Wave Reflection at the Origin of a First-Generation Branch Artery and Target Organ Protection
Michael A. Haidar, Mark A. van Buchem, Sigurður Sigurðsson, John D. Gotal, Vilmundur Guðnason, Lenore J. Launer, Gary F. Mitchell
Abstract
Excessive pressure and flow pulsatility in first-generation branch arteries are associated with microvascular damage in high-flow organs like brain and kidneys. However, the contribution of local wave reflection and rereflection to microvascular damage remains controversial. Aortic flow, carotid pressure, flow and hydraulic power, brain magnetic resonance images, and cognitive scores were assessed in AGES-Reykjavik study participants without history of stroke, transient ischemic attack, or dementia (N=668, 378 women, 69–93 years of age). The aorta-carotid interface was generalized as a markedly asymmetrical bifurcation, with a large parent vessel (proximal aorta) branching into small (carotid) and large (distal aorta) daughter vessels. Local reflection coefficients were computed from aortic and carotid characteristic impedances. The bifurcation reflection coefficient, which determines pressure amplification in both daughter vessels, was low (0.06±0.03). The carotid flow transmission coefficient was low (0.11±0.04) and associated with markedly lower carotid versus aortic flow pulsatility (waveform SD, 7.2±2.0 versus 98.7±21.8 mL/s, P <0.001), pulsatility index (1.8±0.5 versus 4.5±0.6, P <0.001), and pulsatile power percentage (10±4% versus 25±5%, P <0.001). Transmitted as compared to incident pulsatile power (19.0±9.8 versus 35.9±17.8 mW, P <0.001) was further reduced by reflection (−4.3±2.7 mW) and rereflection (−12.5±8.1 mW) within the carotid. Higher carotid flow pulsatility correlated with lower white matter volume (R=−0.130, P <0.001) and lower memory scores (R=−0.161, P <0.001). Marked asymmetry of characteristic impedances at aorta-branch artery bifurcations limits amplification of pressure, markedly reduces absolute and relative pulsatility of transmitted flow and hydraulic power into first-generation branch arteries, and thereby protects the downstream local microcirculation from pulsatile damage.