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.read more
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Journal ArticleDOI
TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control.
Patrick Lugenbiel,Fabian Wenz,Pascal Syren,Pascal Geschwill,Katharina Govorov,Claudia Seyler,Derk Frank,Patrick A. Schweizer,Jennifer Franke,Tanja Weis,Claus Bruehl,Bastian Schmack,Arjang Ruhparwar,Matthias Karck,Norbert Frey,Hugo A. Katus,Dierk Thomas +16 more
TL;DR: Mechanistic and potential therapeutic significance of TREK-1 channels are suggested in a subgroup of AF patients with HF and prolonged atrial effective refractory periods, consistent with prior observations in humans with HF.
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Management of atrial fibrillation in the year 2033: new concepts, tools, and applications leading to personalized medicine.
TL;DR: Viewpoint Management of Atrial Fibrillation in the Year 2033: New Concepts, Tools, and Applications Leading to Personalized Medicine
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Neuronal Na+ Channels Are Integral Components of Pro-Arrhythmic Na+/Ca2+ Signaling Nanodomain That Promotes Cardiac Arrhythmias During β-Adrenergic Stimulation
Przemysław B. Radwański,Hsiang-Ting Ho,Rengasayee Veeraraghavan,Lucia Brunello,Bin Liu,Andriy E. Belevych,Sathya D. Unudurthi,Michael A. Makara,Silvia G. Priori,Pompeo Volpe,Antonis A. Armoundas,Wolfgang H. Dillmann,Bjorn C. Knollmann,Peter J. Mohler,Thomas J. Hund,Sándor Györke +15 more
TL;DR: Data suggest that the arrhythmogenic alteration in Na+/Ca2+ handling evidenced ruing β-AR stimulation results, at least in part, from enhanced Na+ influx through nNav, and selective inhibition of these channels and of Nav1.6 in particular can serve as a potential antiarrhythmic therapy.
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Systems biology and cardiac arrhythmias
TL;DR: The identification of key candidate genes for monogenic arrhythmia syndromes shows that to bring basic biology to the clinic is a powerful approach and allows for systematic analysis that could transform treatment strategies that are often still empirical into management based on molecular evidence.
Journal ArticleDOI
High Familial Risk of Atrial Fibrillation/Atrial Flutter in Multiplex Families: A Nationwide Family Study in Sweden
Bengt Zöller,Henrik Ohlsson,Jan Sundquist,Jan Sundquist,Kristina Sundquist,Kristina Sundquist +5 more
TL;DR: Family history of atrial fibrillation/atrial flutter increases the odds of AF/AFl in first‐degree relatives in multiplex families in the entire Swedish population.
References
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Journal ArticleDOI
Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins
Michel Haïssaguerre,Pierre Jaïs,D. C. Shah,Atsushi Takahashi,Mélèze Hocini,G Quiniou,S. Garrigue,A Le Mouroux,P Le Métayer,Jacques Clementy +9 more
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.
Journal ArticleDOI
Secular Trends in Incidence of Atrial Fibrillation in Olmsted County, Minnesota, 1980 to 2000, and Implications on the Projections for Future Prevalence
Yoko Miyasaka,Marion E. Barnes,Bernard J. Gersh,Stephen S. Cha,Kent R. Bailey,Walter P. Abhayaratna,James B. Seward,Teresa S.M. Tsang +7 more
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
MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts
Thomas Thum,Carina Gross,Jan Fiedler,Thomas Fischer,Stephan Kissler,Markus Bussen,Paolo Galuppo,Steffen Just,Wolfgang Rottbauer,Stefan Frantz,Mirco Castoldi,Jürgen Soutschek,Victor Koteliansky,Andreas Rosenwald,M. Albert Basson,Jonathan D. Licht,John T. R. Pena,Sara H. Rouhanifard,Martina U. Muckenthaler,Thomas Tuschl,Gail R. Martin,Johann Bauersachs,Stefan Engelhardt,Stefan Engelhardt +23 more
TL;DR: It is shown that microRNA-21 regulates the ERK–MAP kinase signalling pathway in cardiac fibroblasts, which has impacts on global cardiac structure and function and confirms miR-21 as a disease target in heart failure and establishes the therapeutic efficacy of microRNA therapeutic intervention in a cardiovascular disease setting.
Journal ArticleDOI
Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis
Eva van Rooij,Lillian B. Sutherland,Jeffrey E. Thatcher,J. Michael DiMaio,R. Haris Naseem,William S. Marshall,Joseph A. Hill,Eric N. Olson +7 more
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.