A Novel Toroidal-Flow Left Ventricular Assist Device Minimizes Blood Trauma: Implications of Improved Ventricular Assist Device Hemocompatibility
A Novel Toroidal-Flow Left Ventricular Assist Device Minimizes Blood Trauma: Implications of Improved Ventricular Assist Device Hemocompatibility
复制标题
DOI：
10.1016/j.athoracsur.2018.11.053
复制
发表时间：
2019-06-01
影响因子：
4.6
通讯作者：
Smalling, Richard
中科院分区：
文献类型：
--
作者：
Bartoli, Carlo R.;Hennessy-Strahs, Samson;Smalling, Richard
背景连续流左心室辅助装置（LVAD）会导致血液创伤，包括血管性血友病因子降解、血小板活化和亚临床溶血。血液创伤导致出血、血栓形成和中风，这导致显著的发病率和死亡率。TORVAD（Windmill Cardiovascular Systems，Inc，Austin，TX）是首款设计用于最大限度减少血液创伤的环形流LVAD。我们测试了TORVAD比HeartMate II（Abbott Laboratories，普莱森顿，CA）LVAD引起更少血液创伤的假设。使用HeartMate II（n = 8; 10，000 rpm，70 +/- 6 mm Hg，4.0 +/- 0.1 L/min）或TORVAD（n = 6;144 rpm，72 +/- 0.0 mm Hg，43 +/- 0.0 L/min），在离体循环回路中使人全血循环6小时。用电泳和免疫印迹定量测定血管性血友病因子降解。通过分化簇（CD）41/61酶联免疫吸附试验（ELISA）定量血小板活化。用酶联免疫吸附法测定血浆游离血红蛋白含量。TORVAD导致高分子量血管性血友病因子多聚体的降解显著减少（-10% +/- 1% vs -21% +/-1%，p < 0.0001），低分子量血管性血友病因子多聚体的积累（22% +/- 2% vs 45% +/-2%，p < 0.0001）和血管性血友病因子降解片段的积累（7% +/- 1% vs 25% +/-6%，p < 0.05）。TORVAD不活化血小板，而HeartMate II引起显著的血小板活化（CD 41/61：645 +/- 20 ng/mL vs 1，581 +/- 150 ng/mL，p < 0.001;正常人CD 41/61，593 ng/mL;范围：400 - 800 ng/mL）。类似地，TORVAD引起最小的溶血，而HeartMate II引起显著的溶血（血浆游离血红蛋白：11 +/- 2 vs 109 +/- 10 mg/dL，p < 0.0001;正常人血浆游离血红蛋白：11 +/- 2 vs 109 +/- 10 mg/dL，p < 0.0001）。
Background. Continuous-flow left ventricular assist devices (LVADs) cause blood trauma that includes von Willebrand factor degradation, platelet activation, and subclinical hemolysis. Blood trauma contributes to bleeding, thrombosis, and stroke, which cause significant morbidity and mortality. The TORVAD (Windmill Cardiovascular Systems, Inc, Austin, TX) is a first-of-its kind, toroidal-flow LVAD designed to minimize blood trauma. We tested the hypothesis that the TORVAD causes less blood trauma than the HeartMate II (Abbott Laboratories, Pleasanton, CA) LVAD.Methods. Whole human blood was circulated for 6 hours in ex vivo circulatory loops with a HeartMate II (n = 8; 10,000 rpm, 70 +/- 6 mm Hg, 4.0 +/- 0.1 L/min) or TORVAD (n = 6;144 rpm, 72 +/- 0.0 mm Hg, 43 +/- 0.0 L/min). von Willebrand factor degradation was quantified with electrophoresis and immunoblotting. Platelet activation was quantified by cluster of differentiation (CD) 41/61 enzyme-linked immunosorbent assay (ELISA). Hemolysis was quantified by plasma free hemoglobin ELISA.Results. The TORVAD caused significantly less degradation of high-molecular-weight von Willebrand factor multimers (-10% +/- 1% vs -21% +/- 1%, p < 0.0001), accumulation of low-molecular-weight von Willebrand factor multimers (22% +/- 2% vs 45% +/- 2%, p < 0.0001), and accumulation of von Willebrand factor degradation fragments (7% +/- 1% vs 25% +/- 6%, p < 0.05) than the HeartMate II. The TORVAD did not activate platelets, whereas the HeartMate II caused significant platelet activation (CD 41/61: 645 +/- 20 ng/mL vs 1,581 +/- 150 ng/mL, p < 0.001; normal human CD 41/61, 593 ng/mL; range, 400 to 800 ng/mL). Similarly, the TORVAD caused minimal hemolysis, whereas the HeartMate II caused significant hemolysis (plasma free hemoglobin: 11 +/- 2 vs 109 +/- 10 mg/dL, p < 0.0001; normal human plasma free hemoglobin