Back to the future: the role of the autonomic nervous system in atrial fibrillation.
The purpose of this manuscript is to review the current literature regarding the role of the autonomic nervous system (ANS) in atrial fibrillation (AF). We will be reviewing its effect on initiation, maintenance, and termination of AF, with emphasis on the role of baroreflex gain (BRG) and autonomic reflexes in the maintenance of this arrhythmia. While it is generally accepted that the ANS plays an important role in AF, the extent of that role remains controversial. Much of the controversy could be explained by the time frame during which the autonomic measurements were made, the differences in patient population, and possibly the differential effect of the autonomic changes on the trigger versus the substrate. While vagal stimulation results in shortening of the atrial effective refractory period and increased dispersion of refractoriness, its effect on the "trigger" might be antiarrhythmic. During AF, cardiac filling pressure increases while arterial blood pressure decreases sending conflicting messages to the medulla. The acute effect is an increase in sympathetic activity to ensure adequate hemodynamic stability. On the other hand, the long-term effects might be impairment in the cardiopulmonary BRG and changes that accentuate the presence of AF. While radiofrequency ablation has provided us with a unique insight into the role of possible denervation in AF suppression, the exact mechanisms involved are far from being completely understood. Today, in an era where great technological advances have occurred, our need to understand the role of the ANS in AF is greater than ever.
Chen
Jay
J
Department of Internal Medicine, Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Wasmund
Stephen L
SL
Hamdan
Mohamed H
MH
D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D005246:Feedback; D006321:Heart / Q000294:innervation*; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular