背景：越来越多的证据表明，颈动脉斑块破裂继之以动脉-动脉血栓栓塞是形成缺血性中风的重要机制。炎症机制在将结构脆弱的斑块转变为功能不稳定的斑块中起关键作用。本研究的目的是评估颈动脉斑块易损性和炎症在急性缺血性中风发病中的作用。方法：调查了52例影响前循环的急性缺血性卒中患者（中风组）和44例无症状性颈动脉狭窄（无症状组）。使用双工超声检查来评估颈动脉斑块的特征和分级颈动脉狭窄程度。斑块回声被评估为可回声，主要是可回声，主要是可回声或可产生回声。斑块表面被分类为光滑，不规则或溃疡。所有受试者均具有双相测定的50％至99％的颈动脉狭窄。测量了血清血清基质金属蛋白酶9（MMP-9），组织金属蛋白酶抑制剂（TIMP-1），可溶性CD40配体（sCD40L）和高敏C反应蛋白（hsCRP）的水平。结果：中风组的斑块是可回声的或主要是回声的，而无症状组的斑块的主要是回声或回声的斑块（P <0.05）。中风患者中经常发现斑块不规则和溃疡，而无症状患者中经常发现光滑斑块（P <0.05）。脑卒中患者的MMP-9，sCD40L，hsCRP水平高于无症状患者。相比之下，无症状的血清TIMP-1水平显着高于中风组。结论：结果表明炎症在颈动脉斑块易损性中起着至关重要的作用，并且与颈动脉斑块的形态学一起在急性缺血性中风的发病机理中起着至关重要的作用。

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