Increased vulnerability to atrial fibrillation in transgenic mice with selective atrial fibrosis caused by overexpression of TGF-β1
Increased vulnerability to atrial fibrillation in transgenic mice with selective atrial fibrosis caused by overexpression of TGF-β1
复制标题
DOI：
10.1161/01.res.0000129579.59664.9d
复制
发表时间：
2004-06-11
影响因子：
20.1
通讯作者：
Olgin, JE
中科院分区：
文献类型：
--
作者：
Verheule, S;Sato, T;Olgin, JE
对患者和大型动物模型的研究表明心房纤维化在心房颤动（AF）发展中的重要性。为了研究增加的纤维化是否足以产生 AF 的底物，我们研究了 MHC-TGFcys(33)ser 转基因小鼠 (Tx) 的心脏电生理学 (EP) 和房性心律失常的诱导性，这些转基因小鼠的心房纤维化增加，但心室纤维化没有增加。在麻醉小鼠中，野生型 (Wt) 和 Tx 的表面心电图参数没有表现出显着差异。对于经食管心房起搏，除了 Tx 小鼠的校正窦房结恢复时间显着减少外，EP 参数没有观察到显着差异。突发起搏在 29 只 Tx 小鼠中的 14 只中诱导了 AF，而在 Wt 同窝小鼠中未诱导 AF（P
Studies on patients and large animal models suggest the importance of atrial fibrosis in the development of atrial fibrillation (AF). To investigate whether increased fibrosis is sufficient to produce a substrate for AF, we have studied cardiac electrophysiology (EP) and inducibility of atrial arrhythmias in MHC-TGFcys(33)ser transgenic mice (Tx), which have increased fibrosis in the atrium but not in the ventricles. In anesthetized mice, wild-type (Wt) and Tx did not show significant differences in surface ECG parameters. With transesophageal atrial pacing, no significant differences were observed in EP parameters, except for a significant decrease in corrected sinus node recovery time in Tx mice. Burst pacing induced AF in 14 of 29 Tx mice, whereas AF was not induced in Wt littermates (P