Do genetics help to better understand the underlying mechanisms of atrial fibrillation?

Abstract

Atrial fibrillation (AF) commonly occurs in the context of structural heart disease and is accompanied by atrial remodelling. The latter refers to any change in atrial function that promotes AF or occurs as a consequence of the arrhythmia.1 Atrial remodelling in the aged heart and during heart failure is characterized by pronounced fibrosis leading to heterogeneous slowing conduction of and prolongation of effective refractory period (ERP). In contrast, atrial remodelling induced by tachycardia is associated with shorter ERP and impaired rate adaptation. Nevertheless, atrial remodelling cannot be an absolute prerequisite for AF because the arrhythmia may also occur in structurally normal hearts, alluding to the existence of acquired or genetically determined predisposing factors. Current knowledge of the molecular identity of the predisposing factors is, however, limited. Fatini et al .2 provide evidence that susceptibility to non-valvular AF (NVAF) may be enhanced in association with certain single nucleotide polymorphisms in the genes encoding the accessory K+ channel subunit minK and the endothelial nitric oxide synthase (eNOS). They studied a serine to glycine exchange in position 38 of minK protein (minK S38G) and several polymorphisms in the eNOS gene including … *Corresponding author. Tel: +49 351 4586279; fax: +49 351 4586315. E-mail address : dobrev{at}rcs.urz.tu-dresden.de