Role of the Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties
Identifieur interne : 001199 ( Istex/Corpus ); précédent : 001198; suivant : 001200Role of the Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties
Auteurs : Karim Khalife ; Jacques Billette ; Djamila Medkour ; Karyne Martel ; Maurice Tremblay ; Jun Wang ; Li-Jen LinSource :
- Journal of Cardiovascular Electrophysiology [ 1045-3873 ] ; 1999-11.
English descriptors
Abstract
AV Nodal Conduction and Dual Pathways. Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (<300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P < 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P < 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. Conclusion: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.
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DOI: 10.1111/j.1540-8167.1999.tb00203.x
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ISTEX:60F7CE56E8582A8DD3DE41BAF0434C8A376B7383Le document en format XML
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Djamila" uniqKey="Medkour D" first="Djamila" last="Medkour">Djamila Medkour</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Martel, Karyne" sort="Martel, Karyne" uniqKey="Martel K" first="Karyne" last="Martel">Karyne Martel</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Tremblay, Maurice" sort="Tremblay, Maurice" uniqKey="Tremblay M" first="Maurice" last="Tremblay">Maurice Tremblay</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Wang, Jun" sort="Wang, Jun" uniqKey="Wang J" first="Jun" last="Wang">Jun Wang</name><affiliation><mods:affiliation>Department de 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Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties</title><author><name sortKey="Khalife, Karim" sort="Khalife, Karim" uniqKey="Khalife K" first="Karim" last="Khalife">Karim Khalife</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Billette, Jacques" sort="Billette, Jacques" uniqKey="Billette J" first="Jacques" last="Billette">Jacques Billette</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jacques.billette@umontreal.ca</mods:affiliation></affiliation></author><author><name sortKey="Medkour, Djamila" sort="Medkour, Djamila" uniqKey="Medkour D" first="Djamila" last="Medkour">Djamila Medkour</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Martel, Karyne" sort="Martel, Karyne" uniqKey="Martel K" first="Karyne" last="Martel">Karyne Martel</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Tremblay, Maurice" sort="Tremblay, Maurice" uniqKey="Tremblay M" first="Maurice" last="Tremblay">Maurice Tremblay</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Wang, Jun" sort="Wang, Jun" uniqKey="Wang J" first="Jun" last="Wang">Jun Wang</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lin, Li En" sort="Lin, Li En" uniqKey="Lin L" first="Li-Jen" last="Lin">Li-Jen Lin</name><affiliation><mods:affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Cardiovascular Electrophysiology</title><idno type="ISSN">1045-3873</idno><idno type="eISSN">1540-8167</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1999-11">1999-11</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1439">1439</biblScope><biblScope unit="page" to="1451">1451</biblScope></imprint><idno type="ISSN">1045-3873</idno></series><idno type="istex">60F7CE56E8582A8DD3DE41BAF0434C8A376B7383</idno><idno type="DOI">10.1111/j.1540-8167.1999.tb00203.x</idno><idno 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Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (<300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P < 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P < 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. Conclusion: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>KARIM KHALIFE B.Sc.</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string></affiliations></json:item><json:item><name>JACQUES BILLETTE M.D. PH.D.</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string><json:string>E-mail: jacques.billette@umontreal.ca</json:string></affiliations></json:item><json:item><name>DJAMILA MEDKOUR M.D., M.Sc</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string></affiliations></json:item><json:item><name>KARYNE MARTEL B.Sc.</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string></affiliations></json:item><json:item><name>MAURICE TREMBLAY Eng</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string></affiliations></json:item><json:item><name>JUN WANG M.D., Ph.D.</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string></affiliations></json:item><json:item><name>LI‐JEN LIN M.D.</name><affiliations><json:string>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>dual pathways</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ablation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>reentry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>inputs</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>supraventricular tachyarrhythmias</value></json:item></subject><articleId><json:string>JCE1439</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>AV Nodal Conduction and Dual Pathways. Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (>300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P > 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P > 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. 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to="1451">1451</biblScope></imprint></monogr><idno type="istex">60F7CE56E8582A8DD3DE41BAF0434C8A376B7383</idno><idno type="DOI">10.1111/j.1540-8167.1999.tb00203.x</idno><idno type="ArticleID">JCE1439</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1999</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>AV Nodal Conduction and Dual Pathways. Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (<300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P < 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P < 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. Conclusion: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>dual pathways</term></item><item><term>ablation</term></item><item><term>reentry</term></item><item><term>inputs</term></item><item><term>supraventricular tachyarrhythmias</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1999-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/60F7CE56E8582A8DD3DE41BAF0434C8A376B7383/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1540-8167</doi><issn type="print">1045-3873</issn><issn type="electronic">1540-8167</issn><idGroup><id type="product" value="JCE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY">Journal of Cardiovascular Electrophysiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="11011"><doi origin="wiley">10.1111/jce.1999.10.issue-11</doi><numberingGroup><numbering type="journalVolume" number="10">10</numbering><numbering type="journalIssue" number="11">11</numbering></numberingGroup><coverDate startDate="1999-11">November 1999</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0143900" status="forIssue"><doi origin="wiley">10.1111/j.1540-8167.1999.tb00203.x</doi><idGroup><id type="unit" value="JCE1439"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><eventGroup><event type="firstOnline" date="2007-04-20"></event><event type="publishedOnlineFinalForm" date="2007-04-20"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-10"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-29"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-24"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1439">1439</numbering><numbering type="pageLast" number="1451">1451</numbering></numberingGroup><correspondenceTo>Address for correspondence: Jacques Billette, M.D., Ph.D., Pavilion Desmarais 2135, Département de Physiologie (Médecine), Université de Montréal, CP 6128. Succ CV, Montréal, Québec, Canada, H3C 3J7. Fax: 514‐343‐2111; E‐mail: <email>jacques.billette@umontreal.ca</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCE.JCE1439.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Manuscript received 5 February 1999; Accepted for publication July 1999</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="64"></count><count type="linksCrossRef" number="8"></count></countGroup><titleGroup><title type="main">Role of the Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>KARIM</givenNames><familyName>KHALIFE</familyName><degrees>B.Sc.</degrees></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1" corresponding="yes"><personName><givenNames>JACQUES</givenNames><familyName>BILLETTE</familyName><degrees>M.D. PH.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>DJAMILA</givenNames><familyName>MEDKOUR</familyName><degrees>M.D., M.Sc</degrees></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>KARYNE</givenNames><familyName>MARTEL</familyName><degrees>B.Sc.</degrees></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>MAURICE</givenNames><familyName>TREMBLAY</familyName><degrees>Eng</degrees></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>JUN</givenNames><familyName>WANG</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>LI‐JEN</givenNames><familyName>LIN</familyName><degrees>M.D.</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dual pathways</keyword><keyword xml:id="k2">ablation</keyword><keyword xml:id="k3">reentry</keyword><keyword xml:id="k4">inputs</keyword><keyword xml:id="k5">supraventricular tachyarrhythmias</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>AV Nodal Conduction and Dual Pathways. <i>Introduction:</i> The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures.</p><p> <i>Methods and Results:</i> A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (<300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A<sub>2</sub>H<sub>2</sub>max from 159 ± 16 ms to 123 ± 11 msec (P < 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P < 0.01) without affecting A<sub>2</sub>H<sub>2</sub> min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway.</p><p> <i>Conclusion:</i> The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>This work was supported by the Medical Research Council of Canada, the Quebec Heart and Stroke Foundation, and Fonds de la recherche en santé du Québec.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of the Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Role of the Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties</title></titleInfo><name type="personal"><namePart type="given">KARIM</namePart><namePart type="family">KHALIFE</namePart><namePart type="termsOfAddress">B.Sc.</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JACQUES</namePart><namePart type="family">BILLETTE</namePart><namePart type="termsOfAddress">M.D. PH.D.</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><affiliation>E-mail: jacques.billette@umontreal.ca</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DJAMILA</namePart><namePart type="family">MEDKOUR</namePart><namePart type="termsOfAddress">M.D., M.Sc</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KARYNE</namePart><namePart type="family">MARTEL</namePart><namePart type="termsOfAddress">B.Sc.</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MAURICE</namePart><namePart type="family">TREMBLAY</namePart><namePart type="termsOfAddress">Eng</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JUN</namePart><namePart type="family">WANG</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LI‐JEN</namePart><namePart type="family">LIN</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1999-11</dateIssued><edition>Manuscript received 5 February 1999; Accepted for publication July 1999</edition><copyrightDate encoding="w3cdtf">1999</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">64</extent></physicalDescription><abstract lang="en">AV Nodal Conduction and Dual Pathways. Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (<300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P < 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P < 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. Conclusion: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.</abstract><subject lang="en"><genre>keywords</genre><topic>dual pathways</topic><topic>ablation</topic><topic>reentry</topic><topic>inputs</topic><topic>supraventricular tachyarrhythmias</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Cardiovascular Electrophysiology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1045-3873</identifier><identifier type="eISSN">1540-8167</identifier><identifier type="DOI">10.1111/(ISSN)1540-8167</identifier><identifier type="PublisherID">JCE</identifier><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1439</start><end>1451</end><total>13</total></extent></part></relatedItem><identifier type="istex">60F7CE56E8582A8DD3DE41BAF0434C8A376B7383</identifier><identifier type="DOI">10.1111/j.1540-8167.1999.tb00203.x</identifier><identifier type="ArticleID">JCE1439</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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