JACC Cardiovasc Imaging. 2009 Dec;2(12):1381-9. doi: 10.1016/j.jcmg.2009.08.007.
We sought to identify clinical and/or plaque characteristics that affect atherosclerotic disease progression and arterial remodeling in the carotid artery with subclinical stenosis.
Increasing severity of stenosis has been associated with a higher risk of stroke. Factors that drive subclinical lesions to become stenotic plaques remain ambiguous. Carotid magnetic resonance imaging (MRI) has been validated with histology to accurately quantify in vivo arterial morphology and plaque composition.
A total of 67 asymptomatic participants with 16% to 49% carotid stenosis as demonstrated by duplex ultrasonography were imaged at 1.5-T with a carotid MRI protocol at baseline and at 18-month follow-up. Clinical and/or intra-arterial metrics with a significant association with change in plaque burden during multivariate analysis were evaluated for effects on lumen, wall, and total vessel volume.
From multiple regression analysis, intraplaque hemorrhage (IPH) (p < 0.001) and statin therapy (p = 0.015) were identified as key determinants of change in plaque burden. The group with IPH compared with the group without IPH demonstrated luminal narrowing, with a mean +/- SD decrease in lumen volume (-24.9 +/- 21.1 mm(3)/year vs. -0.5 +/- 26.9 mm(3)/year; p = 0.005), a larger increase in wall volume (44.1 +/- 36.1 mm(3)/year vs. 0.8 +/- 34.5 mm(3)/year; p < 0.001), and no difference in total vessel volume (19.3 +/- 27.4 mm(3)/year vs. 0.4 +/- 42.4 mm(3)/year; p = 0.15). The nonstatin group compared with the statin group demonstrated outward remodeling, with an increase in wall volume (22.4 +/- 35.6 mm(3)/year(3)/year vs. 0.9 +/- 38.0 mm(3)/year; p = 0.026) and total vessel volume (19.2 +/- 36.9 mm(3)/year vs. -4.9 +/- 40.4 mm(3)/year; p = 0.019) and no difference in lumen volume (-5.8 +/- 26.6 mm(3)/year vs. -3.2 +/- 29.5 mm(3)/year; p = 0.72).
IPH may represent an indication of accelerated plaque growth and impending luminal compromise in the subclinical carotid artery. Statin therapy may stabilize lesions by slowing or halting lesion progression. This phase of plaque stenosis (16% to 49%) may be a critical stage for intrinsic and extrinsic factors to affect the atherosclerotic disease process.
我们试图确定影响亚临床狭窄颈动脉粥样硬化疾病进展和动脉重构的临床和/或斑块特征。
狭窄程度的增加与中风风险的增加有关。导致亚临床病变发展为狭窄斑块的因素仍不清楚。颈动脉磁共振成像（MRI）已通过组织学得到验证，可准确量化体内动脉形态和斑块成分。
共有 67 名无症状参与者，经双功超声检查显示有 16%至 49%的颈动脉狭窄，在 1.5-T 进行颈动脉 MRI 检查，基线和 18 个月随访时进行检查。对与多元分析中斑块负荷变化有显著相关性的临床和/或动脉内指标进行评估，以确定其对管腔、管壁和总血管体积的影响。
多元回归分析显示，斑块内出血（IPH）（p<0.001）和他汀类药物治疗（p=0.015）是斑块负荷变化的关键决定因素。与无 IPH 组相比，有 IPH 组显示管腔狭窄，管腔容积平均减少（-24.9±21.1mm³/年对-0.5±26.9mm³/年；p=0.005），管壁容积增加更大（44.1±36.1mm³/年对0.8±34.5mm³/年；p<0.001），总血管容积无差异（19.3±27.4mm³/年对0.4±42.4mm³/年；p=0.15）。与他汀组相比，非他汀组显示向外重塑，管壁容积增加（22.4±35.6mm³/年对0.9±38.0mm³/年；p=0.026）和总血管容积增加（19.2±36.9mm³/年对-4.9±40.4mm³/年；p=0.019），管腔容积无差异（-5.8±26.6mm³/年对-3.2±29.5mm³/年；p=0.72）。
IPH 可能代表亚临床颈动脉粥样硬化中斑块生长加速和管腔狭窄的迹象。他汀类药物治疗可能通过减缓或阻止病变进展来稳定病变。这种斑块狭窄阶段（16%至 49%）可能是内在和外在因素影响动脉粥样硬化过程的关键阶段。
