Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. The prevalence of AF increases dramatically with age and is seen in as high as 9% of individuals by the age of 80 years. In high-risk patients, the thromboembolic stroke risk can be as high as 9% per year and is associated with a 2-fold increase in mortality. Although the pathophysiological mechanism underlying the genesis of AF has been the focus of many studies, it remains only partially understood. Conventional theories focused on the presence of multiple re-entrant circuits originating in the atria that are asynchronous and conducted at various velocities through tissues with various refractory periods. Recently, rapidly firing atrial activity in the muscular sleeves at the pulmonary veins ostia or inside the pulmonary veins have been described as potential mechanism,. AF results from a complex interaction between various initiating triggers and development of abnormal atrial tissue substrate. The development of AF leads to structural and electrical changes in the atria, a process known as remodeling. To have effective surgical or catheter ablation of AF good understanding of the possible mechanism(s) is crucial.
Once initiated, AF alters atrial electrical and structural properties that promote its maintenance and recurrence. The role of atrial remodeling (AR) in the development and maintenance of AF has been the subject of many animal and human studies over the past 10-15 years. This review will discuss the mechanisms of AR, the structural, electrophysiologic, and neurohormonal changes associated with AR and it is role in initiating and maintaining AF. We will also discuss briefly the role of inflammation in AR and AF initiation and maintenance, as well as, the possible therapeutic interventions to prevent AR, and hence AF, based on the current understanding of the interaction between AF and AR.
Credits: Bandar A Ghamdi, MD; Walid Hassan, MD, FACP, FACC, FCCP, FAHA