Purpose of review: Atrial fibrillation usually occurs in the context of an atrial substrate produced by alterations in atrial tissue properties referred to as remodeling. Remodeling can result from cardiac disease, cardiac arrhythmias, or biologic processes such as senescence. Recent advances in understanding remodeling have allowed for insights into mechanisms underlying atrial fibrillation that have been transferred from experimental models to humans. This paper reviews recent progress in understanding atrial remodeling, as well as the consequent clinical insights into atrial fibrillation pathophysiology and treatment.
Recent findings: Two principal forms of remodeling have been described in animal models of atrial fibrillation: ionic remodeling, which affects cellular electrical properties, and structural remodeling, which alters atrial tissue architecture. Atrial tachycardias (particularly rapid tachyarrhythmias such as atrial flutter and atrial fibrillation) cause ionic remodeling, which decreases the atrial refractory period and promotes atrial reentry. Congestive heart failure produces atrial interstitial fibrosis, which promotes arrhythmogenesis by interfering with atrial conduction properties. Recent animal studies have provided insights into the pathways involved in remodeling, and have indicated the pathophysiological role of remodeling in specific contexts. In addition, work in animal models has provided information about pharmacological interventions that can prevent the development of remodeling. Clinical studies have shown that novel approaches to remodeling prevention identified in animal work have potential therapeutic value in man.
Summary: Understanding atrial remodeling has the potential to improve our appreciation of the pathophysiology of clinical atrial fibrillation and to allow for the development of useful new therapeutic approaches.