Pathophysiology of Atrial Fibrillation - Current Concepts

Atrial fibrillation (AF) is the most common supraventricular tachycardia and its incidence increases with age. The pathophysiology of AF has been studied extensively and is a subject of continuing research. The primary pathologic change seen in AF is progressive fibrosis of the atria and hence structural remodeling, is the mainstay in many forms of AF. Dilation of the atria can be due to almost any structural abnormality of the heart which includes valvular heart disease, hypertension or congestive heart failure. Electrical remodeling promotes AF by acting on fundamental arrhythmia mechanism: focal ectopic activity and reentry. Rapidly firing foci initiating paroxysmal AF arise most commonly from the atrial myocardial sleeves that extend into pulmonary veins. The evolution of AF from paroxysmal to persistent to permanent forms through atrial remodeling can be caused by the arrhythmia itself and/or progression of underlying heart disease. The development of functional reentry substrates contribute to persistent AF. AF-related reentry is currently thought to occur through two main concepts: (1) the leadingcircle concept and (2) spiral wave reentry. The multiple wavelets hypothesis, particularly in advanced structural and electrical remodelling are present, maintains AF survival, causing the most frequent common final pathway in sustained AF.