Sinus node dysfunction and atrial fibrillation: Which one dominates?

Abstract

Atrial fibrillation (AF) is themost common sustained arrhythmia in clinical practice. After the breakthrough study showing the importance of pulmonary veins (PVs) as the trigger of AF, a huge number of interesting clinical and experimental studies have been done on the pathophysiology and treatment of atrial fibrillation in the last decade [1]. We read the exciting article written by Chen and colleagues evaluating whether sinoatrial node (SAN) electrical activity modulates pulmonary veins' (PVs) arrhythmogenesis [2]. In their experimental animal study, they have used conventional microelectrodes and multi-electrode array system to simultaneously record the electrical activity and conduction properties of rabbit SAN and PV tissue preparations with and without SAN-PV interruptions before and after perfusion with Anemonia sulcata toxin (ATX)-II or isoproterenol. They have found that, after SAN-PV disconnection, ATX-II induced burst firing and early after depolarizations in PVs in 8 out of 9 preparations, as opposed to 5 out of 9 preparations before disconnection, and concluded that SAN electrical activity modulates PV arrhythmogenesis and therefore SAN-PV conduction block can increase PV arrhythmogenesis. We think that this study would prove invaluable in the understanding of the frequent observation of AF in cases with sick sinus syndrome (SSS), i.e. tachycardia–bradycardia syndrome. The key question to answer in a case displaying signs of both SAN dysfunction and AF is which one dominates the other. In other words, the important point is whether AF develops as a result of underlying SAN dysfunction, or vice versa, or does a common pathophysiological process cause both SSS and AF. It has long been recognized that SSS is associatedwith an increased risk of AF [3]. SSS is primarily a disease of the elderly and is presumed to be due to senescence of the sinus node and atrial muscle [4]. Therefore, SSS likely reflects an underlying atrial disease that may be involved as a substrate of AF both functionally and anatomically. An increase in the time window due to sinus bradycardia can strongly facilitate the conditions for AF occurrence by both increasing the atrial ectopy and dispersion of the refractoriness, which are the main functional sources for initiation of AF [5]. Additionally, based on the result of the study done by Chen et al., one can also speculate that sinus node dysfunction itself may also increase PV arrhythmogenesis which will further facilitate the triggering of AF. Senescence of the atrial muscle leading to increasing of the atrial fibrosis will also serve the anatomical substrate for AF.