Muscarinic subtype-2 receptor autoantibodies: actors or bystanders in human atrial fibrillation?

This editorial refers to “Autoantibodies against M2 muscarinic acetylcholine receptors: new upstream targets in atrial fibrillation in patients with dilated cardiomyopathy”1 by A. Baba et al. on page 1108 Atrial fibrillation (AF) is currently the most common cardiac arrhythmia in the clinical setting. It is associated with a shortening of action potential duration (APD) and effective refractory period (ERP) and a loss of physiological rate-dependent adaptation that can be explained by concomitant alterations in ion channel activity.1 These electrophysiological changes (electrical remodelling) promote the induction and the persistence of the arrhythmia. In addition, changes in the autonomic nervous system are important for initiation and perpetuation of AF. Vagal stimulation shortens atrial APD and ERP and increases dispersion of atrial ERPs.2 This creates an arrhythmogenic substrate for re-entry of the excitation wave front which may allow the arrhythmia to became sustained. Although there is no doubt that the parasympathetic nervous system contributes to initiation of AF, its precise role in the chronic state of the arrhythmia is currently unknown.