Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation
Identifieur interne : 000756 ( Istex/Corpus ); précédent : 000755; suivant : 000757Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation
Auteurs : Emoke Posan ; Lorne J. Gula ; Allan C. Skanes ; Andrew D. Krahn ; Raymond Yee ; Basilios Petrellis ; Damian P. Redfearn ; Uwais Mohamed ; Paul A. Gould ; George J. KleinSource :
- Journal of Cardiovascular Electrophysiology [ 1045-3873 ] ; 2006-08.
English descriptors
- KwdEn :
Abstract
Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox. Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre‐ and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013); mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001). Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.
Url:
DOI: 10.1111/j.1540-8167.2006.00492.x
Links to Exploration step
ISTEX:B48FB2053E9197FF284325910055B400156E0503Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title><author><name sortKey="Posan, Emoke" sort="Posan, Emoke" uniqKey="Posan E" first="Emoke" last="Posan">Emoke Posan</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gula, Lorne J" sort="Gula, Lorne J" uniqKey="Gula L" first="Lorne J." last="Gula">Lorne J. Gula</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Skanes, Allan C" sort="Skanes, Allan C" uniqKey="Skanes A" first="Allan C." last="Skanes">Allan C. Skanes</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Krahn, Andrew D" sort="Krahn, Andrew D" uniqKey="Krahn A" first="Andrew D." last="Krahn">Andrew D. Krahn</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Yee, Raymond" sort="Yee, Raymond" uniqKey="Yee R" first="Raymond" last="Yee">Raymond Yee</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Petrellis, Basilios" sort="Petrellis, Basilios" uniqKey="Petrellis B" first="Basilios" last="Petrellis">Basilios Petrellis</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Redfearn, Damian P" sort="Redfearn, Damian P" uniqKey="Redfearn D" first="Damian P." last="Redfearn">Damian P. Redfearn</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Mohamed, Uwais" sort="Mohamed, Uwais" uniqKey="Mohamed U" first="Uwais" last="Mohamed">Uwais Mohamed</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gould, Paul A" sort="Gould, Paul A" uniqKey="Gould P" first="Paul A." last="Gould">Paul A. Gould</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Klein, George J" sort="Klein, George J" uniqKey="Klein G" first="George J." last="Klein">George J. Klein</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B48FB2053E9197FF284325910055B400156E0503</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1111/j.1540-8167.2006.00492.x</idno><idno type="url">https://api-v5.istex.fr/document/B48FB2053E9197FF284325910055B400156E0503/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000756</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000756</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title><author><name sortKey="Posan, Emoke" sort="Posan, Emoke" uniqKey="Posan E" first="Emoke" last="Posan">Emoke Posan</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gula, Lorne J" sort="Gula, Lorne J" uniqKey="Gula L" first="Lorne J." last="Gula">Lorne J. Gula</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Skanes, Allan C" sort="Skanes, Allan C" uniqKey="Skanes A" first="Allan C." last="Skanes">Allan C. Skanes</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Krahn, Andrew D" sort="Krahn, Andrew D" uniqKey="Krahn A" first="Andrew D." last="Krahn">Andrew D. Krahn</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Yee, Raymond" sort="Yee, Raymond" uniqKey="Yee R" first="Raymond" last="Yee">Raymond Yee</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Petrellis, Basilios" sort="Petrellis, Basilios" uniqKey="Petrellis B" first="Basilios" last="Petrellis">Basilios Petrellis</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Redfearn, Damian P" sort="Redfearn, Damian P" uniqKey="Redfearn D" first="Damian P." last="Redfearn">Damian P. Redfearn</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Mohamed, Uwais" sort="Mohamed, Uwais" uniqKey="Mohamed U" first="Uwais" last="Mohamed">Uwais Mohamed</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gould, Paul A" sort="Gould, Paul A" uniqKey="Gould P" first="Paul A." last="Gould">Paul A. Gould</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Klein, George J" sort="Klein, George J" uniqKey="Klein G" first="George J." last="Klein">George J. Klein</name><affiliation><mods:affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, 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 Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2006-08">2006-08</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="847">847</biblScope><biblScope unit="page" to="851">851</biblScope></imprint><idno type="ISSN">1045-3873</idno></series><idno type="istex">B48FB2053E9197FF284325910055B400156E0503</idno><idno type="DOI">10.1111/j.1540-8167.2006.00492.x</idno><idno type="ArticleID">JCE492</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1045-3873</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AV node</term><term>AVN reentry</term><term>AVNRT</term><term>catheter ablation</term><term>conduction</term><term>electrophysiology</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox. Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre‐ and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013); mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001). Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>EMOKE POSAN M.D., Ph.D.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>LORNE J. GULA M.D., M.S., F.R.C.P.C.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>ALLAN C. SKANES M.D., F.R.C.P.C.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>ANDREW D. KRAHN M.D., F.R.C.P.C.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>RAYMOND YEE M.D., F.R.C.P.C.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>BASILIOS PETRELLIS F.R.A.C.P.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>DAMIAN P. REDFEARN M.B., Ch.B.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>UWAIS MOHAMED M.B.B.S., F.R.A.C.P.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>PAUL A. GOULD M.B.B.S., Ph.D., F.R.A.C.P.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>GEORGE J. KLEIN M.D., F.R.C.P.C.