Blood Pressure Is a Major Modifiable Risk Factor Implicated in Pathogenesis of Intraplaque Hemorrhage: An In Vivo Magnetic Resonance Imaging Study.
Blood Pressure Is a Major Modifiable Risk Factor Implicated in Pathogenesis of Intraplaque Hemorrhage: An In Vivo Magnetic Resonance Imaging Study.
复制标题
DOI：
10.1161/atvbaha.115.307043
复制
发表时间：
2016-04
期刊：
影响因子：
--
通讯作者：
Yuan C
中科院分区：
文献类型：
--
作者：
Sun J;Canton G;Balu N;Hippe DS;Xu D;Liu J;Hatsukami TS;Yuan C
有效的预防和管理策略斑块内出血（IPH）仍然难以捉摸，由于我们有限的知识，其病因和影响因素。本研究旨在探讨心血管危险因素与IPH之间的相关性，以提高对IPH发病机制的理解。超声显示狭窄16-79%的无症状受试者使用大覆盖范围三维MRI方案进行颈动脉磁共振成像（MRI）。确定双侧颈动脉中的单个斑块（最大厚度>1.5 mm），并确定IPH的存在。从80名受试者中，测量了176个新发斑块，其中38个（21.6%）含有IPH。在校正年龄、性别和斑块大小的多变量分析中，血压（BP），主要是低舒张压，与IPH相关（比值比[OR和95%置信区间]每10 mmHg ↑：0.51 [0.30-0.88]），在校正抗高血压药物使用和全身动脉粥样硬化后几乎没有变化。在年龄和性别校正模型中，抗血小板药物使用与IPH相关（p=0.018），考虑斑块大小和既往病史后，IPH趋势仍然存在（阿司匹林单药与无治疗的OR：3.1 [0.66-14.8];氯吡格雷或双联治疗与无治疗的OR：5.3 [0.80-35.0]; p=0.083）。低舒张压与IPH独立相关，这不太可能是由于治疗差异或全身动脉粥样硬化引起的血压变化。舒张压降低引起的血流动力学改变可能是其病理生理联系。需要前瞻性系列研究来评估BP和抗血小板药物的使用是否与新发或复发IPH的发生相关。
Effective prevention and management strategies of intraplaque hemorrhage (IPH) remain elusive due to our limited knowledge regarding its etiology and contributing factors. This hypothesis-generating study aimed to investigate associations between cardiovascular risk factors and IPH for improved understanding of the pathogenesis of IPH. Asymptomatic subjects with 16–79% stenosis on ultrasound underwent carotid magnetic resonance imaging (MRI) using a large-coverage, three-dimensional MRI protocol. Individual plaques (maximum thickness>1.5 mm) in bilateral carotid arteries were identified and presence of IPH was determined. From 80 subjects, 176 de novo plaques were measured, of which 38 (21.6%) contained IPH. Blood pressure (BP), primarily low diastolic BP, was associated with IPH in multivariate analysis adjusted for age, sex, and plaque size (odds ratio [OR with 95% confidence interval] per 10 mmHg ↑: 0.51 [0.30–0.88]), which was little changed after adjusting for antihypertensive use and systemic atherosclerosis. Antiplatelet use was associated with IPH in age and sex-adjusted models (p=0.018), for which a trend remained after considering plaque size and past medical history (OR for aspirin alone vs. none: 3.1 [0.66–14.8]; OR for clopidogrel or dual therapy vs. none: 5.3 [0.80–35.0]; p=0.083). Low diastolic BP was independently associated with IPH, which was unlikely due to treatment difference or BP changes from systemic atherosclerosis. Hemodynamic changes from lowering diastolic BP may be the pathophysiological link. Prospective serial studies are needed to assess whether BP and antiplatelet use are associated with the development of new or repeated IPH.