@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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