在患有缺血性心肌病的患者中,心肌细胞的结构重塑
A M Gerdes1, S E Kellerman, J A Moore
1Department of Anatomy, University of South Florida, College of Medicine, Tampa 33612.
Circulation
|August 1, 1992
概括
在缺血性心肌病 (ICM) 中,心室扩张主要是由心肌细胞长度增加引起的,而不是滑落. 肌细胞形状的这种变化有助于增加心脏壁的压力.
科学领域:
- 心血管生物学 心血管生物学
- 进行心脏重塑.
- 心脏衰竭病理生理学 病理生理学
背景情况:
- 慢性缺血性心脏病可以导致心室扩张和充血性心力衰竭,这种情况被称为缺血性心肌病 (ICM).
- 导致ICM中心室扩张的心肌细胞形状的具体变化以前没有被理解.
研究的目的:
- 在缺血性心肌病的背景下,研究心肌细胞尺寸和形状的变化.
- 为了确定细胞内变化 (肌细胞延长) 或细胞外变化 (肌细胞滑动) 是否对ICM中的腔室扩张负责.
主要方法:
- 隔离的左心室肌细胞来自ICM患者的心脏和正常冠状动脉 (NCA) 的不衰竭供体心脏.
- 肌细胞尺寸,包括长度和宽度,经过定量评估,并在ICM和NCA组之间进行了比较.
主要成果:
- 与NCA心脏的肌细胞相比,ICM心脏的肌细胞显著更长 (40%的增加) 并具有更大的长度/宽度比率 (49%的增加).
- 两组之间没有观察到肌细胞宽度或瘤长度的显著差异.
- 观察到的肌细胞长度的增加与ICM患者的末端透气直径的记录增加密切相似.
结论:
- 肌细胞长度增加,一种细胞内变化,是缺血性心肌病中腔室扩张的主要驱动因素.
- 肌细胞形状的不适应性重塑,特别是长宽比的增加,可能会加剧ICM中心脏壁应力升高.
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