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Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

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通过左心室辅助装置的慢性卸载逆转了收缩功能障碍,并改变了末期心力衰竭中的基因表达

P M Heerdt¹, J W Holmes, B Cai

¹Departments of Medicine, Surgery, and Biomedical Engineering, Columbia University, New York, NY, USA. pmheerd@mail.med.cornell.edu

|November 30, 2000

概括

左心室辅助装置 (LVAD) 支持改善心肌强度,并逆转心力衰竭中异常收缩模式. 这种重塑涉及处理蛋白的基因表达增加,SERCA2a蛋白显著增加.

科学领域:

心血管生理学心血管生理学
分子心脏病学分子心脏病学
生物医学工程生物医学工程

背景情况:

心力衰竭的特点是心肌收缩能力受损和处理改变.
左心室辅助器件 (LVAD) 用于支持失败的心脏.

研究的目的:

为了研究LVAD支持对完整的人类心肌的力频关系 (FFR) 的影响.
为了确定LVAD植入是否改变了参与心脏 (Ca2+) 处理的基因的表达.

主要方法:

在LVAD支持之前和之后,从心力衰竭患者的左心室 (LV) 轨道上测量了同度力频率关系 (FFR).
通过使用Northern blot分析了SERCA2a,氨酸受体和Na+-Ca2+交换器的基因表达 (mRNA).
蛋白质水平和sarcoplasmic reticular Ca2+吸收通过西方斑点和功能测试进行了评估.

主要成果:

支持LVAD在1Hz刺激时改善了收缩力,并逆转了末期心力衰竭中观察到的负FFR.
在LVAD植入后,SERCA2a,瑞诺丁受体和Na+-Ca2+交换器的mRNA水平上调.
只有SERCA2a蛋白水平显著增加,与增强的质细胞网状Ca2+吸收相关.

结论:

支持LVAD增强心肌收缩强度,并使终端心力衰竭患者的FFR正常化.
LVADs诱导反向分子重塑,对关键的处理基因进行上调.
增加的SERCA2a蛋白质含量是一个关键的功能适应,有助于改善LVAD后的心脏收缩性.

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