Key result
Higher BP variability links to greater odds of CSVD in APOE4 carriers.
Why the study?
It remains uncertain whether elevated blood pressure variability causes or results from vascular brain injury, or how central autonomic network injury contributes to BPV-associated risk in APOE4 carriers.
Does increased blood pressure variability associate with cerebral small vessel disease in older APOE4 carriers?
Cross-Sectional (n=70)
Yes
Does increased blood pressure variability associate with cerebral small vessel disease in older APOE4 carriers?
Effect estimate: B= 18.92
p-value: p=0.02
Increased beat-to-beat blood pressure variability is associated with greater cerebral small vessel disease burden in older APOE4 carriers, particularly those with lower central autonomic network connectivity.
May inform CSVD risk stratification in APOE4 carriers; leaves open causality and intervention effects.
Background Increased blood pressure variability (BPV) is a risk factor for cerebral small vessel disease (CSVD) and neurodegeneration, independent of age and average blood pressure, particularly in apolipoprotein E4 ( APOE4 ) carriers. However, it remains uncertain whether BPV elevation is a cause or a consequence of vascular brain injury, or to what degree injury to the central autonomic network (CAN) may contribute to BPV-associated risk in APOE4 carriers. Methods Independently living older adults (n=70) with no history of stroke or dementia were recruited from the community and underwent 5 minutes of resting beat-to-beat blood pressure monitoring, genetic testing, and brain MRI. Resting BPV, APOE genotype, CSVD burden on brain MRI, and resting state CAN connectivity by fMRI were analyzed. Causal mediation and moderation analysis evaluated BPV and CAN effects on CSVD in APOE4 carriers (n=37) and non-carriers (n=33). Results Higher BPV was associated with the presence and extent of CSVD in APOE4 carriers, but not non-carriers, independent of CAN connectivity ( B = 18.92, P = .02), and CAN connectivity did not mediate the relationship between BPV and CSVD. In APOE4 carriers, CAN connectivity moderated the relationship between BPV and CSVD, whereby BPV effects on CSVD were greater in those with lower CAN connectivity ( B = 36.43, P = .02). Conclusions Older APOE4 carriers with higher beat-to-beat BPV exhibit more extensive CSVD, independent of average blood pressure, and the strength of CAN connectivity does not mediate these effects. Findings suggest increased BPV is more likely a cause, not a consequence, of CSVD. BPV is more strongly associated with CSVD in APOE4 carriers with lower rsCAN connectivity, suggesting CAN dysfunction and BPV elevation may have synergistic effects on CSVD. Further studies are warranted to understand the interplay between BPV and CAN function in APOE4 carriers.
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Lohman et al. (2023) conducted a cross-sectional in Cerebral small vessel disease (n=70). Blood pressure variability vs. APOE4 non-carriers was evaluated on Odds of CSVD feature presence (B= 18.92, p=0.02). Higher blood pressure variability was associated with greater odds of cerebral small vessel disease presence in APOE4 carriers (B= 18.92, P= .02), independent of central autonomic network connectivity.
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