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【ATVBAHA】中风后颈动脉粥样硬化斑块趋向稳定
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:128.)
Carotid Atherosclerotic Plaques Stabilize After Stroke
Insights Into the Natural Process of Atherosclerotic Plaque Stabilization
Abstract
Objective— Rupture of unstable atherosclerotic plaques is the pathological substrate for acute ischemic events. Underlyingcellular and molecular characteristics of plaque rupture have been studied extensively. However, the natural course of symptomatic plaque remodeling after ischemic events is relatively unexplored.
Methods and Results— Atherosclerotic carotid plaques were obtained from 804 symptomatic (stroke=204 and TIA=426) and asymptomatic (n=174) patients undergoing carotid endarterectomy. The presence of macrophages, smooth muscle cells (SMC), collagen, calcification, and lipid-core size were assessed histologically. At protein level, inflammatory mediators (interleukin [IL]-2, IL-4, IL-5, IL-8, IL-10, IL-12p70, interferon-gamma [INF- ], tumor necrosis factor-alpha [TNF- ], matrix degrading proteinases (MMPs), and an apoptosis marker (caspase-3) were determined. We associated plaque characteristics with time elapsed between the latest event and surgery. Early after stroke and TIA, plaques revealed an unstable phenotype. After stroke, the content of macrophages decreased significantly with time (P=0.02), whereas SMC contenttended to increase. At protein level, IL-6, IL-8 expression levels and caspase activity strongly decreased after stroke or TIA.
Conclusions— Symptomatic carotid lesions remodel into more stable plaques over time after stroke. Changes in IL-6 and IL-8 and caspase preceded the decrease of macrophages. These temporal phenotypic plaque alterations should be taken into account for biomarker and therapeutic target validation studies using human atherosclerotic plaques.
The composition of 804 atherosclerotic plaques from patients who underwent carotid endarterectomy has been related to the time, elapsed between the latest cerebrovascular ischemic event and surgical excision. After stroke as well after TIA, the inflammatory status of the plaque decreased independent from potential confounders at histological and protein level. Carotid Atherosclerotic Plaques Stabilize After Stroke
Insights Into the Natural Process of Atherosclerotic Plaque Stabilization
中风后颈动脉粥样硬化斑块趋向稳定
对粥样硬化斑块稳定化的自然过程的观察
Abstract
Objective— Rupture of unstable atherosclerotic plaques is the pathological substrate for acute ischemic events. Underlyingcellular and molecular characteristics of plaque rupture have been studied extensively. However, the natural course of symptomatic plaque remodeling after ischemic events is relatively unexplored.
目的：不稳定粥样硬化斑块的破裂是急性缺血性事件的病例原因。其斑块破裂背后的分子和细胞特征已经被广泛的研究。然而，在缺血事件发生后，有症状的斑块重塑的自然过程却很少被研究。
Methods and Results— Atherosclerotic carotid plaques were obtained from 804 symptomatic (stroke=204 and TIA=426) and asymptomatic (n=174) patients undergoing carotid endarterectomy. The presence of macrophages, smooth muscle cells (SMC), collagen, calcification, and lipid-core size were assessed histologically. At protein level, inflammatory mediators (interleukin [IL]-2, IL-4, IL-5, IL-8, IL-10, IL-12p70, interferon-gamma [INF- ], tumor necrosis factor-alpha [TNF- ], matrix degrading proteinases (MMPs), and an apoptosis marker (caspase-3) were determined. We associated plaque characteristics with time elapsed between the latest event and surgery. Early after stroke and TIA, plaques revealed an unstable phenotype. After stroke, the content of macrophages decreased significantly with time (P=0.02), whereas SMC contenttended to increase. At protein level, IL-6, IL-8 expression levels and caspase activity strongly decreased after stroke or TIA.
方法和结果：颈动脉粥样硬化斑块来自于804名有症状（中风=204和短暂性脑缺血发作=426）和无症状的病人（n=174），他们都接受了动脉内膜剥脱术。从组织学的角度对巨噬细胞、平滑肌细胞（SMC）、胶原、钙化和脂核的大小都被评价。在蛋白水平，炎症介质如白介素（IL-2、4、5、8、10和12p70，干扰素γ [INF-γ]，肿瘤坏死因子α[TNF-α]，基质金属蛋白酶（MMPs）以及凋亡标志物（caspase-3）被进行了检测。我们将斑块的特征与最后一次事件与手术之间的时间联系后进行观察。在中风和短暂性脑缺血发作的早期，斑块显示出一个不稳定的状态。在中风后，随着时间推移，巨噬细胞的数目明显下降（P=0.02），而SMC上升。在蛋白水平，在中风或TIA后，IL-6、IL-8的表达水平和激酶活性强烈的下降。
Conclusions— Symptomatic carotid lesions remodel into more stable plaques over time after stroke. Changes in IL-6 and IL-8 and caspase preceded the decrease of macrophages. These temporal phenotypic plaque alterations should be taken into account for biomarker and therapeutic target validation studies using human atherosclerotic plaques.
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作者:admin@医学,生命科学 2011-05-27 05:11
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