Abstract

The brain is a high‐flow organ that requires continuous, non‐pulsatile blood flow. Intracranial blood flow pulsatility depends on the ability of the large elastic arteries and cerebrovasculature to dampen pulsatile hemodynamics transmitted from the heart. Aging is accompanied by large artery stiffening and reductions in cerebrovascular dampening, ultimately increasing intracranial pulsatility. It is unclear what hemodynamic forces may be responsible for these age‐related changes in the transmission and dampening of intracranial pulsatility across the lifespan. The purpose of this study was to explore hemodynamic contributors to intracranial pulsatility and pulsatile dampening in 244 adults between 35–85 yr (49% female, 56±12 yr, 27±4.2 kg/m2). Intracranial pulsatile dampening was calculated as the ratio between common carotid and middle cerebral artery (MCA) blood velocity pulsatility index (PI) measured via Doppler. Carotid ultrasound and wave intensity analysis were used to measure carotid diameter, forward compression wave energy (W1), wave reflection index (RIx), and forward traveling expansion wave (W2). Aortic (carotid‐femoral) and carotid pulse wave velocity (PWV) were assessed via tonometry and carotid ultrasound, respectively, and expressed as a ratio (aortic:carotid PWV). Carotid pulse pressure (PP) was measured via tonometry. Multiple regression was used to examine the contributions of 1) age, sex, BMI, aortic:carotid PWV, carotid diameter, PP, and W1 to intracranial pulsatility (MCA PI); and 2) age, sex, BMI, aortic:carotid PWV, carotid diameter, RIx, and W2 to intracranial pulsatile dampening. After entering all variables, significant predictors of MCA PI included age (β,0.44), aortic:carotid PWV (β,0.16), PP (β,0.29), and W1 (β,0.20; R2=0.50, p<0.01). Significant predictors of intracranial pulsatile dampening included age (β,−0.47), sex (β,−0.43), and RIx (β,0.26; R2=0.53, p<0.01). Our data confirms recent literature linking age, exaggerated stiffening of the aorta compared to carotid artery, and extracranial hemodynamics to intracranial pulsatility in the MCA. Moreover, our findings indicate age, sex, and wave reflections in the carotid artery impact the ability of the cerebrovasculature to dampen transmission of pulsatile hemodynamics. These data highlight the potential utility of the large extracranial arteries as therapeutic targets to reduce intracranial pulsatility and importance of carotid wave reflections in dampening intracranial pulsatility.Support or Funding InformationFunded in part by an ACSM Foundation Research Grant (WKL), AHA Predoctoral Fellowship (WKL), and Dairy Research Institute/Dairy management Inc. Grant 1154 (KSH).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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