title: Controlling cardiac transport and plaque formation.
abstract: Macro-particles transported in the bloodstream, such as LDL particles and macrophages, are considered to be one of the initiating factors of atherosclerotic plaque development. LDL infiltration from the bloodstream into a blood vessel's wall, whether the coronary, peripheral, or carotid arteries, is considered a major inflammatory factor, recruiting macrophages from the blood flow and leading to the formation of vulnerable atherosclerotic plaques. Infiltration sites are influenced by patterns of blood flow, as regions of lower shear stresses and high oscillations may give rise to higher infiltration rates through the endothelium, exacerbating the growth of a plaque and its tendency to rupture. Previous studies demonstrated a high prevalence of rupture sites proximal to the minimum lumen area, which raised the question of whether the existence of two distinct adjacent plaques, in which the distal plaque is more severe, can give rise to hemodynamic forces that can push the non-stenotic plaque to rupture. Models of the coronary arteries with one and two eccentric and concentric stenotic narrowings were built into a closed flow loop. The single stenosis model had a 75% area reduction narrowing (representing the vunerable atherosclerotic plaque) with relevant elastic properties. The double stenosis model included an additional distal 84% area reduction narrowing. The flow in the area between the two stenoses was recorded and analyzed using continuous doppler particle image velocimetry (CDPIV), together with the hydrostatic pressure acting on the proximal plaque. Results indicated that the combined shear rates and pressure effects in a model with a significant distal stenosis can contribute to the increase in plaque instability by LDL and enhanced macrophage uptake. The highly oscillatory nature of the disturbed flow near the shoulder of the vulnerable atherosclerotic plaque enriches its lipid soft core, and the high hydrostatic pressures acting on the same lesion in this geometry induce high internal maximal stresses that can trigger the rupture of the plaque.
authors: Department of Biomedical Engineering, Tel Aviv University, Tel Aviv 69978, Israel.
authors: Ze'ev
authors: Z
authors: Aronis
authors: Sagi
authors: S
authors: Raz
authors: Elisha J P
authors: EJ
authors: Martinez
authors: Shmuel
authors: S
authors: Einav
mesh_terms: D054058:Acute Coronary Syndrome / Q000503:physiopathology* / Q000517:prevention & control; D050197:Atherosclerosis / Q000503:physiopathology* / Q000517:prevention & control; D001794:Blood Pressure; D003324:Coronary Artery Disease / Q000503:physiopathology* / Q000517:prevention & control; D023921:Coronary Stenosis / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications; D008077:Lipoproteins, LDL / Q000097:blood; D008955:Models, Cardiovascular; D012307:Risk Factors
chemical_list: D008077:Lipoproteins, LDL