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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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Journal ArticleDOI

Cardiac Ion Channel Regulation in Obesity and the Metabolic Syndrome: Relevance to Long QT Syndrome and Atrial Fibrillation

TL;DR: Cardiac ion channel/Ca handling proteins remodeling that predispose to arrhythmias are reviewed to have a significant medical and economic impact.
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Low level tragus nerve stimulation is a non-invasive approach for anti-atrial fibrillation via preventing the loss of connexins

TL;DR: It is hypothesized that LL-TS exertedanti-atrial fibrillatory effect via the downregulation of atrial Cx40 and Cx43, but also observed that RAP after 9 h could reducethelevel ofatrial level and LL- TS could significantly shorten AFduration and prolong AF cycle length.
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German Cardiac Society Working Group on Cellular Electrophysiology state-of-the-art paper: impact of molecular mechanisms on clinical arrhythmia management.

TL;DR: The significance of cellular electrophysiological findings for clinical arrhythmia management constitutes the main focus of this document and the establishment and support of cellular and translational Electrophysiology programs in clinical rhythmology departments is called for to improve basic-science-guided patient management.
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Anti-arrhythmic strategies for atrial fibrillation: The role of computational modeling in discovery, development, and optimization.

TL;DR: Several examples are offered of how computational modeling can provide a quantitative framework for integrating multiscale data to gain insight intoMultiscale mechanisms of AF and identify and test pharmacological and electrical therapy and interventions and support clinical decisions.
Journal ArticleDOI

Atrial-Selective Potassium Channel Blockers.

TL;DR: The molecular and electrophysiologic characteristics of atrial-selective K(+) channels and their potential pathophysiologic role in AF are reviewed and currently available K(+) channel blockers are summarized focusing on the most important compounds.
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.
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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.
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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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