Hemodynamic modeling of aspirin effects on BOLD responses at 7T

Abstract

AbstractAspirin is considered a potential confound for functional magnetic resonance imaging (fMRI) studies. This is because aspirin affects the synthesis of prostaglandin, a vasoactive mediator centrally involved in neurovascular coupling, a process that underlies the blood oxygenated level dependent (BOLD) response. Aspirin-induced changes in BOLD signal are a potential confound for fMRI studies of patients (e.g. with cardiovascular conditions or stroke) who receive low-dose aspirin prophylactically and are compared to healthy controls that do not take aspirin. To examine the severity of this potential confound, we combined high field (7 Tesla) MRI during a simple hand movement task with a biophysically informed hemodynamic model. Comparing elderly volunteers with vs. without aspirin medication, we tested for putative effects of low-dose chronic aspirin on the BOLD response. Specifically, we fitted hemodynamic models to BOLD signal time courses from 14 regions of the human motor system and examined whether model parameter estimates were significantly altered by aspirin. While our analyses indicate that hemodynamics differed across regions, consistent with the known regional variability of the BOLD response, we neither found a significant main effect of aspirin (i.e., an average effect across brain regions) nor an expected drug×region interaction. While our sample size is not sufficiently large to rule out small-to-medium global effects of aspirin, we had adequate statistical power for detecting the expected interaction. Altogether, our analysis suggests that low-dose aspirin, as used for prophylactic purposes, does not strongly affect BOLD signals and may not represent a critical confound for fMRI studies.