Firbank Michael J, Wiseman Rebecca M, Burton Emma J, Saxby Brian K, O'Brien John T, Ford Gary A
Institute for Ageing and Health, Wolfson Research Centre, Newcastle upon Tyne, NE4 6BE, UK. j.t.o'
J Neurol. 2007 Jun;254(6):713-21. doi: 10.1007/s00415-006-0238-4. Epub 2007 Apr 20.
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 5(th) 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.
高血压是中风和痴呆的主要危险因素,与脑白质高信号(WMH)及脑容量减少有关。我们在参与老年认知与预后研究(SCOPE)的高血压受试者中,测量了接受坎地沙坦或安慰剂治疗以及血压正常对照组在两年内WMH体积的增加和脑萎缩率,这些受试者均接受了磁共振成像(FLAIR和容积T1)检查。我们招募了163名在基线评估后2年和4年进行磁共振成像检查的受试者。通过这两次扫描,确定了WMH的体积变化(n = 133)和脑萎缩率(n = 95)。血压正常组和接受治疗的高血压组的总WMH分数均增加(p < 0.01),中位数变化:脑体积的0.05%[范围:-0.45%至1.51%]。深部WMH在高血压组中增加(p = 0.001),而在血压正常组中未增加。治疗组中总WMH增加处于第5个五分位数的受试者数量存在差异(卡方检验p = 0.006),安慰剂组最高(32%),其次是坎地沙坦组(20%),然后是血压正常组(5%)。回归分析发现,WMH变化的显著预测因素是血压和初始深部WMH,而非治疗组。基线收缩压可预测萎缩率增加(p = 0.02),但与WMH测量值无关。与WMH相似,治疗存在一种趋势,血压正常组的萎缩程度<坎地沙坦组<安慰剂组(斯皮尔曼等级相关系数rho = 0.23,p = 0.026)。老年人高血压与全脑进行性萎缩率增加及WMH增加有关。这些变化是独立的。成功的高血压治疗与WMH进展风险降低以及可能的脑萎缩风险降低有关。