Pathophysiology of atrial fibrillation

Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in the clinic. It is often associated with hemodynamic and neurohormonal cardiovascular abnormalities, including heart failure (HF), hypertension, valvular and ischemic heart disease. These derangements cause or promote the development of AF triggers and atrial remodeling giving rise to the arrhythmogenic substrate. Rapid activation of the atria during AF leads to further electrical and structural remodeling, thus facilitating the maintenance of AF. For his reason, AF is said to beget-AF. Pulmonary veins are the prime source for AF trigger(s) and may also be the source for AF drivers. Pulmonary vein sleeves are thin muscular structures and as such are sensitive to pressure and volume overload-induced stretch, which may account for their exceptional arrhythmogenic proclivity. Long-term maintenance of AF is believed to be due largely to a reentrant mechanism(s), but direct evidence is often lacking and the controversy continues. The development and maintenance of AF are multifactorial and involve dynamic pathophysiologic processes which are in many cases not well defined or understood. This chapter reviews our current understanding of pathophysiology of AF.