Association between systolic blood pressure variability and severity of cerebral amyloid angiopathy in incident intracerebral hemorrhage

Tom J. Moullaali, Rachel Walters, Mark Rodrigues, Neshika Samarasekera, Jose Bernal, Xia Wang, Catherine Humphreys, Joanna M. Wardlaw, Andrew Farrall, Colin Smith, Craig S. Anderson, Rustam Al-Shahi Salman, Brian McKinstry
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Abstract

Introduction The role of systolic blood pressure (SBP) variability in the pathogenesis of cerebral amyloid angiopathy (CAA) as an underlying cause of intracerebral hemorrhage (ICH) is unknown. We studied SBP variability before ICH according to CAA severity at autopsy. Methods We collected office (primary care or hospital clinic) BP readings during 10 years before first-ever ICH onset in adults who died and had brain research autopsy in the Lothian IntraCerebral Hemorrhage, Pathology, Imaging, and Neurological Outcome (LINCHPIN), prospective, population-based, inception cohort study. A neuropathologist assessed CAA severity using a histopathological rating scale, masked to BP readings. Functional principal component analysis was used to model SBP levels by time before ICH, and logistic regression models assessed associations of SBP variability indices with CAA severity (moderate-severe vs. absent-mild) adjusted for age, gender, and mean SBP. Results Among 72 adults (median age 81 [interquartile range 76–86], 56% female, median number of SBP readings 11 [3–19]), patients with moderate-severe CAA had similar mean SBP (143 vs. 145 mmHg, P = 0.588) but lower SBP variability (SBP standard deviation [SD] 14 vs. 17 mmHg, P = 0.033) compared with patients with absent-mild CAA, and their SBP trajectories seemed to differ over 10 years before ICH. The odds of moderate-severe CAA were higher with lower maximum SBP (adjusted OR per 10 mmHg lower: 1.53, 95% confidence interval [CI] 1.09–2.15; P = 0.015) and lower SBP range (1.29 [1.03–1.61]; P = 0.028), but not SBP SD (1.95 [0.87–4.38]; P = 0.11). Discussion Compared with absent-mild autopsy-verified CAA, moderate-severe CAA is associated with lower maximum and range of pre-morbid SBP.
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收缩压变异性与突发脑出血中脑淀粉样血管病严重程度的关系
收缩压(SBP)变异性作为脑出血(ICH)的潜在原因在脑淀粉样血管病(CAA)发病机制中的作用尚不清楚。我们根据尸检时CAA的严重程度研究脑出血前的收缩压变异性。方法:在洛锡安脑出血、病理学、影像学和神经预后(LINCHPIN)的前瞻性、基于人群的初始队列研究中,我们收集了首次脑出血发病前10年的办公室(初级保健或医院诊所)血压读数。神经病理学家使用组织病理学评定量表评估CAA的严重程度,并掩盖BP读数。使用功能主成分分析对脑出血前时间的收缩压水平进行建模,并使用逻辑回归模型评估收缩压变异性指数与CAA严重程度(中度严重vs无轻微)的相关性,并根据年龄、性别和平均收缩压进行调整。结果在72名成人(中位年龄81岁[四分位数范围76-86],56%为女性,中位收缩压读数11[3-19])中,中重度CAA患者的平均收缩压相似(143 vs. 145 mmHg, P = 0.588),但收缩压变异性较低(收缩压标准差[SD] 14 vs. 17 mmHg, P = 0.033)与无轻度CAA患者相比,他们的收缩压轨道在ICH前10年似乎有所不同。中重度CAA的几率随着最大收缩压降低而增加(调整后的OR / 10 mmHg降低:1.53,95%可信区间[CI] 1.09-2.15;P = 0.015)和较低的收缩压范围(1.29 [1.03-1.61];P = 0.028),但SBP SD (1.95 [0.87-4.38];P = 0.11)。与无轻度尸检证实的CAA相比,中度重度CAA与发病前收缩压最大值和范围较低相关。
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