| Cardiac adrenergic control and atrial fibrillation. | |
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MedLine Citation:
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PMID: 19960186 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Atrial fibrillation (AF) is the most common cardiac arrhythmia, and it causes substantial mortality. The autonomic nervous system, and particularly the adrenergic/cholinergic balance, has a profound influence on the occurrence of AF. Adrenergic stimulation from catecholamines can cause AF in patients. In human atrium, catecholamines can affect each of the electrophysiological mechanisms of AF initiation and/or maintenance. Catecholamines may produce membrane potential oscillations characteristic of afterdepolarisations, by increasing Ca(2+) current, [Ca(2+)](i) and consequent Na(+)-Ca(2+) exchange, and may also enhance automaticity. Catecholamines might affect reentry, by altering excitability or conduction, rather than action potential terminal repolarisation or refractory period. However, which arrhythmia mechanisms predominate is unclear, and likely depends on cardiac pathology and adrenergic tone. Heart failure (HF), a major cause of AF, causes adrenergic activation and adaptational changes, remodelling, of atrial electrophysiology, Ca(2+) homeostasis, and adrenergic responses. Chronic AF also remodels these, but differently to HF. Myocardial infarction and AF cause neural remodelling that also may promote AF. beta-Adrenoceptor antagonists (beta-blockers) are used in the treatment of AF, mainly to control the ventricular rate, by slowing atrioventricular conduction. beta-Blockers also reduce the incidence of AF, particularly in HF or after cardiac surgery, when adrenergic tone is high. Furthermore, the chronic treatment of patients with beta-blockers remodels the atria, with a potentially antiarrhythmic increase in the refractory period. Therefore, the suppression of AF by beta-blocker treatment may involve an attenuation of arrhythmic activity that is caused by increased [Ca(2+)](i), coupled with effects of adaptation to the treatment. An improved understanding of the involvement of the adrenergic system and its control in basic mechanisms of AF under differing cardiac pathologies might lead to better treatments. |
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Authors:
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Antony J Workman |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2009-12-04 |
Journal Detail:
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Title: Naunyn-Schmiedeberg's archives of pharmacology Volume: 381 ISSN: 1432-1912 ISO Abbreviation: Naunyn Schmiedebergs Arch. Pharmacol. Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-04-08 Completed Date: 2010-07-01 Revised Date: 2010-09-28 |
Medline Journal Info:
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Nlm Unique ID: 0326264 Medline TA: Naunyn Schmiedebergs Arch Pharmacol Country: Germany |
Other Details:
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Languages: eng Pagination: 235-49 Citation Subset: IM |
Affiliation:
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British Heart Foundation Glasgow Cardiovascular Research Centre, Division of Cardiovascular and Medical Sciences, Faculty of Medicine, University of Glasgow, 126 University Place, Glasgow, G12 8TA, UK. A.J.Workman@clinmed.gla.ac.uk |
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| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials
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drug effects Adrenergic beta-Antagonists / administration & dosage, pharmacology, therapeutic use* Animals Atrial Fibrillation / drug therapy*, metabolism, physiopathology Calcium Signaling / drug effects Catecholamines / metabolism* Humans Receptors, Adrenergic / metabolism* Species Specificity |
| Grant Support | |
ID/Acronym/Agency:
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BS/06/003//British Heart Foundation; BS/06/003/20338//British Heart Foundation |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Antagonists; 0/Catecholamines; 0/Receptors, Adrenergic |
| Comments/Corrections | |
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