Local Innervation and Atrial Fibrillation

A trial fibrillation (AF) is the most common human arrhythmia in the world and, depending on individual demographics, afflicts from 0.1% to 4% of the general population. However, despite its ubiquitous presence in adult medicine, AF remains an enigmatic disease whose pathophysiology is very complex and incompletely understood. Unlike traditional macroreentrant arrhythmias that arise from better understood electrophysiological substrates, AF is a more complex disease arising from multiple, mutually interacting mechanisms. In part, because of our incomplete understanding of the mechanisms underlying AF, therapeutic success rates in patients treated with either antiarrhythmic drug therapy, catheter-based ablation, or both remain highly variable. merging data from the basic science laboratory is starting to shed some light on the mechanistic basis of this disease, which may lead to the development of long-term therapies for patients with AF. One of the ideas that has persisted for several decades about AF, and is fast gaining traction, is that there may be a strong contribution from the autonomic nervous system in both the initiation and maintenance of this disease. he structural basis for this theory stems from the discovery of rich autonomic innervation and ganglionated plexi (GP) associated with the pulmonary veins and sites in the atria from which AF triggers often originate. Although the exact causal relationship between these autonomic connections and the initiation of AF is not well understood, anecdotal clinical and laboratory findings suggest that such a link is plausible. In this review, we will explore our current understanding of the cardiac nervous system and its role in the pathogenesis of AF, with an eye toward future therapeutic strategies that could exploit this relationship.