在左心室辅助装置支期间的机械卸载增加了左心室原交叉连接和心肌硬度
Stefan Klotz1, Robert F Foronjy, Marc L Dickstein
1Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Circulation
|July 7, 2005
概括
左心室辅助装置 (LVAD) 的支持增加了失灵心脏中的原交联和性. 这些变化与改变的矩阵重塑有关,这表明LVAD会影响细胞外矩阵的组成和功能.
科学领域:
- 心血管研究研究心血管研究
- 生物医学工程 生物医学工程
- 心脏外科手术 心脏外科手术
背景情况:
- 左心室辅助装置 (LVAD) 在失败的心脏中促进反向重塑.
- 在LVAD患者中细胞外矩阵 (ECM) 变化尚不清楚.
- 在LVAD后发生的ECM变化的机制和功能后果需要研究.
研究的目的:
- 研究LVAD支持对心肌细胞外矩阵组成和度的影响.
- 阐明观测到的ECM变化背后的机制.
- 探索左心室和右心室之间LVAD影响的潜在差异.
主要方法:
- 分析了患有异常扩展性心肌病 (DCM) 的患者,包括没有LVAD支持的患者,以及没有失败的对照患者的心脏.
- 对左心室和右心室测量出活体压力-体积关系.
- 心肌组织中的原含量,矩阵金属蛋白酶 (MMPs),金属蛋白酶的组织抑制剂 (TIMPs) 和血管素 (Ang) 被量化.
主要成果:
- 支持LVAD导致左心室 (LV) 尺寸,质量和肌细胞直径的减少.
- 总和交叉连接的原蛋白,以及原蛋白类型I和III的比例在LVAD后显著增加.
- 心肌和腔室硬度在LVAD支持下增加,伴随着改变的MMP/TIMP比率和增加的Ang水平.
结论:
- 支持LVAD会增加LV原交联和I/III型原的比率,导致心肌硬度增加.
- 降低原降解 (较低的MMP-1/TIMP-1) 和刺激合成 (较高的Ang) 可能会导致这些ECM变化.
- 血动力学卸载LV,而不是RV,似乎是这些ECM变化的主要调节者.
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