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在 HeartMate II 支持期间,减速并不会恢复高分子量 von Willebrand 多聚体:一项体内研究。

Speed Reduction Does Not Restore High Molecular Weight von Willebrand Multimers During HeartMate II Support: An In Vivo Study.

机构信息

From the Division of Cardiology, Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York.

Department of Pathology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York.

出版信息

ASAIO J. 2018 Sep/Oct;64(5):e123-e125. doi: 10.1097/MAT.0000000000000831.

Abstract

Acquired von Willebrand Syndrome (AVWS) in patients undergoing continuous-flow left ventricular assist device support is due to the loss of von Willebrand factor (vWF) high molecular weight multimers (HMWMs) by shear-mediated mechanisms. We investigated whether reducing speed in vivo would mitigate the shear effect. In outpatients (n = 6) with a HeartMate II, pump speed was decreased to 8,000 rpm for 6 hours. At baseline (9,140 ± 189 rpm), patients had an AVWS as evidenced by low vWF activity:antigen ratios (0.58 ± 0.13, normal >0.7) and reduced HMWMs. After 6 hours, there was no significant change in either the vWF activity:antigen ratio or the HMWMs. Decreasing pump speed does not ameliorate AVWS.

摘要

获得性 von Willebrand 综合征(AVWS)在接受连续流动左心室辅助装置支持的患者中是由于剪切介导的机制导致 von Willebrand 因子(vWF)高分子量多聚体(HMWM)的丢失。我们研究了降低体内速度是否可以减轻剪切效应。在门诊患者(n=6)中,使用 HeartMate II 将泵速降低至 8000 rpm 持续 6 小时。在基线时(9140±189 rpm),患者表现出 AVWS,表现为 vWF 活性:抗原比值降低(0.58±0.13,正常>0.7)和 HMWM 减少。6 小时后,vWF 活性:抗原比值或 HMWM 均无明显变化。降低泵速并不能改善 AVWS。

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