Coronary Artery Disease and Dementia Likely Share Genetic Risk

Genetic risk for coronary artery disease (CAD) is also related to risk for developing dementia, according to results of a study published in Circulation.

Mounting evidence has indicated that CAD and dementia share modifiable and nonmodifiable risk factors, suggesting that they may also share genetic risk.

Investigators from University College London in the United Kingdom (UK) sourced data for this study from the UK Biobank, which is a large population-based cohort of individuals recruited between 2006 and 2010. In this study, individuals (N=365,782) were evaluated for CAD polygenic risk score (PRS) and lifestyle risk score (LRS) on the basis of the American Heart Association Life’s Essential 8 (LE8) concept and for incident dementia during follow-up. A subset of individuals (n=32,028) with magnetic resonance imaging (MRI) data were evaluated for contribution CAD risk factors on neurologic outcomes.

During a median 13.9-year follow-up, 8870 incident dementia cases occurred, in which 4021 were diagnosed with Alzheimer disease (AD) and 1994 with vascular dementia.

The individuals with and without (n=356,912) dementia had mean ages of 65 and 60 years, 48% and 54% were women, 36% and 33% had high CAD genetic risk, and 33% and 31% had high lifestyle risk, respectively.

Risk for all-cause dementia increased with every SD increase in CAD PRS (subhazard ratio [sHR], 1.10; P <.001) and LRS (sHR, 1.04; P =.006). Stratified by type of dementia, risk for AD was associated with every SD of PRS (sHR, 1.09; P <.001) but not LRS (sHR, 0.97; P =.096) whereas risk for vascular dementia was associated with both PRS (sHR, 1.16; P <.001) and LRS (sHR, 1.15; P <.001).

Stratified by tertile, risk for all-cause dementia, AD, and vascular dementia was associated with PRS in tertiles 2 (sHR range, 1.09-1.22; all P £.022) and 3 (sHR range, 1.18-1.33; all P <.001) relative to tertile 1. LRS in tertile 3 was associated with all-cause dementia and vascular dementia risk (sHR range, 1.07-1.40; both P £.017) but tertile 2 was associated with lower risk for AD (sHR, 0.92; P =.039) relative to tertile 1.

When LRS was stratified by the biological and behavioral components, risk for all-cause dementia was increased with every SD of behavioral LRS (sHR, 1.08; P <.001) but decreased with biological LRS (sHR, 0.97; P =.006). Stratified by type of dementia, only vascular dementia was associated with increasing SD of behavioral LRS (sHR, 1.17; P <.001).

No significant interactions between PRS and LRS were observed for any dementia outcomes (all P ³.383).

In the neuroimaging subgroup, white matter hyperintensities increased with every SD increase in PRS (3.3%, P <.001), biological LRS (7.6%; P <.001), and behavioral LRS (4.1%; P <.001); gray matter volume decreased with increasing biological (-0.2%; P <.001) and behavioral (-0.1%; P <.001) LRS; and hippocampal volume decreased with increasing behavioral LRS (-0.1%; P =.012).

The major limitation of this study was the cross-sectional design, which did not allow for causal relationships to be assessed.

The study authors concluded, “…we provide evidence for an association between an elevated genetic risk for CAD and an increased risk of dementia.”

This article originally appeared on The Cardiology Advisor