Abstract

Background Blood pressure variability (BPV) is predictive of cerebrovascular disease and dementia, possibly though cerebral hypoperfusion. Higher BPV is associated with cerebral blood flow (CBF) decline in observational cohorts, but relationships in samples with strictly controlled blood pressure remain understudied. We investigated whether BPV relates to change in CBF in the context of intensive versus standard antihypertensive treatment. Methods and Results In this post hoc analysis of the SPRINT MIND (Systolic Blood Pressure Intervention Trial-Memory and Cognition in Decreased Hypertension) trial, 289 participants (mean, 67.6 [7.6 SD] years, 38.8% women) underwent 4 blood pressure measurements over a 9-month period after treatment randomization (intensive versus standard) and pseudo-continuous arterial spin labeling magnetic resonance imaging at baseline and ≈4-year follow-up. BPV was calculated as tertiles of variability independent of mean. CBF was determined for whole brain, gray matter, white matter, hippocampus, parahippocampal gyrus, and entorhinal cortex. Linear mixed models examined relationships between BPV and change in CBF under intensive versus standard antihypertensive treatment. Higher BPV in the standard treatment group was associated with CBF decline in all regions (ß comparing the first versus third tertiles of BPV in whole brain: -0.09 [95% CI, -0.17 to -0.01]; P=0.03), especially in medial temporal regions. In the intensive treatment group, elevated BPV was related to CBF decline only in the hippocampus (ß, -0.10 [95% CI, -0.18, -0.01]; P=0.03). Conclusions Elevated BPV is associated with CBF decline, especially under standard blood pressure-lowering strategies. Relationships were particularly robust in medial temporal regions, consistent with prior work using observational cohorts. Findings highlight the possibility that BPV remains a risk for CBF decline even in individuals with strictly controlled mean blood pressure levels. Registration URL: http://clinicaltrials.gov. Identifier: NCT01206062.

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