Sinus node dysfunction and atrial fibrillation: two sides of the same coin?

Abstract

This editorial refers to ‘Sinus node dysfunction in atrial fibrillation patients: the evidence of regional atrial substrate remodelling’ by H.-Y. Chang et al ., on page 205–211 The original description of the sinus node by Arthur Keith over a century ago outlined a small structure at the junction of the superior vena cava (SVC) and the right atrium (RA). Intraoperative and clinical mapping studies indicate that the ‘functional’ pacemaker actually encompasses a much larger region of posterolateral RA. This pacemaker complex extends from the SVC-RA junction inferiorly along the long axis of the crista terminalis virtually to the inferior vena cava (IVC)-RA junction.1 This complex was shown to be multi-centric, often demonstrating two or occasionally three sites of virtually simultaneous activation and exit to the atria. Physiological influences can alter the position of the lead pacemaker region, which shows cranial shift under sympathetic influence and caudal shift when the vagus predominates. Thus, there is considerable redundancy in the sino-atrial (SA) pacemaker complex, which may hold evolutionary advantages, an observation underscored by studies demonstrating that extensive ablation is required to affect sinus node function in the normal atrium.2 Recent high-density mapping studies have demonstrated the presence of preferential pathways of conduction between the sinus node and the exit of sinus activity to the atria.3 Although the location of the pacemaker region can vary, the gradual decrease in membrane potential that …