Subclinical compromise in cardiac strain relates to smaller cerebral grey matter volumes in older adults

Abstract

Background: Global longitudinal strain (GLS) is a sensitive measure of regional myocardial function that is associated with cognition in older adults. This study examined if compromised GLS related to structural brain changes among aging adults under the hypothesis that compromised GLS would relate to smaller grey matter volumes in regions affected by normal aging and Alzheimer’s disease (AD) due to subtle reductions in blood flow delivery.

Methods and Results: Vanderbilt Memory & Aging Project participants (n=286, 73±7 years) with normal cognition (NC) and mild cognitive impairment (MCI) underwent cardiac magnetic resonance imaging (MRI) to assess GLS and 3T brain MRI to quantify frontal, parietal, temporal, occipital, and hippocampal volumes and calculate an AD signature reflecting regions affected by AD-related neurodegeneration. Linear regressions related GLS to neuroimaging variables adjusting for age, sex, race/ethnicity, education, Framingham Stroke Risk Profile, cognitive diagnosis, Apolipoprotein E ε4 status, and intracranial volume (for volume models). Models were repeated with a GLS x cognitive diagnosis interaction and stratified by diagnosis. In main effect models, compromised GLS related to the AD signature (p=0.03). The GLS x cognitive diagnosis term related to hippocampal (p=0.03) and temporal lobe volumes (p=0.051), with compromised GLS associated with smaller volumes in regions affected by AD pathology but only among MCI participants (p-values<0.04).

Conclusions: Results are among the first to suggest compromised strain relates to grey matter atrophy in regions vulnerable to AD pathology, especially among participants with the earliest clinical signs of dementia. Future research should examine how subclinical changes in myocardial function relate to molecular biomarkers of AD to better elucidate underlying drivers of associations between subclinical cardiovascular dysfunction and brain aging.

Publication
Submitted to PLOS One