Role of neural modulation in the pathophysiology of atrial fibrillation

Abstract

Atrial-fibrillation (AF) is the most common clinically encountered arrhythmia affecting over 1 per cent of population in the United States and its prevalence seems to be moving only in forward direction. A recent systemic review estimates global prevalence of AF to be 596.2 and 373.1 per 100,000 population in males and females respectively. Multiple mechanisms have been put forward in the pathogenesis of AF, however; multiple wavelet hypothesis is the most accepted theory so far. Similar to the conduction system of the heart, a neural network exists which surrounds the heart and plays an important role in formation of the substrate of AF and when a trigger is originated, usually from pulmonary vein sleeves, AF occurs. This neural network includes ganglionated plexi (GP) located adjacent to pulmonary vein ostia which are under control of higher centers in normal people. When these GP become hyperactive owing to loss of inhibition from higher centers e.g. in elderly, AF can occur. We can control these hyperactive GP either by stimulating higher centers and their connections, e.g. vagus nerve stimulation or simply by ablating these GP. This review provides detailed information about the different proposed mechanisms underlying AF, the exact role of autonomic neural tone in the pathogenesis of AF and the possible role of neural modulation in the treatment of AF.