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Atrial remodeling, fibrosis, and atrial fibrillation

Abstract The fundamental mechanisms governing the perpetuation of atrial fibrillation (AF), the most common arrhythmia seen in clinical practice, are poorly understood, which explains in part why AF prevention and treatment remain suboptimal. Although some clinical parameters have been identified as... Full description

Journal Title: Trends in cardiovascular medicine 2015, Vol.25 (6), p.475-484
Main Author: Jalife, José, MD
Other Authors: Kaur, Kuljeet, PhD
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 1050-1738
Link: https://www.ncbi.nlm.nih.gov/pubmed/25661032
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5658790
title: Atrial remodeling, fibrosis, and atrial fibrillation
format: Article
creator:
  • Jalife, José, MD
  • Kaur, Kuljeet, PhD
subjects:
  • Analysis
  • Anti-Arrhythmia Agents - therapeutic use
  • Article
  • Atrial fibrillation
  • Atrial Fibrillation - physiopathology
  • Atrial Fibrillation - therapy
  • Atrial Remodeling - physiology
  • Cardiac arrhythmia
  • Cardiovascular
  • Catheter Ablation - methods
  • Electrophysiological Phenomena
  • Female
  • Fibroblasts
  • Fibrosis - pathology
  • Fibrosis - physiopathology
  • Gene expression
  • Humans
  • Inflammation
  • Investigations
  • Laboratories
  • Male
  • MicroRNAs
  • MicroRNAs - metabolism
  • Oxidative stress
  • Oxidative Stress - physiology
  • Prognosis
  • Reactive Oxygen Species - metabolism
  • Recurrence
  • Risk Assessment
  • Rodents
  • Severity of Illness Index
  • Signal Transduction
ispartof: Trends in cardiovascular medicine, 2015, Vol.25 (6), p.475-484
description: Abstract The fundamental mechanisms governing the perpetuation of atrial fibrillation (AF), the most common arrhythmia seen in clinical practice, are poorly understood, which explains in part why AF prevention and treatment remain suboptimal. Although some clinical parameters have been identified as predicting a transition from paroxysmal to persistent AF in some patients, the molecular, electrophysiological, and inflammation changes leading to such a progression have not been described in detail. Oxidative stress, atrial dilatation, calcium overload, inflammation, microRNAs, and myofibroblast activation are all thought to be involved in AF-induced atrial remodeling. However, it is unknown to what extent and at which time points such alterations influence the remodeling process that perpetuates AF. Here we postulate a working model that might open new pathways for future investigation into mechanisms of AF perpetuation. We start from the premise that the progression to AF perpetuation is the result of interplay among manifold signaling pathways with differing kinetics. Some such pathways have relatively fast kinetics (e.g., oxidative stress-mediated shortening of refractory period); others likely depend on molecular processes with slower kinetics (e.g., transcriptional changes in myocyte ion channel protein expression mediated through inflammation and fibroblast activation). We stress the need to fully understand the relationships among such pathways should one hope to identify novel, truly effective targets for AF therapy and prevention.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 1050-1738
fulltext: fulltext
issn:
  • 1050-1738
  • 1873-2615
url: Link


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descriptionAbstract The fundamental mechanisms governing the perpetuation of atrial fibrillation (AF), the most common arrhythmia seen in clinical practice, are poorly understood, which explains in part why AF prevention and treatment remain suboptimal. Although some clinical parameters have been identified as predicting a transition from paroxysmal to persistent AF in some patients, the molecular, electrophysiological, and inflammation changes leading to such a progression have not been described in detail. Oxidative stress, atrial dilatation, calcium overload, inflammation, microRNAs, and myofibroblast activation are all thought to be involved in AF-induced atrial remodeling. However, it is unknown to what extent and at which time points such alterations influence the remodeling process that perpetuates AF. Here we postulate a working model that might open new pathways for future investigation into mechanisms of AF perpetuation. We start from the premise that the progression to AF perpetuation is the result of interplay among manifold signaling pathways with differing kinetics. Some such pathways have relatively fast kinetics (e.g., oxidative stress-mediated shortening of refractory period); others likely depend on molecular processes with slower kinetics (e.g., transcriptional changes in myocyte ion channel protein expression mediated through inflammation and fibroblast activation). We stress the need to fully understand the relationships among such pathways should one hope to identify novel, truly effective targets for AF therapy and prevention.
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subjectAnalysis ; Anti-Arrhythmia Agents - therapeutic use ; Article ; Atrial fibrillation ; Atrial Fibrillation - physiopathology ; Atrial Fibrillation - therapy ; Atrial Remodeling - physiology ; Cardiac arrhythmia ; Cardiovascular ; Catheter Ablation - methods ; Electrophysiological Phenomena ; Female ; Fibroblasts ; Fibrosis - pathology ; Fibrosis - physiopathology ; Gene expression ; Humans ; Inflammation ; Investigations ; Laboratories ; Male ; MicroRNAs ; MicroRNAs - metabolism ; Oxidative stress ; Oxidative Stress - physiology ; Prognosis ; Reactive Oxygen Species - metabolism ; Recurrence ; Risk Assessment ; Rodents ; Severity of Illness Index ; Signal Transduction
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descriptionAbstract The fundamental mechanisms governing the perpetuation of atrial fibrillation (AF), the most common arrhythmia seen in clinical practice, are poorly understood, which explains in part why AF prevention and treatment remain suboptimal. Although some clinical parameters have been identified as predicting a transition from paroxysmal to persistent AF in some patients, the molecular, electrophysiological, and inflammation changes leading to such a progression have not been described in detail. Oxidative stress, atrial dilatation, calcium overload, inflammation, microRNAs, and myofibroblast activation are all thought to be involved in AF-induced atrial remodeling. However, it is unknown to what extent and at which time points such alterations influence the remodeling process that perpetuates AF. Here we postulate a working model that might open new pathways for future investigation into mechanisms of AF perpetuation. We start from the premise that the progression to AF perpetuation is the result of interplay among manifold signaling pathways with differing kinetics. Some such pathways have relatively fast kinetics (e.g., oxidative stress-mediated shortening of refractory period); others likely depend on molecular processes with slower kinetics (e.g., transcriptional changes in myocyte ion channel protein expression mediated through inflammation and fibroblast activation). We stress the need to fully understand the relationships among such pathways should one hope to identify novel, truly effective targets for AF therapy and prevention.
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abstractAbstract The fundamental mechanisms governing the perpetuation of atrial fibrillation (AF), the most common arrhythmia seen in clinical practice, are poorly understood, which explains in part why AF prevention and treatment remain suboptimal. Although some clinical parameters have been identified as predicting a transition from paroxysmal to persistent AF in some patients, the molecular, electrophysiological, and inflammation changes leading to such a progression have not been described in detail. Oxidative stress, atrial dilatation, calcium overload, inflammation, microRNAs, and myofibroblast activation are all thought to be involved in AF-induced atrial remodeling. However, it is unknown to what extent and at which time points such alterations influence the remodeling process that perpetuates AF. Here we postulate a working model that might open new pathways for future investigation into mechanisms of AF perpetuation. We start from the premise that the progression to AF perpetuation is the result of interplay among manifold signaling pathways with differing kinetics. Some such pathways have relatively fast kinetics (e.g., oxidative stress-mediated shortening of refractory period); others likely depend on molecular processes with slower kinetics (e.g., transcriptional changes in myocyte ion channel protein expression mediated through inflammation and fibroblast activation). We stress the need to fully understand the relationships among such pathways should one hope to identify novel, truly effective targets for AF therapy and prevention.
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