| Atrial electrophysiologic remodeling: another vicious circle? | |
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MedLine Citation:
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PMID: 9869538 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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With few exceptions, acquired heart disease is the result of gradual changes in the heart, progressing during several months or years. This also includes certain cardiac arrhythmias, as for instance atrial fibrillation (AF). In spite of the important role of slowly progressing pathologic processes, most of our knowledge about mechanisms of cardiac arrhythmias is based on acute experiments. Only recently, the attention also is more focused on long-term adaptation processes like cardiac memory, electrical remodeling, and tachycardia-induced cardiomyopathy. In experimental animal models, it has been shown that AF induces a vicious circle of electrophysiologic and structural changes that inevitably leads to "domestication" of the arrhythmia ("AF begets AF"). In this article, the studies on AF-induced electrophysiologic and cellular remodeling are discussed. |
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Authors:
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M A Allessie |
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Publication Detail:
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Type: Lectures; Review |
Journal Detail:
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Title: Journal of cardiovascular electrophysiology Volume: 9 ISSN: 1045-3873 ISO Abbreviation: J. Cardiovasc. Electrophysiol. Publication Date: 1998 Dec |
Date Detail:
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Created Date: 1999-05-13 Completed Date: 1999-05-13 Revised Date: 2013-05-20 |
Medline Journal Info:
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Nlm Unique ID: 9010756 Medline TA: J Cardiovasc Electrophysiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1378-93 Citation Subset: IM |
Affiliation:
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Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Atrial Fibrillation / physiopathology* Atrial Function* / physiology Calcium Channels / physiology Disease Models, Animal Electrophysiology Gap Junctions / physiology Humans Models, Cardiovascular* Refractory Period, Electrophysiological / physiology |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channels |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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