Pandit Sandeep V, Workman Antony J
Department of Internal Medicine - Cardiology, Center for Arrhythmia Research, University of Michigan, Ann Arbor, MI, USA.
Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
Clin Med Insights Cardiol. 2016 Oct 31;10(Suppl 1):41-46. doi: 10.4137/CMC.S39713. eCollection 2016.
Heart failure (HF) causes complex, chronic changes in atrial structure and function, which can cause substantial electrophysiological remodeling and predispose the individual to atrial fibrillation (AF). Pharmacological treatments for preventing AF in patients with HF are limited. Improved understanding of the atrial electrical and ionic/molecular mechanisms that promote AF in these patients could lead to the identification of novel therapeutic targets. Animal models of HF have identified numerous changes in atrial ion currents, intracellular calcium handling, action potential waveform and conduction, as well as expression and signaling of associated proteins. These studies have shown that the pattern of electrophysiological remodeling likely depends on the duration of HF, the underlying cardiac pathology, and the species studied. In atrial myocytes and tissues obtained from patients with HF or left ventricular systolic dysfunction, the data on changes in ion currents and action potentials are largely equivocal, probably owing mainly to difficulties in controlling for the confounding influences of multiple variables, such as patient's age, sex, disease history, and drug treatments, as well as the technical challenges in obtaining such data. In this review, we provide a summary and comparison of the main animal and human electrophysiological studies to date, with the aim of highlighting the consistencies in some of the remodeling patterns, as well as identifying areas of contention and gaps in the knowledge, which warrant further investigation.
心力衰竭（HF）会导致心房结构和功能发生复杂的慢性变化，这可能会引起显著的电生理重塑，并使个体易患心房颤动（AF）。用于预防HF患者发生AF的药物治疗方法有限。更好地了解促进这些患者发生AF的心房电和离子/分子机制，可能会带来新治疗靶点的发现。HF动物模型已确定心房离子电流、细胞内钙处理、动作电位波形和传导以及相关蛋白的表达和信号传导存在众多变化。这些研究表明，电生理重塑模式可能取决于HF的持续时间、潜在的心脏病理状况以及所研究的物种。在从HF患者或左心室收缩功能障碍患者获取的心房肌细胞和组织中，关于离子电流和动作电位变化的数据大多模棱两可，这可能主要是由于难以控制多个变量的混杂影响，如患者的年龄、性别、病史和药物治疗，以及获取此类数据时的技术挑战。在本综述中，我们对迄今为止主要的动物和人类电生理研究进行了总结和比较，目的是突出一些重塑模式中的一致性，以及确定存在争议的领域和知识空白，这些都值得进一步研究。
