Abstract
Atrial fibrillation (AF) is the most common arrhythmia and a major cause of morbidity and mortality in an aging population. Unfortunately, current treatments for AF are suboptimal, in large part because the molecular mechanisms underlying AF are not well understood. Recent advances in our understanding of the AF disease state have led to the preclinical development of gene-based therapies that are targeted to key molecular mechanisms involved in the genesis and maintenance of AF.