Friction Of Blood Research Articles

Presence of Left Atrial Fibrosis May Contribute to Aberrant Hemodynamics and Increased Risk of Stroke in Atrial Fibrillation Patients.

Atrial fibrillation (AF) patients are at high risk of stroke, with the left atrial appendage (LAA) found to be the most common site of clot formation. Presence of left atrial (LA) fibrosis has also been associated with higher stroke risk. However, the mechanisms for increased stroke risk in patients with atrial fibrotic remodeling are poorly understood. We sought to explore these mechanisms using fluid dynamic analysis and to test the hypothesis that the presence of LA fibrosis leads to aberrant hemodynamics in the LA, contributing to increased stroke risk in AF patients. We retrospectively collected late-gadolinium-enhanced MRI (LGE-MRI) images of eight AF patients (four persistent and four paroxysmal) and reconstructed their 3D LA surfaces. Personalized computational fluid dynamic simulations were performed, and hemodynamics at the LA wall were quantified by wall shear stress (WSS, friction of blood), oscillatory shear index (OSI, temporal directional change of WSS), endothelial cell activation potential (ECAP, ratio of OSI and WSS), and relative residence time (RRT, residence time of blood near the LA wall). For each case, these hemodynamic metrics were compared between fibrotic and non-fibrotic portions of the wall. Our results showed that WSS was lower, and OSI, ECAP, and RRT was higher in the fibrotic region as compared to the non-fibrotic region, with ECAP (p = 0.001) and RRT (p = 0.002) having significant differences. Case-wise analysis showed that these differences in hemodynamics were statistically significant for seven cases. Furthermore, patients with higher fibrotic burden were exposed to larger regions of high ECAP, which represents regions of low WSS and high OSI. Consistently, high ECAP in the vicinity of the fibrotic wall suggest that local blood flow was slow and oscillating that represents aberrant hemodynamic conditions, thus enabling prothrombotic conditions for circulating blood. AF patients with high LA fibrotic burden had more prothrombotic regions, providing more sites for potential clot formation, thus increasing their risk of stroke.

Abstract 16758: Presence of Left Atrial Fibrosis Contributes to Aberrant Hemodynamics and Increased Risk of Stroke in Atrial Fibrillation Patients

Introduction: Atrial fibrillation (AF) patients are at high risk of stroke, with the left atrial appendage (LAA) found to be the most common site of clot formation. Left atrial (LA) fibrosis is also associated with higher stroke risk. However, the mechanisms for increased stroke risk in patients with atrial fibrotic remodeling are poorly understood. We sought to explore these specific mechanisms using fluid dynamics analysis. Hypothesis: The presence of LA fibrosis leads to aberrant hemodynamics in the atria, contributing to increased stroke risk in AF patients. Methods: We retrospectively collected LGE-MRI images of 3 AF patients and reconstructed their 3D LA endocardial surfaces. Fibrotic regions were identified as those with intensity 3 standard deviations greater than the mean LA blood-pool intensity. Personalized computational fluid dynamic simulations were performed, and hemodynamics at the LA wall were quantified by wall shear stress (WSS, friction of blood) and oscillatory shear index (OSI, temporal directional change of WSS). For each case, WSS and OSI were compared between fibrotic and normal regions. Results: WSS was significantly lower in the fibrotic region as compared to normal region for all 3 cases. Additionally, OSI was higher in the fibrotic region as compared to normal region for all 3 cases. However, this different was statistically significant for cases 1 and 3; case 2 was not statistically significantly different. Low WSS and high OSI in the vicinity of the fibrotic wall suggest that local blood-flow was slow and oscillating, enabling pro-thrombotic conditions for circulating blood. Conclusion: LA fibrosis correlates with regions of aberrant hemodynamics, which renders it susceptible to blood thrombosis. AF patients with high LA fibrosis burden will have more pro-thrombotic regions, in addition to low flow in the LAA, providing more sites for a potential clot formation. These conditions might get exacerbated during an AF event and cause stroke.

Mathematical modelling of the influence of yield shear stress on blood friction in a turbulent flow

Measurements of blood rheology indicate that human blood has a yield shear stress. Transport of oxygen in the aorta or a vein depends on blood flow rate. Therefore, it is interesting to find out how blood yield shear stress affects blood transportation if flow is turbulent. The majority of mathematical approaches deal with laminar flow of human blood, which is rather simple compared to turbulent flow modelling. This paper presents a mathematical model of fully developed turbulent flow of human blood in the aorta. The physical model assumes that blood is a non-Newtonian liquid that demonstrates yield shear tress. The main objective of the research is to examine the influence of human blood yield shear stress on turbulent properties, like friction factor, in the aorta. Available blood rheology experimental data for various concentrations of haematocrit were used in order to fit the rheological model. The rheological model together with the momentum equation and the two-equation turbulence model constitute a mathematical model of turbulent flow of human blood. Results of simulations are discussed and presented as figures and conclusions.

Leukocyte Adhesion Under Hemodynamic Flow Conditions.

Vascular endothelial cells (ECs) line the luminal side of all blood vessels and act as a selective barrier between blood and tissue. ECs are constantly exposed to biochemical and biomechanical stimuli from the blood and underlying tissue. Fluid shear stress acts in parallel to the vessel wall, resulting from friction of blood against EC. Despite the importance of flow on normal EC function, much of the information regarding EC function and dysfunction has been derived from cells harvested, grown, and studied in static culture.In order to study the effects of shear stress on EC function a number of in vitro models have been developed. This manuscript provides methodology for use of a system which enables recirculation of leukocytes and cell culture medium over the endothelium for a period of several minutes to days and enables investigation of the effects of prolonged leukocyte coculture on both the endothelial and leukocyte populations.

Molecular mechanisms of the vascular responses to haemodynamic forces

Blood vessels are permanently subjected to mechanical forces in the form of stretch, encompassing cyclic mechanical strain due to the pulsatile nature of blood flow and shear stress. Significant variations in mechanical forces, of physiological or physiopathological nature, occur in vivo. These are accompanied by phenotypical modulation of smooth muscle cells and endothelial cells, producing structural modifications of the arterial wall. In all the cases, vascular remodelling can be allotted to a modification of the tensional strain or shear, and underlie a trend to reestablish baseline mechanical conditions. Vascular cells are equipped with numerous receptors that allow them to detect and respond to the mechanical forces generated by pressure and shear stress. The cytoskeleton and other structural components have an established role in mechanotransduction, being able to transmit and modulate tension within the cell via focal adhesion sites, integrins, cellular junctions and the extracellular matrix. Mechanical forces also initiate complex signal transduction cascades, including nuclear factor-kappaB and mitogen-activated protein kinase pathways, leading to functional changes within the cell.