Abstract

BackgroundCerebrovascular reactivity (CVR) measures blood flow change in response to a vasoactive stimulus. Impairment is associated with several neurological conditions and can be measured using blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI). Field strength affects the BOLD signal, but the effect on CVR is unquantified in patient populations.MethodsWe recruited patients with minor ischemic stroke and assessed CVR magnitude and delay time at 3 and 1.5 Tesla using BOLD MRI during a hypercapnic challenge. We assessed subcortical gray (GM) and white matter (WM) differences using Wilcoxon signed rank tests and scatterplots. Additionally, we explored associations with demographic factors, WM hyperintensity burden, and small vessel disease score.ResultsEighteen of twenty patients provided usable data. At 3T vs. 1.5T: mean CVR magnitude showed less variance (WM 3T: 0.062 ± 0.018%/mmHg, range 0.035, 0.093; 1.5T: 0.057 ± 0.024%/mmHg, range 0.016, 0.094) but was not systematically higher (Wilcoxon signal rank tests, WM: r = −0.33, confidence interval (CI): −0.013, 0.003, p = 0.167); delay showed similar variance (WM 3T: 40 ± 12 s, range: 12, 56; 1.5T: 31 ± 13 s, range 6, 50) and was shorter in GM (r = 0.33, CI: −2, 9, p = 0.164) and longer in WM (r = −0.59, CI: −16, −2, p = 0.010). Patients with higher disease severity tended to have lower CVR at 1.5 and 3T.ConclusionMean CVR magnitude at 3T was similar to 1.5T but showed less variance. GM/WM delay differences may be affected by low signal-to-noise ratio among other factors. Although 3T may reduce variance in CVR magnitude, CVR is readily assessable at 1.5T and reveals comparable associations and trends with disease severity.

Highlights

  • MATERIALS AND METHODSCerebrovascular reactivity (CVR) quantifies the change in blood flow in response to a vasoactive stimulus, providing an indicator of vascular health

  • CVR magnitude is lower in patients with more severe small vessel disease (SVD) features on magnetic resonance imaging (MRI) (Blair et al, 2020), and CVR delay is longer in SVD patients than healthy controls (Sam et al, 2016; Thrippleton et al, 2018; Atwi et al, 2019)

  • Within the individual regions of interest (ROIs), we found generally similar results to the averaged values: mean CVR magnitude was comparable though marginally higher at 3T vs. 1.5T; delay in subcortical GM regions tended to be shorter at 3T than 1.5T; delay in white matter (WM) regions was typically longer at 3T than at 1.5T

Read more

Summary

Introduction

Cerebrovascular reactivity (CVR) quantifies the change in blood flow in response to a vasoactive stimulus, providing an indicator of vascular health. CVR delay, the time between stimulus onset and observing a change in the blood flow, should be considered to avoid underestimating CVR magnitude as response time can vary in different tissues (van Niftrik et al, 2017). Impaired CVR is associated with several conditions, including cerebral small vessel disease (SVD), a major cause of stroke and dementia with no current treatments (Wardlaw et al, 2019). Cerebrovascular reactivity (CVR) measures blood flow change in response to a vasoactive stimulus. Impairment is associated with several neurological conditions and can be measured using blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI). Field strength affects the BOLD signal, but the effect on CVR is unquantified in patient populations

Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call