Platelet activation of mechanical versus bioprosthetic heart valves during systole. 2017

Mohammadali Hedayat, and Hafez Asgharzadeh, and Iman Borazjani
Department of Mechanical and Aerospace Engineering, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.

Thrombus formation is a major concern for recipients of mechanical heart valves (MHVs), which requires them to take anticoagulant drugs for the rest of their lives. Bioprosthetic heart valves (BHVs) do not require life-long anticoagulant therapy but deteriorate after 10-15years. The thrombus formation is initiated by the platelet activation which is thought to be mainly generated in MHVs by the flow through the hinge and the leakage flow during the diastole. However, our results show that the activation in the bulk flow during the systole phase might play an essential role as well. This is based on our results obtained by comparing the thrombogenic performance of a MHV and a BHV (as control) in terms of shear induced platelet activation under exactly the same conditions. Three different mathematical activation models including linear level of activation, damage accumulation, and Soares model are tested to quantify the platelet activation during systole using the previous simulations of the flow through MHV and BHV in a straight aorta under the same physiologic flow conditions. Results indicate that the platelet activation in the MHV at the beginning of the systole phase is slightly less than the BHV. However, at the end of the systole phase the platelet activation by the bulk flow for the MHV is several folds (1.41, 5.12, and 2.81 for linear level of activation, damage accumulation, and Soares model, respectively) higher than the BHV for all tested platelet activation models.

UI MeSH Term Description Entries
D008955 Models, Cardiovascular Theoretical representations that simulate the behavior or activity of the cardiovascular system, processes, or phenomena; includes the use of mathematical equations, computers and other electronic equipment. Cardiovascular Model,Cardiovascular Models,Model, Cardiovascular
D006350 Heart Valve Prosthesis A device that substitutes for a heart valve. It may be composed of biological material (BIOPROSTHESIS) and/or synthetic material. Prosthesis, Heart Valve,Cardiac Valve Prosthesis,Cardiac Valve Prostheses,Heart Valve Prostheses,Prostheses, Cardiac Valve,Prostheses, Heart Valve,Prosthesis, Cardiac Valve,Valve Prostheses, Cardiac,Valve Prostheses, Heart,Valve Prosthesis, Cardiac,Valve Prosthesis, Heart
D006351 Heart Valves Flaps of tissue that prevent regurgitation of BLOOD from the HEART VENTRICLES to the HEART ATRIA or from the PULMONARY ARTERIES or AORTA to the ventricles. Cardiac Valves,Cardiac Valve,Heart Valve,Valve, Cardiac,Valve, Heart,Valves, Cardiac,Valves, Heart
D001011 Aorta The main trunk of the systemic arteries. Aortas
D013599 Systole Period of contraction of the HEART, especially of the HEART VENTRICLES. Systolic Time Interval,Interval, Systolic Time,Intervals, Systolic Time,Systoles,Systolic Time Intervals,Time Interval, Systolic,Time Intervals, Systolic
D015539 Platelet Activation A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. Activation, Platelet,Activations, Platelet,Platelet Activations

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