Topic
Pulsatile flow
About: Pulsatile flow is a research topic. Over the lifetime, 6278 publications have been published within this topic receiving 149638 citations.
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TL;DR: This report identifies the inception and progressive pathology of atherosclerosis resulting from the effects of hydraulic forces inherent in the circulatory system as determined by hydraulic forces.
Abstract: This report identifies the inception and progressive pathology of atherosclerosis resulting from the effects of hydraulic forces inherent in the circulatory system. 1 Vascular dynamics relates the effect of hydraulic forces to the biological response of blood vessels. The forces and principles involved are directly comparable to those which prevail in all hydraulic systems with due regard to local conditions of flow and hydraulic characteristics. 2 The laws of fluid mechanics are fully applicable to the hydrobiological conditions found in the human circulatory system, and the composite effects of their operation are both prerequisite and conducive to atherosclerosis. Previous reports 3,4 have correlated atherosclerotic lesions found at autopsy with their localization in the circulatory system as determined by hydraulic forces. Rigid and flexible model hydraulic systems built to simulate the specifications of human blood vessels with respect to pulsatile flow, volumetric flow, velocity of flow, and anatomical geometry confirm the
92 citations
TL;DR: Integrity of the N-terminus of dystrophin is a useful indicator of both LV and RV function, and in addition to improving LV hemodynamics, LVAD therapy results in amelioration of the myocardial structure of the right cardiac chamber.
92 citations
TL;DR: Comparison of results shows that the behaviors of the two flows are similar at some instances of time, however, important observed differences indicate that for thorough understanding of pulsatile flow behavior in stenosed arteries, the actual physiological flow should be simulated.
92 citations
TL;DR: It is shown that albumin wall flux varies significantly along the arterial section, is strongly dependent upon the different flow regimes and varies considerably during a cardiac cycle.
Abstract: Albumin transport in a stenosed artery configuration is analyzed numerically under steady and pulsatile flow conditions. The flow dynamics is described applying the incompressible Navier-Stokes equations for Newtonian fluids, the mass transport is modelled using the convection diffusion equation. The boundary conditions describing the solute wall flux take into account the concept of endothelial resistance to albumin flux by means of a shear dependent permeability model based on experimental data. The study concentrates on the influence of steady and pulsatile flow patterns and of regional variations in vascular geometry on the solute wall flux and on the ratio of endothelial resistance to concentration boundary layer resistance. The numerical solution of the Navier-Stokes equations and of the transport equation applies the finite element method where stability of the convection dominated transport process is achieved by using an upwind procedure and a special subelement technique. Numerical simulations are carried out for albumin transport in a stenosed artery segment with 75 percent area reduction representing a late stage in the progression of an atherosclerotic disease. It is shown that albumin wall flux varies significantly along the arterial section, is strongly dependent upon the different flow regimes and varies considerably during a cardiac cycle. The comparison of steady results and pulsatile results shows differences up to 30 percent between time-averaged flux and steady flux in the separated flow region downstream the stenosis.
92 citations
TL;DR: Enhanced PP transmission may thus occur and precipitate organ damage at each time that autoregulatory mechanisms, normally protecting the heart from vascular injury, are blunted and explain why increased PP and arterial stiffness are significant predictors of morbidity and mortality in the elderly.
Abstract: Whereas large arteries dampen oscillations resulting from intermittent ventricular ejection, small arteries steadily deliver optimal blood flow to various organs as the heart. The transition from pulsatile to steady pressure is influenced by several factors as wave travel, damping, and reflections, which are mainly determined by the impedance mismatch between large vessels and arteriolar bifurcations. The mechanism(s) behind the dampening of pressure wave in the periphery and the links between central and peripheral pulsatile pressure (PP) may determine cardiac damage. Active pathways participate to pulse widening and changes in pulse amplitude in microvessels. Steady and cyclic stresses operate through different transduction mechanisms, the former being focal adhesion kinase and the latter being free radicals and oxidative stress. Independently of mechanics, calcifications and attachment molecules contribute to enhance vessel wall stiffness through changes in collagen cross-links, proteoglycans, integrins, and fibronectin. Enhanced PP transmission may thus occur and precipitate organ damage at each time that autoregulatory mechanisms, normally protecting the heart from vascular injury, are blunted. Such circumstances, observed in old subjects with systolic hypertension and/or Type 2 diabetes mellitus, particularly under high-sodium diet, cause cardiac damage and explain why increased PP and arterial stiffness are significant predictors of morbidity and mortality in the elderly.
91 citations