• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Chronic cardiac resynchronization therapy and reverse ventricular remodeling in a model of nonischemic cardiomyopathy
【24h】

Chronic cardiac resynchronization therapy and reverse ventricular remodeling in a model of nonischemic cardiomyopathy

机译：非缺血性心肌病模型中的慢性心脏再同步治疗和心室重构

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

While cardiac resynchronization therapy (CRT) has been shown to reduce morbidity and mortality in heart failure (HF) patients, the fundamental mechanisms for the efficacy of CRT are poorly understood. The lack of understanding of these basic mechanisms represents a significant barrier to our understanding of the pathogenesis of HF and potential recovery mechanisms. Our purpose was to determine cellular mechanisms for the observed improvement in chronic HF after CRT. We used a canine model of chronic nonischemic cardiomyopathy. After 15 months, dogs were randomized to continued RV tachypacing (untreated HF) or CRT for an additional 9 months. Six minute walk tests, echocardiograms, and electrocardiograms were done to assess the functional response to therapy. Left ventricular (LV) midmyocardial myocytes were isolated to study electrophysiology and intracellular calcium regulation. Compared to untreated HF, CRT improved HF-induced increases in LV volumes, diameters and mass (p<0.05). CRT reversed HF-induced prolongations in LV myocyte repolarization (p<0.05) and normalized HF-induced depolarization (p<0.03) of the resting membrane potential. CRT improved HF-induced reductions in calcium (p<0.05). CRT did not attenuate the HF-induced increases in LV interstitial fibrosis. Using a translational approach in a chronic HF model, CRT significantly improved LV structure; this was accompanied by improved LV myocyte electrophysiology and calcium regulation. The beneficial effects of CRT may be attributable, in part, to improved LV myocyte function. (C) 2007 Elsevier Inc. All rights reserved.
机译：尽管心脏再同步治疗（CRT）可以降低心力衰竭（HF）患者的发病率和死亡率，但对CRT疗效的基本机制了解甚少。缺乏对这些基本机制的理解为我们对HF的发病机理和潜在的恢复机制提供了重要的障碍。我们的目的是确定观察到的CRT后慢性HF改善的细胞机制。我们使用了慢性非缺血性心肌病的犬模型。 15个月后，将狗随机分组，继续进行RV tachypacping（未经治疗的HF）或CRT，持续9个月。进行六分钟步行测试，超声心动图和心电图，以评估对治疗的功能反应。分离左心室（LV）心肌中层细胞，以研究电生理和细胞内钙调节。与未治疗的HF相比，CRT改善了HF诱发的LV体积，直径和质量增加（p <0.05）。 CRT逆转了HF诱导的左室心肌细胞复极化的延长（p <0.05）和归一化的HF诱导的静息膜电位的去极化（p <0.03）。 CRT改善了HF诱导的钙减少（p <0.05）。 CRT不能减弱HF引起的LV间质纤维化的增加。在慢性HF模型中使用平移方法，CRT显着改善了LV结构。这伴随着改善的LV肌细胞电生理和钙调节。 CRT的有益作用可能部分归因于LV心肌细胞功能的改善。 （C）2007 Elsevier Inc.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号