Respiration Can Trigger Cerebrovascular Reactivity: A Novel Method to Quantify Cerebrovascular Resistance Dynamics...

To directly quantify respiration-driven cerebrovascular resistance dynamics (CRD) using a gas-free MRI framework based on the internal-to-external artery carotid flow ratio (ratio_Q).

Two independent datasets (n = 10 and n = 17) were used to evaluate repeatability and to compare breathing conditions. Real-time phase-contrast MRI (RT-PC) was performed at the C2-C3 level, and a dedicated in-house software was used to extract the respiratory-frequency components of internal and external carotid artery flow (Q_ICA and Q_ECA). The flow ratio (ratio_Q = Q_ICA/Q_ECA) was derived to attenuate cardiac-driven inflow effects. Its mean value (aver_ratio_Q) reflected baseline cerebrovascular resistance, while its pulsatility index (PI_ratio_Q = amplitude/mean) quantified respiration-driven CRD.

In Dataset 1, ratio_Q showed excellent within-session repeatability for its mean value (ICC(3,1) = 0.96) and good repeatability for its pulsatility index (ICC(3,1) = 0.79). In Dataset 2, sustained deep breathing increased mean cerebrovascular resistance, evidenced by a decrease in aver_ratio_Q from 2.5 ± 0.9 to 1.7 ± 0.9. Specifically, aver_Q_ICA decreased by 30% (p < 0.001), whereas aver_Q_ECA showed no significant change (a 5% increase, p = 0.094). Respiration-driven CRD was enhanced during sustained deep breathing, with PI_ratio_Q increasing by ≈69% compared with free breathing (from 13.6 ± 5.0 to 23.0 ± 7.3, p < 0.001).

This gas-free RT-PC approach using the ICA-to-ECA flow ratio provides a stable and reproducible index of respiration-driven CRD, enabling isolation of cerebrovascular resistance modulation from cardiac effects and supporting its potential role in the development of faster and more accessible CVR assessment strategies.