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Conference Paper: Effects of class I anti-arrhythmic drugs in infarcted tissue

TitleEffects of class I anti-arrhythmic drugs in infarcted tissue
Authors
Issue Date1991
PublisherCanadian Medical Association. The Journal's web site is located at http://www.csci-scrc.medical.org/english/cim.html
Citation
Clinical And Investigative Medicine, 1991, v. 14 n. 5, p. 466-475 How to Cite?
AbstractAn in vitro model was used to examine the electrophysiological effects of anti-arrhythmic drugs in infarcted tissue. After 24 h of coronary artery occlusion in the dog, endocardial preparations were removed from the infarcted zone. Intracellulr action potentials recorded from surviving Purkinje fibres on the endocardial surface showed reduced maximum upstroke velocity (V̇(max)), increased action potential duration and enhanced automaticity. The rate-dependent effect of lidocaine on V̇(max) and conduction was more prominent in Purkinje fibres that survived myocardial infarction than in normal Purkinje fibres. Tocainide, flecainide, and O-demethyl encainide reduced V̇(max) in both normal Purkinje fibres and Purkinje fibres surviving infarction. Similar to lidocaine, these drugs showed the greatest reduction of V̇(max) in Purkinje fibres surviving infarction at the shortest stimulation cycle length tested. In contrast, maximal drug effects on action potential duration were observed when long stimulation cycle lengths were used. Our results indicate that most Class I anti-arrhythmic drugs showed rate-dependent properties in normal Purkinje fibres as well as in Purkinje fibres surviving infarction. The increased sensitivity of the ischemic myocardium to anti-arrhythmic drugs resulting in greater reductions of V̇(max) and conduction may contribute to a greater potency of anti-arrhythmic drugs in the suppression of arrhythmias associated with ischemia. Conversely, while slowing of conduction can abolish re-entry arrhythmias by producing a bidirectional block, further slowing of conduction by anti-arrhythmic drugs can favour the development of new re-entry pathways and may contribute to their pro-arrhythmic effects.
Persistent Identifierhttp://hdl.handle.net/10722/173492
ISSN
2015 Impact Factor: 1.191
2015 SCImago Journal Rankings: 0.502
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMan, RYKen_US
dc.contributor.authorBril, Aen_US
dc.date.accessioned2012-10-30T06:32:20Z-
dc.date.available2012-10-30T06:32:20Z-
dc.date.issued1991en_US
dc.identifier.citationClinical And Investigative Medicine, 1991, v. 14 n. 5, p. 466-475en_US
dc.identifier.issn0147-958Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/173492-
dc.description.abstractAn in vitro model was used to examine the electrophysiological effects of anti-arrhythmic drugs in infarcted tissue. After 24 h of coronary artery occlusion in the dog, endocardial preparations were removed from the infarcted zone. Intracellulr action potentials recorded from surviving Purkinje fibres on the endocardial surface showed reduced maximum upstroke velocity (V̇(max)), increased action potential duration and enhanced automaticity. The rate-dependent effect of lidocaine on V̇(max) and conduction was more prominent in Purkinje fibres that survived myocardial infarction than in normal Purkinje fibres. Tocainide, flecainide, and O-demethyl encainide reduced V̇(max) in both normal Purkinje fibres and Purkinje fibres surviving infarction. Similar to lidocaine, these drugs showed the greatest reduction of V̇(max) in Purkinje fibres surviving infarction at the shortest stimulation cycle length tested. In contrast, maximal drug effects on action potential duration were observed when long stimulation cycle lengths were used. Our results indicate that most Class I anti-arrhythmic drugs showed rate-dependent properties in normal Purkinje fibres as well as in Purkinje fibres surviving infarction. The increased sensitivity of the ischemic myocardium to anti-arrhythmic drugs resulting in greater reductions of V̇(max) and conduction may contribute to a greater potency of anti-arrhythmic drugs in the suppression of arrhythmias associated with ischemia. Conversely, while slowing of conduction can abolish re-entry arrhythmias by producing a bidirectional block, further slowing of conduction by anti-arrhythmic drugs can favour the development of new re-entry pathways and may contribute to their pro-arrhythmic effects.en_US
dc.languageengen_US
dc.publisherCanadian Medical Association. The Journal's web site is located at http://www.csci-scrc.medical.org/english/cim.htmlen_US
dc.relation.ispartofClinical and Investigative Medicineen_US
dc.subject.meshAction Potentials - Drug Effectsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Arrhythmia Agents - Pharmacologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDogsen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshMyocardial Infarction - Physiopathologyen_US
dc.subject.meshPurkinje Fibers - Drug Effects - Physiopathologyen_US
dc.titleEffects of class I anti-arrhythmic drugs in infarcted tissueen_US
dc.typeConference_Paperen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid1742923-
dc.identifier.scopuseid_2-s2.0-0025944307en_US
dc.identifier.volume14en_US
dc.identifier.issue5en_US
dc.identifier.spage466en_US
dc.identifier.epage475en_US
dc.identifier.isiWOS:A1991GM70100013-
dc.publisher.placeCanadaen_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.scopusauthoridBril, A=7006161753en_US

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