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Recent advances in the molecular pathophysiology of atrial fibrillation
Reza Wakili, … , Dobromir Dobrev, Stanley Nattel
Reza Wakili, … , Dobromir Dobrev, Stanley Nattel
Published August 1, 2011
Citation Information: J Clin Invest. 2011;121(8):2955-2968. https://doi.org/10.1172/JCI46315.
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Science in Medicine

Recent advances in the molecular pathophysiology of atrial fibrillation

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Abstract

Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in understanding the underlying molecular pathobiology. This article reviews the basic mechanisms and molecular processes causing AF. We discuss the ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia. We conclude with a discussion of the potential therapeutic implications that might arise from an improved mechanistic understanding.

Authors

Reza Wakili, Niels Voigt, Stefan Kääb, Dobromir Dobrev, Stanley Nattel

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Figure 4

Tissue mechanisms leading to AF and clinical forms.

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Tissue mechanisms leading to AF and clinical forms.
(A) Ectopic activity...
(A) Ectopic activity can act as a driver maintaining AF or as a trigger on a vulnerable substrate resulting in reentry (single- or multiple-circuit). Local driver mechanisms (ectopic or single-circuit reentrant) produce irregular fibrillatory activity via fibrillatory conduction. Rapid atrial activity (tachycardia) causes atrial remodeling, promoting multiple-circuit reentry. (B) Clinical AF can manifest as paroxysmal AF (self-terminating), persistent AF (requires drug therapy or electrical cardioversion to terminate), and permanent AF (non-terminating). Focal ectopic drivers are principally associated with paroxysmal forms, functional reentrant substrates with persistent AF, and increasingly fixed substrates with permanent forms.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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