Differential effects of lignocaine and hypercalcaemia on anisotropic conduction and reentry in the ischaemically damaged canine ventricle

Anisotropic conduction characteristics, which may be expressed as the ratio of conduction velocities in the longitudinal (Vlong) and transverse (Vtrans) fibre directions, have been shown to stabilise reentry and favour the induction of sustained, uniform ventricular tachycardia. The aim of this stud...

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Veröffentlicht in:Cardiovascular research 1995-03, Vol.29 (3), p.359-372
Hauptverfasser: HELIE, F, COSSETTE, J, VERMEULEN, M, CARDINAL, R
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COSSETTE, J
VERMEULEN, M
CARDINAL, R
description Anisotropic conduction characteristics, which may be expressed as the ratio of conduction velocities in the longitudinal (Vlong) and transverse (Vtrans) fibre directions, have been shown to stabilise reentry and favour the induction of sustained, uniform ventricular tachycardia. The aim of this study was to investigate whether interventions affecting either excitability (lignocaine) or both excitability and cell coupling (hypercalcaemia) might produce differential effects on the Vlong/Vtrans ratio, and whether an intervention reducing this ratio might prevent the induction of sustained reentrant ventricular tachycardia. The effects of hypercalcaemia [8.2(SD 3.8) mmol.litre-1] and lignocaine infusion [to 24.4(19) and 42.3(29) mumol.litre-1] on Vlong and Vtrans were determined from 127 electrograms recorded with a plaque electrode on the anterior left ventricular wall of healthy dogs or 3 d after occlusion of the left anterior descending coronary artery. Vlong and Vtrans were computed from isochronal maps displaying ellipsoid patterns with a long axis corresponding to longitudinal conduction and a short axis corresponding to transverse conduction, as determined during basic (S1) and premature (S2) stimulation from the centre of the plaque electrode. Infarcted heart preparations were subjected to programmed stimulation for induction of reentrant ventricular tachycardias. Hypercalcaemia reduced both Vlong and Vtrans (P < 0.05) but did not modify either the Vlong/Vtrans ratio or the induction and patterns of ventricular tachycardias. Lignocaine reduced Vlong and the Vlong/Vtrans ratio during premature stimulation (S2) of infarcted heart preparations (P < 0.05) and stabilised reentrant ventricular tachycardias in preparations in which only nonsustained, multiform ventricular tachycardias were induced under control conditions. Conduction velocities in the longitudinal and transverse directions can be differentially affected by selected pharmacological interventions, but the Vlong/Vtrans ratio is not a representative index of the facilitating influence of tissue anisotropy on reentry. Therefore, the role of anisotropy in this model of reentry is not confined to establishing disparity of a functional character between conduction velocities in the longitudinal and transverse directions.
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Vascular system</subject><subject>Coronary heart disease</subject><subject>Dogs</subject><subject>Electrophysiology</subject><subject>Female</subject><subject>Heart</subject><subject>Heart Conduction System - drug effects</subject><subject>Heart Conduction System - physiopathology</subject><subject>Hypercalcemia - metabolism</subject><subject>Lidocaine - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - metabolism</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardium - metabolism</subject><subject>Tachycardia, Ventricular - physiopathology</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kctOHDEQRa0oCIZJ_iCRvIgiWDTx291LRHhJSGzI2vK4y4yjbnuwe5DmE_hr3DCalctV9x6VbiH0g5ILSqj6QwhpG8UVP-vUedvKjjfsC1pQLWXDmZBf0eIgOUGnpfyvXym1OEbHWreVQRbo7W_wHjLEKdgBQ63dVHDyeAjPMTkbImAbe7zebSA7OzgLY7A4xdoNJU05bYLDLsV-66bw0e5xhsrLOxwintaAQ3Hr2Vbtww73drTP0GNXARX-OkuDG-AbOvJ2KPB9_y7Rv5vrp6u75uHx9v7q8qFxtJNTwxR4ooRXDOyKc6eB9UwTTTsqV5J4al0nqeLUC-BetQQY1a13jGgvbC_4Ev3-5G5yetlCmcxYF4RhsBHSthita3hKdFUoPoUup1IyeLPJYbR5Zygx8wXMHK-Z4zWdMh8XMKzafu7529UI_cG0j7zOf-3nttREfLbRhXKQcVEX0Jy_A9h9kKY</recordid><startdate>199503</startdate><enddate>199503</enddate><creator>HELIE, F</creator><creator>COSSETTE, J</creator><creator>VERMEULEN, M</creator><creator>CARDINAL, R</creator><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199503</creationdate><title>Differential