Ding Jie, Mitchell Gary F, Bots Michiel L, Sigurdsson Sigurdur, Harris Tamara B, Garcia Melissa, Eiriksdottir Gudny, van Buchem Mark A, Gudnason Vilmundur, Launer Lenore J
From the Intramural Research Program, Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Bethesda, MD (J.D., T.B.H., M.G., L.J.L.); Cardiovascular Engineering, Inc, Norwood, MA (G.F.M.); Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands (M.L.B.); Icelandic Heart Association, Kopavogur, Iceland (S.S., G.E., V.G.); Department of Radiology, Leiden University Medical Centre, Leiden, The Netherlands (M.A.v.B.); and Faculty of Medicine, University of Iceland, Reykjavik, Iceland (V.G.).
Arterioscler Thromb Vasc Biol. 2015 Aug;35(8):1889-95. doi: 10.1161/ATVBAHA.115.305451. Epub 2015 Jun 25.
Age and high blood pressure are major risk factors for cerebral microbleeds (CMBs). However, the underlying mechanisms remain unclear and arterial stiffness may be important. We investigated whether carotid arterial stiffness is associated with incidence and location of CMBs.
In the prospective, population-based Age, Gene/Environment Susceptibility (AGES)-Reykjavik study, 2512 participants aged 66 to 93 years underwent a baseline brain MRI examination and carotid ultrasound in 2002 to 2006 and returned for a repeat brain MRI in 2007 to 2011. Common carotid arterial stiffness was assessed using a standardized protocol and expressed as carotid arterial strain, distensibility coefficient, and Young elastic modulus. Modified Poisson regression was applied to relate carotid arterial stiffness parameters to CMB incidence. During a mean follow-up of 5.2 years, 463 people (18.4%) developed new CMBs, of whom 292 had CMBs restricted to lobar regions and 171 had CMBs in a deep or infratentorial region. After adjusting for age, sex, and follow-up interval, arterial stiffness measures were associated with incident CMBs (risk ratio per SD decrease in carotid arterial strain, 1.11 [95% confidence interval, 1.01-1.21]; per SD decrease in natural log-transformed distensibility coefficient, 1.14 [1.05-1.24]; and per SD increase in natural log-transformed Young elastic modulus, 1.13 [1.04-1.23]). These measures were also significantly associated with incident deep CMBs (1.18 [1.02-1.37]; 1.24 [1.08-1.42]; and 1.23 [1.07-1.42]) but not with lobar CMBs. When further adjusted for blood pressure and other baseline vascular risk factors, carotid plaque, prevalent CMBs, subcortical infarcts, and white matter hyperintensities, the associations persisted.
Our findings support the hypothesis that localized increases in carotid arterial stiffness may contribute to the development of CMBs, especially in a deep location attributable to hypertension.
年龄和高血压是脑微出血（CMB）的主要危险因素。然而，其潜在机制仍不清楚，动脉僵硬度可能起重要作用。我们研究了颈动脉僵硬度是否与CMB的发生率及部位相关。
在基于人群的前瞻性年龄、基因/环境易感性（AGES）-雷克雅未克研究中，2512名年龄在66至93岁的参与者于2002年至2006年接受了基线脑MRI检查和颈动脉超声检查，并于2007年至2011年再次接受脑MRI检查。采用标准化方案评估颈总动脉僵硬度，并以颈动脉应变、扩张系数和杨氏弹性模量表示。应用修正泊松回归分析将颈动脉僵硬度参数与CMB发生率相关联。在平均5.2年的随访期间，463人（18.4%）出现了新的CMB，其中292人的CMB局限于脑叶区域，171人的CMB位于深部或幕下区域。在调整年龄、性别和随访间隔后，动脉僵硬度指标与新发CMB相关（颈动脉应变每标准差降低的风险比为1.11 [95%置信区间，1.01 - 1.21]；自然对数转换后的扩张系数每标准差降低为1.14 [1.05 - 1.24]；自然对数转换后的杨氏弹性模量每标准差增加为1.13 [1.04 - 1.23]）。这些指标也与新发深部CMB显著相关（1.18 [1.02 - 1.37]；1.24 [1.08 - 1.42]；1.23 [1.07 - 1.42]），但与脑叶CMB无关。当进一步调整血压和其他基线血管危险因素、颈动脉斑块、既往CMB、皮质下梗死和白质高信号后，这些关联仍然存在。
我们的研究结果支持以下假设，即颈动脉僵硬度的局部增加可能促成CMB的发生，尤其是在因高血压导致的深部位置。
