Baczko István, Leprán István, Kiss Loránd, Muntean Danina M, Light Peter E
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Szeged, Dom ter 12., 6720 Szeged, Hungary.
Curr Pharm Des. 2015;21(8):1011-29. doi: 10.2174/1381612820666141029101305.
Heart failure (HF) is a clinical syndrome characterized by significant impairment of cardiac ventricular function. Atrial fibrillation (AF) is the most commonly observed sustained arrhythmia in clinical practice. Both HF and AF are associated with increased morbidity and mortality and their prevalence increases with age. Approximately 50% of patients with moderate HF die due to ventricular fibrillation that leads to sudden cardiac death. Patients with AF exhibit increased mortality due to HF and stroke. HF and AF often co-exist, and the development of the other condition further deteriorates prognosis. Both chronic HF and AF lead to structural and electrophysiological changes in the heart called remodeling, modifying therapeutic targets including those for antiarrhythmic intervention. Current pharmacological treatment of arrhythmias has major limitations due to low efficacy and serious adverse effects. In this review, the main aspects of electrical remodeling in HF and AF are discussed along with possible novel targets identified for future pharmacological antiarrhythmic therapy.
心力衰竭（HF）是一种以心室功能严重受损为特征的临床综合征。心房颤动（AF）是临床实践中最常见的持续性心律失常。HF和AF均与发病率和死亡率增加相关，且其患病率随年龄增长而升高。约50%的中度HF患者死于导致心源性猝死的心室颤动。AF患者因HF和中风而死亡率增加。HF和AF常并存，另一种疾病的发生会进一步恶化预后。慢性HF和AF都会导致心脏发生结构和电生理变化，即重构，从而改变治疗靶点，包括抗心律失常干预的靶点。目前心律失常的药物治疗由于疗效低和严重不良反应而存在重大局限性。在本综述中，将讨论HF和AF电重构的主要方面以及为未来抗心律失常药物治疗确定的可能新靶点。
