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Article: Ionic current abnormalities associated with prolonged action potentials in cardiomyocytes from diseased human right ventricles

TitleIonic current abnormalities associated with prolonged action potentials in cardiomyocytes from diseased human right ventricles
Authors
Issue Date2004
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/heartrhythmjournal
Citation
Heart Rhythm, 2004, v. 1 n. 4, p. 460-468 How to Cite?
AbstractObjectives: This study was designed to determine whether ionic currents in right ventricular myocytes from explanted human transplant recipient hearts are related to right ventricular histopathology and function. Background: Cardiac action potential duration (APD) is prolonged in ventricular tissues/cells from patients with heart failure, but the ionic mechanisms are not well documented. Methods: Membrane currents and transmembrane action potentials in myocytes from right ventricular epicardium of explanted human hearts were recorded using whole-cell patch clamp technique. Data from cells from right ventricles with severe histologic and functional abnormalities (abnormal histology group [AH]) and from right ventricles with preserved histology and function (relatively normal histology group [RNH]) were compared. Results: We found that APD at 50% (APD 50) and 90% repolarization (APD 90) were significantly longer in AH cells than in RNH cells. Early afterdepolarizations (EADs) were observed in 20% of AH cells and none of the RNH cells. Inwardly rectifying K + current (I K1) was decreased (both inward and outward components). Both transient outward K + current K + (I to1) and slowly delayed rectifier K + current (I Ks) were down-regulated in AH cells. L-type Ca 2+ (I Ca.L was not altered in AH cells. Conclusions: I K1, I to1, and I Ks are down-regulated in AH cells of human heart failure. This down-regulation contributes to APD prolongation that favors the occurrence of arrhythmogenic EADs and suggests a link between human cardiac histopathologic/functional abnormalities and arrhythmogenic ionic remodeling. © 2004 Heart Ryhthm Society. All rigths reserved.
Persistent Identifierhttp://hdl.handle.net/10722/85485
ISSN
2015 Impact Factor: 4.391
2015 SCImago Journal Rankings: 2.756
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLeung, TKen_HK
dc.contributor.authorNattel, Sen_HK
dc.date.accessioned2010-09-06T09:05:38Z-
dc.date.available2010-09-06T09:05:38Z-
dc.date.issued2004en_HK
dc.identifier.citationHeart Rhythm, 2004, v. 1 n. 4, p. 460-468en_HK
dc.identifier.issn1547-5271en_HK
dc.identifier.urihttp://hdl.handle.net/10722/85485-
dc.description.abstractObjectives: This study was designed to determine whether ionic currents in right ventricular myocytes from explanted human transplant recipient hearts are related to right ventricular histopathology and function. Background: Cardiac action potential duration (APD) is prolonged in ventricular tissues/cells from patients with heart failure, but the ionic mechanisms are not well documented. Methods: Membrane currents and transmembrane action potentials in myocytes from right ventricular epicardium of explanted human hearts were recorded using whole-cell patch clamp technique. Data from cells from right ventricles with severe histologic and functional abnormalities (abnormal histology group [AH]) and from right ventricles with preserved histology and function (relatively normal histology group [RNH]) were compared. Results: We found that APD at 50% (APD 50) and 90% repolarization (APD 90) were significantly longer in AH cells than in RNH cells. Early afterdepolarizations (EADs) were observed in 20% of AH cells and none of the RNH cells. Inwardly rectifying K + current (I K1) was decreased (both inward and outward components). Both transient outward K + current K + (I to1) and slowly delayed rectifier K + current (I Ks) were down-regulated in AH cells. L-type Ca 2+ (I Ca.L was not altered in AH cells. Conclusions: I K1, I to1, and I Ks are down-regulated in AH cells of human heart failure. This down-regulation contributes to APD prolongation that favors the occurrence of arrhythmogenic EADs and suggests a link between human cardiac histopathologic/functional abnormalities and arrhythmogenic ionic remodeling. © 2004 Heart Ryhthm Society. All rigths reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/heartrhythmjournalen_HK
dc.relation.ispartofHeart Rhythmen_HK
dc.rightsHeart Rhythm. Copyright © Elsevier Inc.en_HK
dc.subject.meshAction Potentialsen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCalcium - physiologyen_HK
dc.subject.meshCalcium Channels, L-Type - physiologyen_HK
dc.subject.meshElectrophysiologic Techniques, Cardiacen_HK
dc.subject.meshHeart Ventricles - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIon Channel Gatingen_HK
dc.subject.meshMembrane Potentialsen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMyocytes, Cardiac - pathologyen_HK
dc.subject.meshPotassium Channels, Voltage-Gated - physiologyen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTransplantationen_HK
dc.subject.meshVentricular Dysfunction, Right - pathologyen_HK
dc.titleIonic current abnormalities associated with prolonged action potentials in cardiomyocytes from diseased human right ventriclesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1547-5271&volume=1&issue=4&spage=460&epage=468&date=2004&atitle=Ionic+Current+Abnormalities+Associated+With+Prolonged+Action+Potentials+In+Cardiomyocytes+From+Diseased+Human+Right+Ventriclesen_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.hrthm.2004.06.003en_HK
dc.identifier.pmid15851200-
dc.identifier.scopuseid_2-s2.0-7744235724en_HK
dc.identifier.hkuros101179en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-7744235724&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1en_HK
dc.identifier.issue4en_HK
dc.identifier.spage460en_HK
dc.identifier.epage468en_HK
dc.identifier.isiWOS:000226395900012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLeung, TK=7202110185en_HK
dc.identifier.scopusauthoridNattel, S=36947837400en_HK
dc.identifier.citeulike10845197-

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