Late-Life Blood Pressure and Cerebral Amyloid Angiopathy: Findings from the U.S. National Alzheimer’s Coordinating Center Uniform Dataset

Author:

Sin Mo-Kyung1ORCID,Dowling N.23,Roseman Jeffrey4,Ahmed Ali567ORCID,Zamrini Edward568ORCID

Affiliation:

1. College of Nursing, Seattle University, Seattle, WA 98122, USA

2. Department of Acute & Chronic Care, School of Nursing, George Washington University, Washington, DC 20147, USA

3. Department of Epidemiology & Biostatistics, Milken School of Public Health, George Washington University, Washington, DC 20147, USA

4. Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA

5. Center for Data Science and Outcomes Research, Veterans Affairs Medical Center, Washington, DC 20242, USA

6. Department of Medicine, School of Medicine & Health Sciences, George Washington University, Washington, DC 20052, USA

7. Department of Medicine, School of Medicine, Georgetown University, Washington, DC 20057, USA

8. Biomedical Informatics Center, School of Medicine & Health Sciences, George Washington University, Washington, DC 20052, USA

Abstract

High blood pressure (BP) and cerebral amyloid angiopathy (CAA) are two common risk factors for intracranial hemorrhage, potentially leading to cognitive impairment. Less is known about the relationship between BP and CAA, the examination of which was the objective of this study. We analyzed data from 2510 participants in the National Alzheimer’s Coordinating Center (NACC) who had information on longitudinal BP measurements before death and on CAA from autopsy. Using the average of four systolic BPs (SBPs) prior to death, SBP was categorized into three groups: <120 mmHg (n = 435), 120–139 mmHg (n = 1335), and ≥140 mmHg (n = 740). CAA was diagnosed using immunohistochemistry in 1580 participants and categorized as mild (n = 759), moderate (n = 529), or severe (n = 292). When adjusted for age at death, sex, APOE genotype, Braak, CERAD, antihypertensive medication use, and microinfarcts, the odds ratios (95% CIs) for CAA associated with SBPs of 120–139 and ≥140 mmHg were 0.91 (0.74–1.12) and 1.00 (0.80–1.26), respectively. Findings from predictor effect plots show no variation in the probability of CAA between the three SBP categories. Microbleeds had no association with CAA, but among those with SBP ≥ 130 mmHg, the proportion of those with microbleeds was numerically greater in those with more severe CAA (p for trend, 0.084). In conclusion, we found no evidence of an association between SBP and CAA. Future studies need to develop non-invasive laboratory tests to diagnose CAA and prospectively examine this association and its implication on the pathophysiology and outcome of Alzheimer’s disease.

Funder

National Institute on Aging of the National Institutes of Health

Publisher

MDPI AG

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