Abstract

[Figure: see text].

Highlights

  • Excessive pressure and flow pulsatility in first-generation branch arteries are associated with microvascular damage in high-flow organs like brain and kidneys

  • The general structure of markedly asymmetrical bifurcations at stiff first-generation branch arteries arising from a compliant aorta optimally limits pulsatile power transmission into the branch vasculature and protects the fragile microcirculation

  • Others have observed that bifurcations in the arterial system are generally impedance-matched in the forward, but not the backward direction, optimally transmitting forward hydraulic power while causing backward-traveling power to be trapped in daughter arteries by rereflection.[12,13,14,15]

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Summary

Introduction

Excessive pressure and flow pulsatility in first-generation branch arteries are associated with microvascular damage in high-flow organs like brain and kidneys. Age-related dementias affect ≈5.8 million people in the United States.[1] By 2050, the prevalence is projected to increase to over 13.8 million.[1] Cardiovascular risk factors, including arterial stiffness, are risk factors for dementias of all types and represent important potentially modifiable targets for intervention.[2] Pressure and flow pulsatility in the macrocirculation and microcirculation are associated with microvascular damage in target organs like the brain and kidneys.[3,4,5,6,7] Wave reflection at the origin of a first-generation branch artery (FGBA) arising from the aorta represents a possible mechanism that could limit the pulsatility of flow and power transmitted into these arteries.[8] some have speculated that since the aorta-carotid bifurcation is relatively well matched, with a reflection coefficient of 0% to 15%, any effect of local wave reflection on transmitted power at the junction is trivial, with 97% and 100% of incident power transmitted.[9,10] larger bifurcation reflection coefficients increase transmitted pulsatile pressure, which should be deleterious. Cardiovascular disease risk factors associated with aortic stiffening represent important potentially modifiable targets for intervention

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