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
Citations
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Journal ArticleDOI
Tracking Atrial Fibrillation Mechanisms: a Computational Method for Locating Rotors and Ectopic Activity Using Curl and Divergence Operators
TL;DR: In this article , an approach for locating functional rotors (FR) and ectopic foci (EF) in potential maps, which were tested with mathematical phantoms, was proposed.
Journal ArticleDOI
Analyses of m6A regulatory genes and subtype classification in atrial fibrillation
TL;DR: In this paper , the role of m6A regulatory genes in atrial fibrillation (AF) was explored by two genotyping methods associated with m6AA regulatory genes and explored their clinical significance.
Journal ArticleDOI
The heart and the osteoclasts.
TL;DR: The genetic background of atrial fibrillation, considered unlikely to be an important factor and largely unknown only just a few years ago, has become evident and robustly supported and a novel and interesting signaling system has been demonstrated.
Posted Content
Modelling the progression of atrial fibrillation: A stochastic individual-based approach
TL;DR: The model operates at patient level over a lifetime and is based on elements of the physiology and biophysics of AF, making contact with existing mechanistic models, with a view towards model-based personalised medicine.
Journal ArticleDOI
Pitx2c deficiency confers cellular electrophysiological hallmarks of atrial fibrillation to isolated atrial myocytes.
Carmen Tarifa,Selma A. Serra,Adela Herraiz-Martínez,Estefanía Lozano-Velasco,Raul Benitez,Amelia Aránega,Diego Franco,Leif Hove-Madsen +7 more
TL;DR: In this paper , a mouse model with conditional atrial-specific deletion of the transcription factor Pitx2c was used to investigate the relationship between defective calcium homeostasis and electrical activity in isolated atrial myocytes.
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.
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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
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.
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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.
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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.