Mechanisms of atrial remodeling and clinical relevance. Nattel, S., Shiroshita-Takeshita, A., Cardin, S., & Pelletier, P. Curr Opin Cardiol, 20(1):21–5, 2005. abstract bibtex This paper reviews recent progress in understanding atrial remodeling, as well as the consequent clinical insights into atrial fibrillation pathophysiology and treatment. RECENT FINDINGS: Two principal forms of remodeling have been described in animal models of atrial fibrillation: ionic remodeling, which affects cellular electrical properties, and structural remodeling, which alters atrial tissue architecture. Atrial tachycardias (particularly rapid tachyarrhythmias such as atrial flutter and atrial fibrillation) cause ionic remodeling, which decreases the atrial refractory period and promotes atrial reentry. Congestive heart failure produces atrial interstitial fibrosis, which promotes arrhythmogenesis by interfering with atrial conduction properties. Recent animal studies have provided insights into the pathways involved in remodeling, and have indicated the pathophysiological role of remodeling in specific contexts. In addition, work in animal models has provided information about pharmacological interventions that can prevent the development of remodeling. Clinical studies have shown that novel approaches to remodeling prevention identified in animal work have potential therapeutic value in man. SUMMARY: Understanding atrial remodeling has the potential to improve our appreciation of the pathophysiology of clinical atrial fibrillation and to allow for the development of useful new therapeutic approaches.
@Article{RSM:Nat2005a,
author = "S. Nattel and A. Shiroshita-Takeshita and S. Cardin
and P. Pelletier",
title = "Mechanisms of atrial remodeling and clinical
relevance",
journal = "Curr Opin Cardiol",
volume = "20",
number = "1",
pages = "21--5",
abstract = "This paper reviews recent progress in understanding
atrial remodeling, as well as the consequent clinical
insights into atrial fibrillation pathophysiology and
treatment. RECENT FINDINGS: Two principal forms of
remodeling have been described in animal models of
atrial fibrillation: ionic remodeling, which affects
cellular electrical properties, and structural
remodeling, which alters atrial tissue architecture.
Atrial tachycardias (particularly rapid
tachyarrhythmias such as atrial flutter and atrial
fibrillation) cause ionic remodeling, which decreases
the atrial refractory period and promotes atrial
reentry. Congestive heart failure produces atrial
interstitial fibrosis, which promotes arrhythmogenesis
by interfering with atrial conduction properties.
Recent animal studies have provided insights into the
pathways involved in remodeling, and have indicated the
pathophysiological role of remodeling in specific
contexts. In addition, work in animal models has
provided information about pharmacological
interventions that can prevent the development of
remodeling. Clinical studies have shown that novel
approaches to remodeling prevention identified in
animal work have potential therapeutic value in man.
SUMMARY: Understanding atrial remodeling has the
potential to improve our appreciation of the
pathophysiology of clinical atrial fibrillation and to
allow for the development of useful new therapeutic
approaches.",
year = "2005",
}
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