Department of Cardiology, Medical University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
Heidelberg Center for Heart Rhythm Disorders (HCR), University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
Cells. 2021 Oct 15;10(10):2767. doi: 10.3390/cells10102767.
Ventricular arrhythmias contribute significantly to morbidity and mortality in patients with heart failure (HF). Pathomechanisms underlying arrhythmogenicity in patients with structural heart disease and impaired cardiac function include myocardial fibrosis and the remodeling of ion channels, affecting electrophysiologic properties of ventricular cardiomyocytes. The dysregulation of ion channel expression has been associated with cardiomyopathy and with the development of arrhythmias. However, the underlying molecular signaling pathways are increasingly recognized. This review summarizes clinical and cellular electrophysiologic characteristics observed in dilated cardiomyopathy (DCM) with ionic and structural alterations at the ventricular level. Furthermore, potential translational strategies and therapeutic options are highlighted.
室性心律失常是心力衰竭（HF）患者发病率和死亡率的重要原因。结构性心脏病和心功能受损患者心律失常的发生机制包括心肌纤维化和离子通道重构，从而影响心室肌细胞的电生理特性。离子通道表达的失调与心肌病和心律失常的发生有关。然而，其潜在的分子信号通路正在逐渐被认识。本文总结了伴有离子和结构改变的扩张型心肌病（DCM）的临床和细胞电生理特征，并强调了潜在的转化策略和治疗选择。
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