Abstract

Aortic stiffness increases with age and is a robust predictor of brain pathology including Alzheimer’s and other dementias. Aging causes disproportionate stiffening of the aorta compared with the carotid arteries, reducing protective impedance mismatches at their interface and affecting transmission of destructive pulsatile energy to the cerebral circulation. Recent clinical studies have measured regional stiffness within the aortic arch using pulse wave velocity (PWV) and have found a stronger association with cerebrovascular events than global stiffness measures. However, effects of aortic arch PWV on the transmission of harmful excessive pulsatile energy to the brain is not well-understood. In this study, we use an energy-based analysis of hemodynamic waves to quantify the effect of aortic arch stiffening on transmitted pulsatility to cerebral vasculature, employing a computational approach using a one-dimensional model of the human vascular network. Results show there exists an optimum wave condition—occurring near normal human heart rates—that minimizes pulsatile energy transmission to the brain. This indicates the important role of aortic arch biomechanics on heart-brain coupling. Our results also suggest that energy-based indices of pulsatility combining pressure and flow data are more sensitive to increased stiffness than using flow or pressure pulsatility indices in isolation.

Highlights

  • Www.nature.com/scientificreports brain microvasculature from high pulsatile energy

  • In the Dallas Heart Study[14], it has been shown that aortic arch pulse wave velocity (PWV) and increased blood pressure have independent associations with brain vascular insult

  • Our results suggest that: (1) there exists an optimum wave condition in the aorta that minimizes the harmful pulsatile energy transmission to the brain, (2) at different wave conditions, this optimum wave condition occurs around a value near the normal human heart rate (HR) (75 bpm), and (3) an index based on pulsatile power is a more sensitive measure for excessive pulsatility transmission to the brain compared to conventional measures such as pressure and flow pulsatility indices alone

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Summary

Introduction

Www.nature.com/scientificreports brain microvasculature from high pulsatile energy. Disproportionate age-related stiffening of the aorta (relative to the carotid arteries) is theorized to reduce this protective impedance mismatch at the interface and thereby affect the wave reflection[8]. In the Dallas Heart Study[14], it has been shown that aortic arch PWV (which is a contributor to the pulsatile portion of the net power) and increased blood pressure (which is a contributor to the steady portion of the power) have independent associations with brain vascular insult Due to this independence, we put the focus of the current study only on the pulsatile portion of the transmitted power in order to capture the dynamic effects of arterial stiffening on pulsatility transmitted to the cerebral vasculature. We put the focus of the current study only on the pulsatile portion of the transmitted power in order to capture the dynamic effects of arterial stiffening on pulsatility transmitted to the cerebral vasculature This analysis considers the combined effects of flow and pressure propagation into the brain and demonstrates greater sensitivity to increased stiffness than using a pressure or flow pulsatility index alone.

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