</name><affiliations><json:string>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>catheter ablation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AVNRT</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>electrophysiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AVN reentry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>AV node</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>conduction</value></json:item></subject><articleId><json:string>JCE492</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox. Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre‐ and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P > 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P > 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013); mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001). Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.</abstract><qualityIndicators><score>6.401</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594.006 x 783.008 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1694</abstractCharCount><pdfWordCount>3401</pdfWordCount><pdfCharCount>21000</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>254</abstractWordCount></qualityIndicators><title>Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title><genre><json:string>article</json:string></genre><host><title>Journal of Cardiovascular Electrophysiology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1540-8167</json:string></doi><issn><json:string>1045-3873</json:string></issn><eissn><json:string>1540-8167</json:string></eissn><publisherId><json:string>JCE</json:string></publisherId><volume>17</volume><issue>8</issue><pages><first>847</first><last>851</last><total>5</total></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>cardiac & cardiovascular systems</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>cardiovascular system & hematology</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1111/j.1540-8167.2006.00492.x</json:string></doi><id>B48FB2053E9197FF284325910055B400156E0503</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/B48FB2053E9197FF284325910055B400156E0503/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/B48FB2053E9197FF284325910055B400156E0503/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/B48FB2053E9197FF284325910055B400156E0503/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><availability><p>WILEY</p></availability><date>2006</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title><author xml:id="author-1"><persName><forename type="first">EMOKE</forename><surname>POSAN</surname></persName><roleName type="degree">M.D., Ph.D.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">LORNE J.</forename><surname>GULA</surname></persName><roleName type="degree">M.D., M.S., F.R.C.P.C.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">ALLAN C.</forename><surname>SKANES</surname></persName><roleName type="degree">M.D., F.R.C.P.C.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-4"><persName><forename type="first">ANDREW D.</forename><surname>KRAHN</surname></persName><roleName type="degree">M.D., F.R.C.P.C.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">RAYMOND</forename><surname>YEE</surname></persName><roleName type="degree">M.D., F.R.C.P.C.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-6"><persName><forename type="first">BASILIOS</forename><surname>PETRELLIS</surname></persName><roleName type="degree">F.R.A.C.P.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-7"><persName><forename type="first">DAMIAN P.</forename><surname>REDFEARN</surname></persName><roleName type="degree">M.B., Ch.B.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-8"><persName><forename type="first">UWAIS</forename><surname>MOHAMED</surname></persName><roleName type="degree">M.B.B.S., F.R.A.C.P.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-9"><persName><forename type="first">PAUL A.</forename><surname>GOULD</surname></persName><roleName type="degree">M.B.B.S., Ph.D., F.R.A.C.P.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author><author xml:id="author-10"><persName><forename type="first">GEORGE J.</forename><surname>KLEIN</surname></persName><roleName type="degree">M.D., F.R.C.P.C.</roleName><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation></author></analytic><monogr><title level="j">Journal of Cardiovascular Electrophysiology</title><idno type="pISSN">1045-3873</idno><idno type="eISSN">1540-8167</idno><idno type="DOI">10.1111/(ISSN)1540-8167</idno><imprint><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><date type="published" when="2006-08"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="847">847</biblScope><biblScope unit="page" to="851">851</biblScope></imprint></monogr><idno type="istex">B48FB2053E9197FF284325910055B400156E0503</idno><idno type="DOI">10.1111/j.1540-8167.2006.00492.x</idno><idno type="ArticleID">JCE492</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox. Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre‐ and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013); mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001). Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>catheter ablation</term></item><item><term>AVNRT</term></item><item><term>electrophysiology</term></item><item><term>AVN reentry</term></item><item><term>AV node</term></item><item><term>conduction</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-08">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/B48FB2053E9197FF284325910055B400156E0503/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 Inc</publisherName><publisherLoc>Malden, USA</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="08008"><doi origin="wiley">10.1111/jce.2006.17.issue-8</doi><numberingGroup><numbering type="journalVolume" number="17">17</numbering><numbering type="journalIssue" number="8">8</numbering></numberingGroup><coverDate startDate="2006-08">August 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="8" status="forIssue"><doi origin="wiley">10.1111/j.1540-8167.2006.00492.x</doi><idGroup><id type="unit" value="JCE492"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title><title type="tocHeading2"><i>Clinical</i></title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-04"></event><event type="publishedOnlineFinalForm" date="2006-04-04"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.4 mode:FullText source:FullText result:FullText" date="2010-03-30"></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="847">847</numbering><numbering type="pageLast" number="851">851</numbering></numberingGroup><correspondenceTo>Address for correspondence: Lorne J. Gula, M.D., M.S., F.R.C.P.C., London Health Sciences Centre, 339 Windermere Road, London, Ontario N6A 5A5, Canada. Fax: (519) 434‐3278; E‐mail: <email>lgula@uwo.ca</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCE.JCE492.