| Ventricular tachyarrhythmias in a canine model of LQT3: arrhythmogenic effects of sympathetic activity and therapeutic effects of mexiletine. | |
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MedLine Citation:
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PMID: 12604879 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The ventricular tachyarrhythmias associated with the LQT3 syndrome are typically bradycardia-dependent. However, some episodes can be associated with exercise or emotional stress, suggesting a different arrhythmogenic mechanism when sympathetic activity predominates. This study examined the potential arrhythmogenic mechanisms during periods of autonomically mediated transient heart rate acceleration in a canine anthopleurin-A model of LQT3 syndrome. Using plunge needle electrodes, transmural unipolar electrograms of the left ventricle were recorded from endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) sites. The activation-recovery interval (ARI) was measured to estimate local refractoriness. The cardiac cycle length was gradually shortened by cessation of vagal stimulation (vagal stimulation protocol (VSP)), and intramural electrograms and onset mode of ventricular tachyarrhythmias were analyzed in 7 experiments. The VSP was performed 8 times before and 5 times after administration of mexiletine in each experiment. Before mexiletine, vagal stimulation slowed the heart rate and created large transmural ARI dispersion because of a greater ARI prolongation at Mid rather than Epi/Endo sites. After cessation of vagal stimulation, unipolar electrograms started to show ARI alternans and ventricular premature beats developed sporadically. Sustained ventricular tachyarrhythmias were induced in 12 of the 56 trials of the VSP. Initiation of ventricular tachyarrhythmias was associated with delayed conduction at Mid/Endo sites. Mexiletine attenuated transmural ARI dispersion, and neither ARI alternans nor ventricular tachyarrhythmias was observed during all 35 trials of the VSP after mexiletine administration. Heart rate acceleration induced by an abrupt shift to a state of predominant sympathetic activity enhances arrhythmias in this LQT3 model. Mexiletine homogenizes ventricular repolarization, suppresses premature complexes and was antiarrhythmic during ventricular tachyarrhythmias induced by the VSP. |
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Authors:
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Masaomi Chinushi; Minoru Tagawa; Hirotaka Sugiura; Satoru Komura; Yukio Hosaka; Takashi Washizuka; Yoshifusa Aizawa |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Circulation journal : official journal of the Japanese Circulation Society Volume: 67 ISSN: 1346-9843 ISO Abbreviation: Circ. J. Publication Date: 2003 Mar |
Date Detail:
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Created Date: 2003-02-26 Completed Date: 2003-12-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101137683 Medline TA: Circ J Country: Japan |
Other Details:
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Languages: eng Pagination: 263-8 Citation Subset: IM |
Affiliation:
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School of Health Science, Niigata University School of Medicine, Japan. masaomi@clg.niigata-u.ac.jp |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Arrhythmia Agents / pharmacology* Cardiac Complexes, Premature / drug therapy Dogs Electrocardiography Heart Rate Long QT Syndrome / complications*, physiopathology Mexiletine / pharmacology* Models, Animal Sympathetic Nervous System Tachycardia, Ventricular / drug therapy, etiology*, physiopathology Vagus Nerve / physiopathology |
| Chemical | |
Reg. No./Substance:
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0/Anti-Arrhythmia Agents; 31828-71-4/Mexiletine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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