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Article: Electrophysiological properties of the fibrillating atrium: Implications for therapy

TitleElectrophysiological properties of the fibrillating atrium: Implications for therapy
Authors
Issue Date1998
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEP
Citation
Clinical And Experimental Pharmacology And Physiology, 1998, v. 25 n. 5, p. 293-302 How to Cite?
Abstract1. Atrial fibrillation (AF) is the most commonly occurring cardiac dysrhythmia and remains a challenge to medical therapy. Although the disorder has been recognized for over 100 years, surprisingly very little is understood about its pathophysiology. Over the past decade, a variety of experimental and animal models of AF have been developed and these have provided insights into the mechanism of AF. 2. The pathophysiology of AF is complex. Atrial fibrillation can be caused either by a single source of very rapid impulses or, in the majority of cases, by multiple random re-entering wavelets. The notion that AF may be initiated by a single rapid firing focus and the perpetuation of AF may be partly dependent on macro re-entry around the natural atrial orifices provides a new potential curative therapy for AF by radiofrequency ablation. 3. Shortening of atrial wavelength, either by slow atrial conduction velocities, short atrial refractory periods or both, seems to predispose to development of intra-atrial re-entry and, thus, AF. The functional mechanism by which anti-arrhythmic drugs terminate AF appears to be by prolonging the wavelength and decreasing the number of re-entry wavelets. These understandings are important for the future development of effective anti-arrhythmic agents against AF. 4. The presence of a short and variable excitable gap during AF may be potentially important for termination of AF by pacing. 5. New insights are being gained into the potential role and mechanism of electrical remodelling of the atrium due to AF. Repented induction of AF by rapid atrial pacing leads to a shortening of atrial refractoriness with loss of rate adaptation, which favours the induction and maintenance of AF. These electrophysiological changes were assumed to occur during repeated AF and to facilitate the generation of multiple re-entrant wavelets. These data suggest that prompt restoration of sinus rhythm and new novel therapy that prevents or diminishes electrical remodelling may promote maintenance of sinus rhythm after successful cardioversion.
Persistent Identifierhttp://hdl.handle.net/10722/77048
ISSN
2012 Impact Factor: 2.16
2015 SCImago Journal Rankings: 0.944
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CPen_HK
dc.date.accessioned2010-09-06T07:27:43Z-
dc.date.available2010-09-06T07:27:43Z-
dc.date.issued1998en_HK
dc.identifier.citationClinical And Experimental Pharmacology And Physiology, 1998, v. 25 n. 5, p. 293-302en_HK
dc.identifier.issn0305-1870en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77048-
dc.description.abstract1. Atrial fibrillation (AF) is the most commonly occurring cardiac dysrhythmia and remains a challenge to medical therapy. Although the disorder has been recognized for over 100 years, surprisingly very little is understood about its pathophysiology. Over the past decade, a variety of experimental and animal models of AF have been developed and these have provided insights into the mechanism of AF. 2. The pathophysiology of AF is complex. Atrial fibrillation can be caused either by a single source of very rapid impulses or, in the majority of cases, by multiple random re-entering wavelets. The notion that AF may be initiated by a single rapid firing focus and the perpetuation of AF may be partly dependent on macro re-entry around the natural atrial orifices provides a new potential curative therapy for AF by radiofrequency ablation. 3. Shortening of atrial wavelength, either by slow atrial conduction velocities, short atrial refractory periods or both, seems to predispose to development of intra-atrial re-entry and, thus, AF. The functional mechanism by which anti-arrhythmic drugs terminate AF appears to be by prolonging the wavelength and decreasing the number of re-entry wavelets. These understandings are important for the future development of effective anti-arrhythmic agents against AF. 4. The presence of a short and variable excitable gap during AF may be potentially important for termination of AF by pacing. 5. New insights are being gained into the potential role and mechanism of electrical remodelling of the atrium due to AF. Repented induction of AF by rapid atrial pacing leads to a shortening of atrial refractoriness with loss of rate adaptation, which favours the induction and maintenance of AF. These electrophysiological changes were assumed to occur during repeated AF and to facilitate the generation of multiple re-entrant wavelets. These data suggest that prompt restoration of sinus rhythm and new novel therapy that prevents or diminishes electrical remodelling may promote maintenance of sinus rhythm after successful cardioversion.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEPen_HK
dc.relation.ispartofClinical and Experimental Pharmacology and Physiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnti-Arrhythmia Agents - therapeutic useen_HK
dc.subject.meshAtrial Fibrillation - physiopathology - therapyen_HK
dc.subject.meshCardiac Pacing, Artificialen_HK
dc.subject.meshElectric Stimulationen_HK
dc.subject.meshElectrophysiologyen_HK
dc.subject.meshHeart Conduction System - physiopathologyen_HK
dc.subject.meshHumansen_HK
dc.titleElectrophysiological properties of the fibrillating atrium: Implications for therapyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0305-1870&volume=25&spage=293&epage=302&date=1998&atitle=Electrophysiological+properties+of+the+fibrillating+atrium:+implications+for+therapyen_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1440-1681.1998.tb02355.x-
dc.identifier.pmid9612655-
dc.identifier.scopuseid_2-s2.0-0031895106en_HK
dc.identifier.hkuros39282en_HK
dc.identifier.hkuros41433-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031895106&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue5en_HK
dc.identifier.spage293en_HK
dc.identifier.epage302en_HK
dc.identifier.isiWOS:000073418800001-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK

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