Intramural Research Program, Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland.
Icelandic Heart Association, Kopavogur, Iceland.
JAMA Neurol. 2015 Jun;72(6):682-8. doi: 10.1001/jamaneurol.2015.0174.
The spatial distribution of cerebral microbleeds (CMBs), which are asymptomatic precursors of intracerebral hemorrhage, reflects specific underlying microvascular abnormalities of cerebral amyloid angiopathy (lobar structures) and hypertensive vasculopathy (deep brain structures). Relatively little is known about the occurrence of and modifiable risk factors for developing CMBs, especially in a lobar location, in the general population of older people.
To investigate whether lifestyle and lipid factors predict new CMBs in relation to their anatomic location.
DESIGN, SETTING, AND PARTICIPANTS: We enrolled 2635 individuals aged 66 to 93 years from the population-based Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study in a brain imaging study. Participants underwent a baseline magnetic resonance imaging (MRI) examination of the brain from September 1, 2002, through February 28, 2006, and returned for a second MRI examination from April 1, 2007, through September 30, 2011.
Lifestyle and lipid factors assessed at baseline included smoking, alcohol consumption, body mass index, and serum levels of total cholesterol, high- and low-density lipoprotein cholesterol, and triglycerides.
Incident CMBs detected on MRIs, which were further categorized as exclusively lobar or as deep.
During a mean follow-up of 5.2 years, 486 people (18.4%) developed new CMBs, of whom 308 had lobar CMBs only and 178 had deep CMBs. In the multivariate logarithm-binomial regression model adjusted for baseline cardiovascular risk factors, including blood pressure, antihypertensive use, prevalent CMBs, and markers of cerebral ischemic small-vessel disease, heavy alcohol consumption (vs light to moderate consumption; relative risk [RR], 2.94 [95% CI, 1.23-7.01]) was associated with incident CMBs in a deep location. Baseline underweight (vs normal weight; RR, 2.41 [95% CI, 1.21-4.80]), current smoking (RR, 1.47 [95% CI, 1.11-1.94]), an elevated serum level of high-density lipoprotein cholesterol (RR per 1-SD increase, 1.13 [95% CI, 1.02-1.25]), and a decreased triglyceride level (RR per 1-SD decrease in natural logarithm-transformed triglyceride level, 1.17 [95% CI, 1.03-1.33]) were significantly associated with an increased risk for lobar CMBs exclusively but not for deep CMBs.
Lifestyle and lipid risk profiles for CMBs were similar to those for symptomatic intracerebral hemorrhage and differed for lobar and deep CMBs. Modification of these risk factors could have the potential to prevent new-onset CMBs, particularly those occurring in a lobar location.
脑微出血（CMB）是脑出血的无症状前体，其空间分布反映了脑淀粉样血管病（脑叶结构）和高血压血管病（深部脑结构）的特定潜在微血管异常。相对而言，人们对老年人一般人群中 CMB 的发生和可改变的危险因素知之甚少，特别是在脑叶部位。
研究生活方式和血脂因素是否与 CMB 的解剖位置有关。
设计、地点和参与者：我们从基于人群的年龄、基因/环境易感性（AGES）-雷克雅未克研究中招募了 2635 名年龄在 66 至 93 岁之间的个体，进行脑成像研究。参与者在 2002 年 9 月 1 日至 2006 年 2 月 28 日期间接受了基线磁共振成像（MRI）脑检查，并在 2007 年 4 月 1 日至 2011 年 9 月 30 日期间返回进行第二次 MRI 检查。
基线评估的生活方式和血脂因素包括吸烟、饮酒、体重指数以及总胆固醇、高低密度脂蛋白胆固醇和甘油三酯的血清水平。
MRI 检测到的新 CMB，并进一步分为仅脑叶或深部。
在平均 5.2 年的随访期间，486 人（18.4%）出现新的 CMB，其中 308 人仅出现脑叶 CMB，178 人出现深部 CMB。在调整了包括血压、降压药物使用、现有的 CMB 和脑小血管缺血性疾病标志物在内的基线心血管危险因素的多变量对数二项式回归模型中，大量饮酒（与轻至中度饮酒相比；相对风险 [RR]，2.94 [95%CI，1.23-7.01]）与深部 CMB 有关。基线体重不足（与正常体重相比；RR，2.41 [95%CI，1.21-4.80]）、当前吸烟（RR，1.47 [95%CI，1.11-1.94]）、高密度脂蛋白胆固醇血清水平升高（每增加 1-SD 的 RR，1.13 [95%CI，1.02-1.25]）和甘油三酯水平降低（每降低 1-SD 对数转换甘油三酯水平的 RR，1.17 [95%CI，1.03-1.33]）与脑叶 CMB 风险增加显著相关，但与深部 CMB 无关。
CMB 的生活方式和血脂风险特征与症状性脑出血相似，且脑叶和深部 CMB 之间存在差异。这些危险因素的改变有可能预防新出现的 CMB，特别是在脑叶部位发生的 CMB。
