Department of Medical Physiology, University Medical Center, Utrecht, The Netherlands.
J Cardiovasc Pharmacol. 2011 Jun;57(6):630-8. doi: 10.1097/FJC.0b013e318207a35f.
In this review article about fibrosis and arrhythmias, we show that the amount of collagen, a normal element of the heart muscle, increases with age and in heart disease. The relation between fibrosis and electrophysiological parameters such as conduction, fractionation of electrograms, abnormal impulse initiation as well as arrhythmogenicity is discussed. Next to the amount of fibrosis, we offer data suggesting that collagen texture too plays a role in conduction slowing and arrhythmia vulnerability. Data are shown revealing that fibrosis can also be induced by reduced sodium channel and connexin43 expression. Finally contrast-enhanced magnetic resonance to detect fibrosis and ventricular tachycardia vulnerability in a noninvasive way as well as a reduction of fibrosis and arrhythmogenicity by inhibition of the renin-angiotensin-aldosterone system is discussed.
在这篇关于纤维化和心律失常的综述文章中,我们表明,胶原蛋白(心肌的正常成分)的含量会随着年龄的增长和心脏病的发生而增加。讨论了纤维化与电生理参数(如传导、心电图的分段、异常冲动起始以及致心律失常性)之间的关系。除了纤维化的程度,我们还提供了一些数据,表明胶原纤维的结构也在传导减慢和心律失常易感性中起作用。研究数据表明,纤维化也可以由减少钠通道和连接蛋白 43 的表达而引起。最后,还讨论了通过对比增强磁共振以非侵入性方式检测纤维化和室性心动过速易感性,以及通过抑制肾素-血管紧张素-醛固酮系统来减少纤维化和致心律失常性。