Electrophysiological changes in heart failure and their implications for arrhythmogenesis

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1832

Review

Coronel, R.¹  Wilders, Ronald²  Verkerk, Arie O.²  Wiegerinck, Rob F.³  Benoist, David^4,5  Bernus, Olivier^4,5 

[1] Univ Amsterdam, Acad Med Ctr, Dept Expt Cardiol, Ctr Heart, NL-1105 AZ Amsterdam, Netherlands

[2] Univ Amsterdam, Acad Med Ctr, Dept Anat Embryol & Physiol, NL-1105 AZ Amsterdam, Netherlands

[3] Maastricht Univ, Cardiovasc Res Inst Maastricht CARIM, Dept Physiol, Maastricht, Netherlands

[4] Univ Bordeaux, INSERM, U1045, Ctr Rech Cardiothorac, Bordeaux, France

[5] Univ Bordeaux, Inst Rythmol & Modelisat Cardiaque, Bordeaux, France

关键词: Heart failure;    Arrhythmia mechanism;    Intercellular coupling;    Diet;    Stretch;    Pulmonary hypertension;   

DOI  :  10.1016/j.bbadis.2013.04.002

来源: Elsevier

【 摘 要 】

Heart failure is the final common pathway of various cardiac pathologies and is associated with sudden cardiac death, mostly caused by ventricular arrhythmias. In this paper we briefly review the electrophysiological remodeling and the alterations in intracellular calcium handling, and the resulting arrhythmogenic mechanisms associated with heart failure. Intercellular uncoupling and fibrosis are identified as a major arrhythmogenic factors. Diet and ventricular wall stretch are discussed as modulating factors. Finally, emphasis is placed on the hitherto poorly studied aspects of right ventricular failure. This article is part of a Special Issue entitled: Heart failure pathogenesis and emerging diagnostic and therapeutic interventions. (C) 2013 Elsevier B.V. All rights reserved.

【 授权许可】

Free