Abstract

Numerous pathophysiologic observations in humans and animals led to the formulation of the response-to-injury hypothesis of atherosclerosis, which proposed that endothelial denu- dation by the blood flow was the first step in atherosclerosis. At present it is impossible to describe hemodynamics only by the Navier-Stokes or Oldroyd-B equations because in the large arteries blood flow is unsteady, with the flow separation and waveform propagation of the thyxotropic mass. The purpose of this paper is to study the impact of the arterial pulse wave on the blood flow and initial factors of atherosclerosis. In 12 healthy men (25-39 years of age) peak velocity, mean velocity, mean flow and net flow in the aorta have been investigated by МR angiography. Initial velocity was registered after 43msec of the ECG-R wave, and it differed from zero at all sites of the aorta, although net flow was equal to zero. Womersley’s number from the ascending to the thoracic aorta decreased from 12.5 ± 1.5 to 7.3 ± 1.2; flow modified from inertio-elastic to viscous. In the aortic arch in protodiastole blood flow separated into the opposite directed streams resulting in wave superposition with the high net flow. At the isthmus area separated waves interferences and reflects to anterograde direction. Here flow acceleration in protodiastole is 6 times higher than in systole. Pulse waves move on artery walls fifteen or more times more rapidly than the blood flow. Pulse oscillation increases strain rate to the contiguous vessel wall flow layers. At the sites with the flow wave negative interference vessel pulse oscillation attenuates and at the boundary reflection flow wave can shift the vessel wall.

Keywords

Arterial pulse; Blood flow; Wave Propagation; Blood/Arterial Wall Viscoelasticity; Endothelial Denudation; Magnetic Resonance Imaging; Atherosclerosis

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Conflicts of Interest

The authors declare no conflicts of interest.

References