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="23"></count><count type="linksCrossRef" number="32"></count></countGroup><titleGroup><title type="main">Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>EMOKE</givenNames><familyName>POSAN</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>LORNE J.</givenNames><familyName>GULA</familyName><degrees>M.D., M.S., F.R.C.P.C.</degrees></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>ALLAN C.</givenNames><familyName>SKANES</familyName><degrees>M.D., F.R.C.P.C.</degrees></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>ANDREW D.</givenNames><familyName>KRAHN</familyName><degrees>M.D., F.R.C.P.C.</degrees></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>RAYMOND</givenNames><familyName>YEE</familyName><degrees>M.D., F.R.C.P.C.</degrees></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>BASILIOS</givenNames><familyName>PETRELLIS</familyName><degrees>F.R.A.C.P.</degrees></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>DAMIAN P.</givenNames><familyName>REDFEARN</familyName><degrees>M.B., Ch.B.</degrees></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>UWAIS</givenNames><familyName>MOHAMED</familyName><degrees>M.B.B.S., F.R.A.C.P.</degrees></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1"><personName><givenNames>PAUL A.</givenNames><familyName>GOULD</familyName><degrees>M.B.B.S., Ph.D., F.R.A.C.P.</degrees></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a1"><personName><givenNames>GEORGE J.</givenNames><familyName>KLEIN</familyName><degrees>M.D., F.R.C.P.C.</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1"><i>catheter ablation</i></keyword><keyword xml:id="k2"><i>AVNRT</i></keyword><keyword xml:id="k3"><i>electrophysiology</i></keyword><keyword xml:id="k4"><i>AVN reentry</i></keyword><keyword xml:id="k5"><i>AV node</i></keyword><keyword xml:id="k6"><i>conduction</i></keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!-- Persistent Slow Pathway After AVNRT Ablation. 
<p> <i>Background:</i> AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox.</p><p> <i>Methods and Results:</i> Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre‐ and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013<i>)</i>; mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016<i>).</i> Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001).</p><p> <i>Conclusions:</i> Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.</p><!-- (J Cardiovasc Electrophysiol, Vol. 17, pp. 847-851, August 2006)
</abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>Manuscript received 26 January 2006; Revised manuscript received 12 February 2006; Accepted for publication 15 February 2006.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation</title></titleInfo><name type="personal"><namePart type="given">EMOKE</namePart><namePart type="family">POSAN</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LORNE J.</namePart><namePart type="family">GULA</namePart><namePart type="termsOfAddress">M.D., M.S., F.R.C.P.C.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ALLAN C.</namePart><namePart type="family">SKANES</namePart><namePart type="termsOfAddress">M.D., F.R.C.P.C.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ANDREW D.</namePart><namePart type="family">KRAHN</namePart><namePart type="termsOfAddress">M.D., F.R.C.P.C.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RAYMOND</namePart><namePart type="family">YEE</namePart><namePart type="termsOfAddress">M.D., F.R.C.P.C.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BASILIOS</namePart><namePart type="family">PETRELLIS</namePart><namePart type="termsOfAddress">F.R.A.C.P.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DAMIAN P.</namePart><namePart type="family">REDFEARN</namePart><namePart type="termsOfAddress">M.B., Ch.B.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">UWAIS</namePart><namePart type="family">MOHAMED</namePart><namePart type="termsOfAddress">M.B.B.S., F.R.A.C.P.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PAUL A.</namePart><namePart type="family">GOULD</namePart><namePart type="termsOfAddress">M.B.B.S., Ph.D., F.R.A.C.P.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GEORGE J.</namePart><namePart type="family">KLEIN</namePart><namePart type="termsOfAddress">M.D., F.R.C.P.C.</namePart><affiliation>Division of Cardiology, Department of Medicine, London Health Sciences Centre, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Inc</publisher><place><placeTerm type="text">Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2006-08</dateIssued><copyrightDate encoding="w3cdtf">2006</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="figures">2</extent><extent unit="tables">2</extent><extent unit="references">23</extent></physicalDescription><abstract lang="en">Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox. Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre‐ and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013); mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001). Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining tachycardia.</abstract><subject lang="en"><genre>keywords</genre><topic>catheter ablation</topic><topic>AVNRT</topic><topic>electrophysiology</topic><topic>AVN reentry</topic><topic>AV node</topic><topic>conduction</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>2006</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>847</start><end>851</end><total>5</total></extent></part></relatedItem><identifier type="istex">B48FB2053E9197FF284325910055B400156E0503</identifier><identifier type="DOI">10.1111/j.1540-8167.2006.00492.x</identifier><identifier type="ArticleID">JCE492</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000756 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000756 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:B48FB2053E9197FF284325910055B400156E0503
|texte= Characteristics of Slow Pathway Conduction After Successful AVNRT Ablation
}}
| This area was generated with Dilib version V0.6.29. |  |