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收缩期机械瓣膜与生物瓣膜的血小板激活情况

Platelet activation of mechanical versus bioprosthetic heart valves during systole.

作者信息

Hedayat Mohammadali, Asgharzadeh Hafez, Borazjani Iman

机构信息

Department of Mechanical and Aerospace Engineering, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.

Department of Mechanical and Aerospace Engineering, University at Buffalo, State University of New York, Buffalo, NY 14260, USA.

出版信息

J Biomech. 2017 May 3;56:111-116. doi: 10.1016/j.jbiomech.2017.03.002. Epub 2017 Mar 11.

Abstract

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.

摘要

血栓形成是机械心脏瓣膜(MHV)接受者的主要担忧,这要求他们终身服用抗凝药物。生物人工心脏瓣膜(BHV)不需要终身抗凝治疗,但在10 - 15年后会退化。血栓形成是由血小板活化引发的,人们认为这主要是在MHV中由通过铰链的血流和舒张期的泄漏血流产生的。然而,我们的结果表明,收缩期主流中的活化也可能起着至关重要的作用。这是基于我们在完全相同的条件下,通过比较MHV和BHV(作为对照)在剪切诱导血小板活化方面的血栓形成性能所获得的结果。测试了三种不同的数学活化模型,包括线性活化水平、损伤累积和苏亚雷斯模型,以使用先前在相同生理血流条件下通过直主动脉中的MHV和BHV的血流模拟来量化收缩期的血小板活化。结果表明,收缩期开始时MHV中的血小板活化略低于BHV。然而,在收缩期末期,对于所有测试的血小板活化模型,MHV中由主流引起的血小板活化比BHV高几倍(线性活化水平、损伤累积和苏亚雷斯模型分别为1.41、5.12和2.81)。

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