Key result
Pulmonary vein triggers and functional re-entry drive atrial fibrillation pathogenesis and progressive remodeling.
This review summarizes current mechanistic theories of atrial fibrillation pathophysiology and their clinical implications.
Supports vein-targeted ablation in practice; leaves open a unifying AF mechanism.
Atrial fibrillation (AF) is the most common sustained dysrhythmia in adults. It is ironic, then, that although mechanisms and effective treatments for most other supraventricular tachyarrhythmias have been discovered, AF remains incompletely understood and poorly treated. Nonetheless, our understanding of the pathophysiology of AF has improved in the last half-century, including some groundbreaking observations made in the last 10 years. Indeed, for some patients, the potential for cure now appears to be available. Because no unifying mechanism of AF has been proven, the aim of this review is to describe some of the common and important concepts behind current mechanistic theories of AF and how they contribute to our clinical understanding of AF.
No takes yet. Share an insight, caveat, or question.
George D. Veenhuyzen (2004) conducted a review in Atrial fibrillation. Current understanding of atrial fibrillation attributes its pathophysiology to functional re-entry and focal triggers primarily from the pulmonary veins, leading to electrical and structural remodeling.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: