Abstract
Background Atherosclerosis is a build-up of low-density lipoproteins (LDL) in the channels of blood vessels. This occludes the vessels and, occurring in the carotid arteries, portends conditions that favour stroke. This work is an attempt to mathematically represent the physiological process of atherosclerosis caused by plaques on the walls of the human arteries. Aim Provide insight into the effect of blood flow velocity on wall shear stress and its implications on atherosclerosis progression in a human carotid artery via computational simulation. Methods The effect of blood velocity on plaque growth and progression is simulated using COMSOL multi-physics. The human carotid was modeled in 2-D with Stokes law for model flow. The simulation began with a plaque-free vessel with velocities of 30 m/s – 125 m/s. Results Results showed that the rate of plaque initiation dropped as the blood velocity increased from 30 m/s to 125 m/s; higher inlet velocities gave lower plaque growth; the highest degree of 30% stenosis was recorded at a blood velocity of 30 m/s. Plaque height significantly affects the Plaque wall Stress, PWS, and its distribution around the plaque and arterial wall; higher plaque heights experience higher velocity distribution around the plaque, causing a higher force associated with blood flow around the plaque, resulting in higher compression stress. More compressional stresses are localized around the root, which would encourage growth as well as possible rupture at higher velocities. These ruptured plaques potentially narrow or block the arteries and prevent blood flow. This is atherosclerosis and can lead to a heart attack. Conclusion Results from this study can find significant use in the understanding, management, and treatment of atherosclerosis since the regulation of blood velocity and pressure plays a major role in the progress of atherosclerosis in the carotid artery which raises the risk of stroke.