期刊论文详细信息
JACC-CARDIOVASCULAR IMAGING 卷:5
Sustained Acceleration in Carotid Atherosclerotic Plaque Progression With Intraplaque Hemorrhage A Long-Term Time Course Study
Article
Sun, Jie2  Underhill, Hunter R.3  Hippe, Daniel S.2  Xue, Yunjing2  Yuan, Chun2  Hatsukami, Thomas S.1 
[1] Univ Washington, Vasc Imaging Lab, Dept Surg, Seattle, WA 98109 USA
[2] Univ Washington, Dept Radiol, Seattle, WA 98109 USA
[3] Univ Washington, Dept Med, Div Med Genet, Seattle, WA 98109 USA
关键词: atherosclerosis;    carotid arteries;    intraplaque hemorrhage;    magnetic resonance imaging;   
DOI  :  10.1016/j.jcmg.2012.03.014
来源: Elsevier
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【 摘 要 】

OBJECTIVES This study sought to determine the immediate and long-term effects of intraplaque hemorrhage (IPH) on plaque progression in the carotid artery. BACKGROUND Previous studies have associated IPH in the carotid artery with more rapid plaque progression. However, the time course and long-term effect remain unknown. Carotid magnetic resonance imaging is a noninvasive imaging technique that has been validated with histology for the accurate in vivo detection of IPH and measurement of plaque burden. METHODS Asymptomatic subjects with 50% to 79% carotid stenosis underwent carotid magnetic resonance imaging at baseline and then serially every 18 months for a total of 54 months. Subjects with IPH present in at least 1 carotid artery at 54 months were selected. Subsequently, presence/absence of IPH and wall volume were determined independently in all time points for both sides. A piece-wise progression curve was fit by using a linear mixed model to compare progression rates described as annualized changes in wall volume between periods defined by their relationship to IPH development. RESULTS From 14 subjects who exhibited IPH at 54 months, 12 arteries were found to have developed IPH during the study period. The progression rates were -20.5 +/- 13.1, 20.5 +/- 13.6, and 16.5 +/- 10.8 mm(3)/year before, during, and after IPH development, respectively. The progression rate during IPH development tended to be higher than the period before (p = 0.080) but comparable to the period after (p = 0.845). The progression rate in the combined period during/after IPH development was 18.3 +/- 6.5 mm(3)/year, which indicated significant progression (p = 0.008 compared with a slope of 0) and was higher than the period before IPH development (p = 0.018). No coincident ischemic events were noted for new IPH. CONCLUSIONS The development of IPH posed an immediate and long-term promoting effect on plaque progression. IPH seems to alter the biology and natural history of carotid atherosclerosis. Early identification of patients with IPH may prove invaluable in optimizing management to minimize future sequelae. (J Am Coll Cardiol Img 2012; 5: 798-804) (C) 2012 by the American College of Cardiology Foundation

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