Year of Publication

2017

College

Public Health

Degree Name

Master of Public Health (M.P.H.)

Committee Chair

Daniela Moga, MD, PhD

Committee Member

Erin Abner, MPH, PhD

Committee Member

Wayne Sanderson, MS, CIH, PhD

Abstract

Background

Dementia is a growing public health concern as the population ages. Vascular dementia is the second most common type of dementia behind Alzheimer’s, and is caused by cerebrovascular damage, such as infarcts and hemorrhages. As in systemic cardiovascular disease, diabetes and hypertension are leading risk factors for cerebrovascular pathology. Anti-hypertensive treatment (AHT), therefore, may have a role in preventing cerebrovascular damage.

Methods

A case-control study design was utilized to evaluate any association between AHT during life and cerebrovascular pathology in autopsy in diabetic participants from the National Alzheimer’s Coordinating Centers (NACC). Pathology outcomes included infarcts of various sizes and arteriolosclerosis. Exposure was classified as any reported use, use at last visit, and percentage of visits with reported use. Adjusted logistic regression was used to compare cases and controls.

Results

Among 484 study participants, 74-90% reported exposure to AHT. Among exposed participants, CVD (54% vs 23%) and hypercholesterolemia (76% vs 61%) were more common. In unadjusted logistic analyses, any infarct and large infarct cases were associated with 1.64 and 2.22 times greater odds of exposure reported at last visit than controls. In multiple adjusted analyses, only cases with large infarct pathology were associated with greater odds of exposure reported at last visit [OR, 95% CI = 2.59 (1.02- Cerebrovascular pathology and AHT 4 6.59)]. Large infarcts were also associated with increasing percentage of visits with reported AHT.

Conclusions

Large infarct pathology was associated with exposure to AHT at last visit and with increased percentage visits with reported AHT. Though not significant for all pathology or exposure definitions, consistent direction and magnitude of effects were seen, suggesting that cerebrovascular pathology may be associated with AHT exposure. Most notably, the odds of exposure to AHT for participants with large infarcts were consistently more than double the odds for controls, regardless of exposure definition or adjustment.

Based on pathophysiology of cardiovascular and cerebrovascular disease, an association between pathology and AHT is surprising and questionable. Despite adjustment for confounders, residual confounding is likely present. This result highlights the complicated time course cerebrovascular pathology and the importance of accurate measurement of risk factors and exposure during life.

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