effects of lignocaine and hypercalcaemia on anisotropic conduction and reentry in the ischaemically damaged canine ventricle</title><author>HELIE, F ; COSSETTE, J ; VERMEULEN, M ; CARDINAL, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c195t-26ef064f62eab33c7e2d27071915b50f1ac951631f4e3f680e2178fc207f4ad43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Anisotropy</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Dogs</topic><topic>Electrophysiology</topic><topic>Female</topic><topic>Heart</topic><topic>Heart Conduction System - drug effects</topic><topic>Heart Conduction System - physiopathology</topic><topic>Hypercalcemia - metabolism</topic><topic>Lidocaine - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Ischemia - metabolism</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardium - metabolism</topic><topic>Tachycardia, Ventricular - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HELIE, F</creatorcontrib><creatorcontrib>COSSETTE, J</creatorcontrib><creatorcontrib>VERMEULEN, M</creatorcontrib><creatorcontrib>CARDINAL, R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HELIE, F</au><au>COSSETTE, J</au><au>VERMEULEN, M</au><au>CARDINAL, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential effects of lignocaine and hypercalcaemia on anisotropic conduction and reentry in the ischaemically damaged canine ventricle</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>1995-03</date><risdate>1995</risdate><volume>29</volume><issue>3</issue><spage>359</spage><epage>372</epage><pages>359-372</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>Anisotropic conduction characteristics, which may be expressed as the ratio of conduction velocities in the longitudinal (Vlong) and transverse (Vtrans) fibre directions, have been shown to stabilise reentry and favour the induction of sustained, uniform ventricular tachycardia. 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Infarcted heart preparations were subjected to programmed stimulation for induction of reentrant ventricular tachycardias. Hypercalcaemia reduced both Vlong and Vtrans (P &lt; 0.05) but did not modify either the Vlong/Vtrans ratio or the induction and patterns of ventricular tachycardias. Lignocaine reduced Vlong and the Vlong/Vtrans ratio during premature stimulation (S2) of infarcted heart preparations (P &lt; 0.05) and stabilised reentrant ventricular tachycardias in preparations in which only nonsustained, multiform ventricular tachycardias were induced under control conditions. Conduction velocities in the longitudinal and transverse directions can be differentially affected by selected pharmacological interventions, but the Vlong/Vtrans ratio is not a representative index of the facilitating influence of tissue anisotropy on reentry. Therefore, the role of anisotropy in this model of reentry is not confined to establishing disparity of a functional character between conduction velocities in the longitudinal and transverse directions.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>7781010</pmid><doi>10.1016/0008-6363(96)88593-2</doi><tpages>14</tpages></addata></record>
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subjects Animals
Anisotropy
Biological and medical sciences
Cardiology. Vascular system
Coronary heart disease
Dogs
Electrophysiology
Female
Heart
Heart Conduction System - drug effects
Heart Conduction System - physiopathology
Hypercalcemia - metabolism
Lidocaine - pharmacology
Male
Medical sciences
Myocardial Ischemia - metabolism
Myocardial Ischemia - physiopathology
Myocardium - metabolism
Tachycardia, Ventricular - physiopathology
title Differential effects of lignocaine and hypercalcaemia on anisotropic conduction and reentry in the ischaemically damaged canine ventricle
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