Brain atrophy and white matter hyperintensity change in older adults and relationship to blood pressure

Brain atrophy and white matter hyperintensity change in older adults and relationship to blood pressure
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DOI:
10.1007/s00415-006-0238-4
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发表时间:
2007-06-01
影响因子:
6
通讯作者:
Ford, Gary A.
Ford, Gary A.
中科院分区:
医学2区
文献类型:
--
作者:
Firbank, Michael J.;Wiseman, Rebecca M.;Ford, Gary A.

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高血压是中风和痴呆的主要危险因素,并与白色物质高信号(WMH)和脑容量减少有关。我们测量了参加老年人认知和预后研究(SCOPE)的高血压受试者(接受坎地沙坦或安慰剂)和血压正常对照者的WMH体积增加和脑萎缩率。我们招募了163名在基线评估后2年和4年进行MRI(FLAIR和体积T1)的受试者。从这两个扫描中,WMH体积变化(n = 133)和脑萎缩率(n = 95)进行了测定。总WMH分数增加正常血压和治疗高血压组(p < 0.01),中位数变化:0.05%的脑体积[范围:-0.45%至1.51%]。高血压组的深部WMH增加(p = 0.001),但血压正常组没有。治疗组之间第5个五分位数中总WMH增加的受试者数量不同(卡方p = 0.006),安慰剂组最多(32%),然后是坎地沙坦(20%),然后是血压正常(5%)。回归分析发现WMH变化的显著预测因素是血压和初始深度WMH,但不是治疗组。通过基线收缩压预测萎缩率增加(p = 0.02),但与WMH指标无关。与WMH相似,治疗有一个趋势,血压正常<坎地沙坦<安慰剂中出现萎缩(斯皮尔曼rho = 0.23,p = 0.026)。老年人的高血压与进行性全脑萎缩率增加和WMH增加有关。这些变化是独立的。成功的高血压治疗与WMH进展和可能的脑萎缩风险降低相关。
Hypertension is a major risk factor for stroke and dementia and is associated with white matter hyperintensities (WMH) and reduced brain volumes. We measured the increase in WMH volume, and rate of cerebral atrophy over two years, in hypertensive subjects participating in the Study on COgnition and Prognosis in the Elderly (SCOPE), receiving candesartan or placebo, and normotensive controls. We recruited 163 subjects who had MRI (FLAIR and volumetric T1) at 2 and 4 years after baseline assessment. From these two scans, volumetric change in WMH (n = 133) and brain atrophy rates (n = 95) were determined.Total WMH fraction increased in both normotensive and treated hypertensive groups (p < 0.01) median change: 0.05% of brain volume [range: -0.45% to 1.51%]. Deep WMH increased in hypertensive (p = 0.001) but not the normotensive group. The number of subjects with an increase of total WMH in the 5th quintile differed between the treatment groups (chi square p = 0.006), being greatest in the placebo group (32%), then candesartan (20%) then normotensive (5%). Regression analysis found significant predictors of change in WMH to be blood pressure and initial deep WMH, but not treatment group. Increased atrophy rate was predicted by baseline systolic blood pressure (p = 0.02) but was not associated with measures of WMH. Similar to WMH, there was a trend with treatment, with atrophy in normotensive < Candesartan < Placebo (Spearman's rho = 0.23, p = 0.026). Hypertension in older people is associated with increased rates of progressive whole brain atrophy and an increase in WMH. These changes are independent. Successful hypertension treatment was associated with reduced risk of WMH progression and possibly brain atrophy.