Abstract
Coronary bifurcations are prone to atherosclerotic plaque growth, experiencing regions of reduced wall shear stress (WSS) and increased platelet adhesion. This study compares effects across different rheological approaches on hemodynamics, combined with a shear stress exposure history model of platelets within a stenosed porcine bifurcation. Simulations used both single/multiphase blood models to determine which approach best predicts phenomena associated with atherosclerosis and atherothrombosis. A novel Lagrangian platelet tracking model was used to evaluate residence time and shear history of platelets indicating likely regions of thrombus formation. Results show a decrease in area of regions with pathologically low time-averaged WSS with the use of multiphase models, particularly in a stenotic bifurcation. Significant non-Newtonian effects were observed due to low-shear and varying hematocrit levels found on the outer walls of the bifurcation and distal to the stenosis. Platelet residence time increased 11% in the stenosed artery, with exposure times to low-shear sufficient for red blood cell aggregation (>1.5 s). increasing the risk of thrombosis. This shows stenotic artery hemodynamics are inherently non-Newtonian and multiphase, with variations in hematocrit (0.163–0.617) and elevated vorticity distal to stenosis (+15%) impairing the function of the endothelium via reduced time-averaged WSS regions, rheological properties and platelet activation/adhesion.
Highlights
Cardiovascular diseases were responsible for an estimated 18.8 million deaths in 2017 [1], with heart disease being the leading cause of death in the USA in the same year [2]
In addition to plaque rupture causing myocardial infarction or sudden death [2], the altered hemodynamics arising from inflammatory plaque growth impacts the behaviour and activation of platelets; catalysing plaque/fibrin growth through increased platelet adhesion and increased risk of thrombus formation [10], with a detailed review of these phenomena provided by Davi and Patrono [11]
This study presents for the first time, a Lagrangian platelet tracking model to assess the likely regions of platelet activation and indicate potential regions with an increased risk of clotting/thrombus formation alongside a comprehensive examination of the relation between blood rheology red blood cells (RBC) aggregation/concentration and hemodynamics
Summary
Cardiovascular diseases were responsible for an estimated 18.8 million deaths in 2017 [1], with heart disease being the leading cause of death in the USA in the same year [2]. Of particular relevance to cardiovascular health are the coronary arteries, two major blood vessels which bifurcate into multiple smaller branches. The coronary arteries have been associated with several clinical pathologies, including atherosclerotic plaques/lesions [3, 4], arterial stiffening [5] and increased thrombosis [6] (clot formation). Blood rheology and platelet activation in a coronary bifurcation time-averaged wall shear stress [7] (TAWSS) occurring around the branching of the artery [8] or distal to regions of stenosis [9]. In addition to plaque rupture causing myocardial infarction or sudden death [2], the altered hemodynamics arising from inflammatory plaque growth impacts the behaviour and activation of platelets; catalysing plaque/fibrin growth through increased platelet adhesion and increased risk of thrombus formation [10] (atherothrombosis), with a detailed review of these phenomena provided by Davi and Patrono [11]
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