Ding Shifang, Zhang Mei, Zhao Yuxia, Chen Wenqiang, Yao Guihua, Zhang Cheng, Zhang Pengfei, Zhang Yun
Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Qilu Hospital, Shandong University, Jinan, Shandong, People's Republic of China.
Am J Med Sci. 2008 Jul;336(1):27-31. doi: 10.1097/MAJ.0b013e31815b60a1.
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.
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.
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.
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.
越来越多的证据表明，颈动脉斑块破裂继发动脉-动脉血栓栓塞是缺血性卒中发生的重要机制。炎症机制在将结构上易损的斑块转变为功能上不稳定的斑块过程中起关键作用。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卒中发病机制中的作用。
对52例影响前循环的急性缺血性卒中患者（卒中组）和44例无症状性颈动脉狭窄患者（无症状组）进行了研究。采用双功超声评估颈动脉斑块特征并对颈动脉狭窄程度进行分级。斑块回声分为无回声、以无回声为主、以强回声为主或强回声。斑块表面分为光滑、不规则或溃疡型。所有受试者双功超声测定的颈动脉狭窄率为50%至99%。检测血清基质金属蛋白酶-9（MMP-9）、金属蛋白酶组织抑制剂（TIMP-1）、可溶性CD40配体（sCD40L）和高敏C反应蛋白（hsCRP）水平。
卒中组斑块为无回声或以无回声为主，而无症状组斑块以强回声为主或为强回声斑块（P<0.05）。卒中患者中不规则和溃疡型斑块常见，而无症状患者中光滑斑块常见（P<0.05）。卒中患者血清MMP-9、sCD40L、hsCRP水平高于无症状患者。相比之下，无症状组血清TIMP-1水平显著高于卒中组。
结果表明，炎症在颈动脉斑块易损性中起关键作用，并与颈动脉斑块形态一起在急性缺血性卒中发病机制中起作用。
