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KMID : 1225120110030010045
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Vascular Neurology
2011 Volume.3 No. 1 p.45 ~ p.50
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Evaluation of Regression of Advanced Carotid Atherosclerotic Plaques
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Pae Hye-Kyoung
Cho Kyoung-Joo
Lee Su-Kyung
Kim Gyung-Whan
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Abstract
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Objective: Recent studies have determined evidences of effects of hypolipidemic drug on atherosclerotic plaque as well as marked change in composition that affects plaque stability. In particular, high dose statin treatment plays an important role in regression of advanced atherosclerotic plaque. In this study, we aimed to investigate the relationship between the disruption of atherosclerotic plaque and inflammatory molecules and propose the reliable guideline of therapy of advanced (calcified) carotid atheroma.
Methods: The outpatients of 23 who had advanced carotid atherosclerotic plaque were selected from the neurology outpatient clinic and were treated statin, aspirin, and clopidogrel for secondary prevention for a year. All participants were measured carotid artery intima-media thickness, plaque morphology, and thickness of carotid plaque by an external B-mode ultrasound and were assessed express P-selectin expression (CD62p), platelet-leukocyte aggregation, CD11b and CD40L by flow cytometry and by the platelet function analyzer.
Results: The outpatients of 23 were more than 60 years old (69.8±6.9, male=16, female=7). The average of carotid artery intima-media thickness was 0.93 mm at left and 0.91 at right. We found the significant fact that the number of total plaques in all subjects was 83. The distribution of plaques in different arterial segments was: common carotid artery, 21.7%; bulb, 54.2%; and internal carotid artery, 24.1. 77.1% (n=64) of total plaques were heterogeneous with hyperechoic morphology and 14.5% (n=12) of those were hypoechoic plaques in echogenicity. High sensitivity C-reactive protein of participants was 1.9±2.3. The difference of carotid atherosclerotic plaque thickness before and after intensive statin treatment was 2.6±0.8 and 2.4±0.7 (p=0.001). The level of CD11b and CD40L in monocyte decreased significantly after high dose statin therapy.
Conclusions: These findings support the central role of statin to reduce plaque thickness and the level of inflammatory markers. Intensive statin therapy is crucial for patients with advanced atherosclerotic plaques in carotid artery. Thus, it is urgent to establish optimal dose of stain for each patient without undergoing adverse reactions.
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KEYWORD
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Atherosclerosis, Calcified carotid artery atheroma, Circulation inflammatory molecules, Stroke
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