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Recent advances in the molecular pathophysiology of atrial fibrillation

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TLDR
The ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia are discussed, including the potential therapeutic implications that might arise from an improved mechanistic understanding.
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.

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Citations
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Journal ArticleDOI

A brain-stellate ganglion-atrium network regulates atrial fibrillation vulnerability through macrophages in acute stroke.

TL;DR: A brain-stellate ganglion-atrium network may increase AF vulnerability through macrophage activation after acute stroke through increased left stellate Ganglion activity, higher Macrophage infiltration and higher levels of inflammatory cytokines in the atrium.
Journal ArticleDOI

Age-dependent myocardial transcriptomic changes in the rat. Novel insights into atrial and ventricular arrhythmias pathogenesis

TL;DR: The results indicate the induction of an up-regulation transcriptional response in atrial but not ventricular myocytes with advancing age, suggesting that the two chambers undergo different molecular remodeling programs.
Dissertation

Atrial fibrillation and systolic heart failure: the role of myocardial fibrosis and catheter ablation

TL;DR: In this article, the role of catheter ablation as a treatment for systolic dysfunction was evaluated in patients with atrial fibrillation and concurrent Systolic Dysfunction.
Journal ArticleDOI

Should concomitant surgical ablation for atrial fibrillation be performed in elderly patients

TL;DR: The safety and efficacy of concomitant surgical atrial fibrillation ablation in elderly patients was safe and effective independently of age, and Sinus rhythm at discharge and bipolar ablation were significant predictors for successful ablation.
Journal ArticleDOI

Influence of Zoledronic Acid on Atrial Electrophysiological Parameters and Electrocardiographic Measurements.

TL;DR: Zoledronic acid (ZA) has been shown to affect atrial electrophysiological parameters and electrocardiographic measurements in guinea pigs as mentioned in this paper, including APD, ERP, and P wave dispersion.
References
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Journal ArticleDOI

Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins

TL;DR: The pulmonary veins are an important source of ectopic beats, initiating frequent paroxysms of atrial fibrillation and these foci respond to treatment with radio-frequency ablation.
Journal ArticleDOI

Atrial Fibrillation Begets Atrial Fibrillation A Study in Awake Chronically Instrumented Goats

TL;DR: Artificial maintenance of AF leads to a marked shortening of AERP, a reversion of its physiological rate adaptation, and an increase in rate, inducibility and stability of AF.
Journal ArticleDOI

Secular Trends in Incidence of Atrial Fibrillation in Olmsted County, Minnesota, 1980 to 2000, and Implications on the Projections for Future Prevalence

TL;DR: The age-adjusted incidence of AF increased significantly in Olmsted County during 1980 to 2000 and the projected number of persons with AF for the United States will exceed 10 million by 2050, underscoring the urgent need for primary prevention strategies against AF development.
Journal ArticleDOI

Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis

TL;DR: It is concluded that miR-29 acts as a regulator of cardiac fibrosis and represents a potential therapeutic target for tissue fibrosis in general.
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