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
Bioptic Study of Left and Right Atrial Interstitium in Cardiac Patients with and without Atrial Fibrillation: Interatrial but Not Rhythm-Based Differences.
Natalia Smorodinova,Lucie Lantova,Martin Bláha,Vojtěch Melenovský,Jan Hanzelka,Jan Pirk,Josef Kautzner,Tomáš Kučera +7 more
TL;DR: No significant changes in atrial extracellular matrix fiber content, microvascular density and angiogenic signaling, attributable to AF, were found in this cohort of patients with structural heart disease, which suggests that interstitial fibrosis and other morphological changes inAtrial tissue are rather linked to structuralHeart disease than to AF per se.
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Pioglitazone inhibits angiotensin II-induced atrial fibroblasts proliferation via NF-κB/TGF-β1/TRIF/TRAF6 pathway.
TL;DR: The exact mechanisms underlying inhibitory effects of pioglitazone (Pio) on atrial fibrosis are complex and remain largely unknown as discussed by the authors, however, the effect of Pio on the effects of atrial cancer was examined in vivo and in vitro.
Journal ArticleDOI
Atrial arrhythmia prevalence and characteristics for human immunodeficiency virus-infected persons and matched uninfected controls.
Jes M. Sanders,Alexandra B Steverson,Anna Pawlowski,Daniel Schneider,Chad J. Achenbach,Donald M. Lloyd-Jones,Matthew J. Feinstein +6 more
TL;DR: HIV-related immunosuppression (nadir CD4 T cell count <200 cells/mm3) and traditional CVD risk factors are associated with significantly elevated odds of AF/AFL among HIV+ persons.
Journal ArticleDOI
Canonical Transient Receptor Potential Channels and Their Link with Cardio/Cerebro-Vascular Diseases
TL;DR: This review will provide an overview of current knowledge about the underlying pathogenesis of TRPCs in cardio/cerebrovascular diseases, including hypertension, pulmonary arterial hypertension, cardiac hypertrophy, atherosclerosis, arrhythmia, and cerebrov vascular ischemia reperfusion injury.
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Pinocembrin attenuates autonomic dysfunction and atrial fibrillation susceptibility via inhibition of the NF-κB/TNF-α pathway in a rat model of myocardial infarction.
TL;DR: Findings indicate that pinocembrin treatment decreases autonomic remodeling, lowers atrial fibrosis, ameliorates atrial electrical remodelling, and suppresses MI-induced inflammatory responses, which suggests a potential novel strategy for atrial arrhythmias.
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.
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.
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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.