University of California, San Francisco, Department of Veterans Affairs Medical Center, 4150 Clement Street (114M), San Francisco, CA 94121, USA.
Stroke. 2012 Nov;43(11):2865-70. doi: 10.1161/STROKEAHA.112.659722. Epub 2012 Sep 13.
The purpose of this study was to investigate whether the Framingham Cardiovascular Risk Profile and carotid artery intima-media thickness are associated with cortical volume and thickness.
Consecutive subjects participating in a prospective cohort study of aging and mild cognitive impairment enriched for vascular risk factors for atherosclerosis underwent structural MRI scans at 3-T and 4-T MRI at 3 sites. Freesurfer (Version 5.1) was used to obtain regional measures of neocortical volumes (mm3) and thickness (mm). Multiple linear regression was used to determine the association of Framingham Cardiovascular Risk Profile and carotid artery intima-media thickness with cortical volume and thickness.
One hundred fifty-two subjects (82 men) were aged 78 (±7) years, 94 had a clinical dementia rating of 0, 58 had a clinical dementia rating of 0.5, and the mean Mini-Mental State Examination was 28±2. Framingham Cardiovascular Risk Profile score was inversely associated with total gray matter volume and parietal and temporal gray matter volume (adjusted P<0.04). Framingham Cardiovascular Risk Profile was inversely associated with parietal and total cerebral gray matter thickness (adjusted P<0.03). Carotid artery intima-media thickness was inversely associated with thickness of parietal gray matter only (adjusted P=0.04). Including history of myocardial infarction or stroke and radiological evidence of brain infarction, or apolipoprotein E genotype did not alter relationships with Framingham Cardiovascular Risk Profile or carotid artery intima-media thickness.
Increased cardiovascular risk was associated with reduced gray matter volume and thickness in regions also affected by Alzheimer disease independent of infarcts and apolipoprotein E genotype. These results suggest a "double hit" toward developing dementia when someone with incipient Alzheimer disease also has high cardiovascular risk.
本研究旨在探讨弗雷明汉心血管风险概况和颈动脉内膜中层厚度与皮质体积和厚度的关系。
连续参加血管性危险因素动脉粥样硬化性痴呆的前瞻性队列研究的受试者在 3 个地点接受了 3-T 和 4-T MRI 结构 MRI 扫描。使用 Freesurfer（版本 5.1）获得新皮质体积（mm3）和厚度（mm）的区域测量值。多元线性回归用于确定弗雷明汉心血管风险概况和颈动脉内膜中层厚度与皮质体积和厚度的关系。
152 名受试者（82 名男性）年龄为 78（±7）岁，94 名临床痴呆评定量表评分为 0，58 名临床痴呆评定量表评分为 0.5，平均简易精神状态检查评分为 28±2。弗雷明汉心血管风险评分与总灰质体积以及顶叶和颞叶灰质体积呈负相关（调整后 P<0.04）。弗雷明汉心血管风险评分与顶叶和总脑灰质厚度呈负相关（调整后 P<0.03）。颈动脉内膜中层厚度仅与顶叶灰质厚度呈负相关（调整后 P=0.04）。包括心肌梗死或中风病史以及影像学证据的脑梗死或载脂蛋白 E 基因型并没有改变与弗雷明汉心血管风险评分或颈动脉内膜中层厚度的关系。
心血管风险增加与阿尔茨海默病相关区域的灰质体积和厚度减少有关，与梗死和载脂蛋白 E 基因型无关。这些结果表明，当一个患有早期阿尔茨海默病的人同时具有高心血管风险时，会对痴呆的发展产生“双重打击”。
