Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome
Identifieur interne : 000525 ( Main/Corpus ); précédent : 000524; suivant : 000526Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome
Auteurs : Takashi Hamada ; Tatsuro Hiraki ; Hisao Ikeda ; Ichiro Kubara ; Teruhisa Yoshida ; Masanobu Ohga ; Tsutomu ImaizumiSource :
- Journal of Cardiovascular Electrophysiology [ 1045-3873 ] ; 2002-03.
English descriptors
Abstract
Atrial Fibrillation and WPW Syndrome. Introduction: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff‐Parkinson‐White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). Methods and Results: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long‐term follow‐up (17 ± 7 months). Conclusion: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP‐dependent atrial vulnerability, and the other is intrinsic and AP‐independent atrial vulnerability.
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DOI: 10.1046/j.1540-8167.2002.00223.x
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Ikeda</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kubara, Ichiro" sort="Kubara, Ichiro" uniqKey="Kubara I" first="Ichiro" last="Kubara">Ichiro Kubara</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yoshida, Teruhisa" sort="Yoshida, Teruhisa" uniqKey="Yoshida T" first="Teruhisa" last="Yoshida">Teruhisa Yoshida</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ohga, Masanobu" sort="Ohga, Masanobu" uniqKey="Ohga M" first="Masanobu" last="Ohga">Masanobu Ohga</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Imaizumi, Tsutomu" sort="Imaizumi, Tsutomu" uniqKey="Imaizumi T" first="Tsutomu" last="Imaizumi">Tsutomu Imaizumi</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:07856F7CAABB980894830A85F063623FC87FA87B</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1046/j.1540-8167.2002.00223.x</idno><idno type="url">https://api.istex.fr/document/07856F7CAABB980894830A85F063623FC87FA87B/fulltext/pdf</idno><idno 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last="Ikeda">Hisao Ikeda</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kubara, Ichiro" sort="Kubara, Ichiro" uniqKey="Kubara I" first="Ichiro" last="Kubara">Ichiro Kubara</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yoshida, Teruhisa" sort="Yoshida, Teruhisa" uniqKey="Yoshida T" first="Teruhisa" last="Yoshida">Teruhisa Yoshida</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ohga, Masanobu" sort="Ohga, Masanobu" uniqKey="Ohga M" first="Masanobu" last="Ohga">Masanobu Ohga</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</mods:affiliation></affiliation></author><author><name sortKey="Imaizumi, Tsutomu" sort="Imaizumi, Tsutomu" uniqKey="Imaizumi T" first="Tsutomu" last="Imaizumi">Tsutomu Imaizumi</name><affiliation><mods:affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</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 Science Inc</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-03">2002-03</date><biblScope unit="volume">13</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="223">223</biblScope><biblScope unit="page" to="229">229</biblScope></imprint><idno type="ISSN">1045-3873</idno></series><idno type="istex">07856F7CAABB980894830A85F063623FC87FA87B</idno><idno type="DOI">10.1046/j.1540-8167.2002.00223.x</idno><idno type="ArticleID">JCE223</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1045-3873</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Wolff‐Parkinson‐White syndrome</term><term>atrial fibrillation</term><term>catheter ablation</term><term>recurrence</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Atrial Fibrillation and WPW Syndrome. Introduction: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff‐Parkinson‐White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). Methods and Results: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long‐term follow‐up (17 ± 7 months). Conclusion: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP‐dependent atrial vulnerability, and the other is intrinsic and AP‐independent atrial vulnerability.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>TAKASHI HAMADA M.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item><json:item><name>TATSURO HIRAKI M.D., Ph.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item><json:item><name>HISAO IKEDA M.D., Ph.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item><json:item><name>ICHIRO KUBARA M.D., Ph.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item><json:item><name>TERUHISA YOSHIDA M.D., Ph.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item><json:item><name>MASANOBU OHGA M.D., Ph.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item><json:item><name>TSUTOMU IMAIZUMI M.D., Ph.D.</name><affiliations><json:string>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Wolff‐Parkinson‐White syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>atrial fibrillation</value></json:item><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>recurrence</value></json:item></subject><articleId><json:string>JCE223</json:string></articleId><language><json:string>eng</json:string></language><abstract>Atrial Fibrillation and WPW Syndrome. Introduction: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff‐Parkinson‐White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). Methods and Results: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P > 0.0001 and P > 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P > 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long‐term follow‐up (17 ± 7 months). Conclusion: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP‐dependent atrial vulnerability, and the other is intrinsic and AP‐independent atrial vulnerability.</abstract><qualityIndicators><score>7.638</score><pdfVersion>1.2</pdfVersion><pdfPageSize>572.031 x 776.126 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1983</abstractCharCount><pdfWordCount>4638</pdfWordCount><pdfCharCount>29205</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>300</abstractWordCount></qualityIndicators><title>Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White 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Medicine, Kurume, Japan</affiliation></author><author><persName><forename type="first">MASANOBU</forename><surname>OHGA</surname></persName><roleName type="degree">M.D., Ph.D.</roleName><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation></author><author><persName><forename type="first">TSUTOMU</forename><surname>IMAIZUMI</surname></persName><roleName type="degree">M.D., Ph.D.</roleName><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</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 Science Inc</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2002-03"></date><biblScope unit="volume">13</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="223">223</biblScope><biblScope unit="page" to="229">229</biblScope></imprint></monogr><idno type="istex">07856F7CAABB980894830A85F063623FC87FA87B</idno><idno type="DOI">10.1046/j.1540-8167.2002.00223.x</idno><idno type="ArticleID">JCE223</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Atrial Fibrillation and WPW Syndrome. Introduction: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff‐Parkinson‐White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). Methods and Results: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long‐term follow‐up (17 ± 7 months). Conclusion: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP‐dependent atrial vulnerability, and the other is intrinsic and AP‐independent atrial vulnerability.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Wolff‐Parkinson‐White syndrome</term></item><item><term>atrial fibrillation</term></item><item><term>catheter ablation</term></item><item><term>recurrence</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2002-03">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-3">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/07856F7CAABB980894830A85F063623FC87FA87B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component found"><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 Science Inc</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="03003"><doi origin="wiley">10.1111/jce.2002.13.issue-3</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2002-03">March 2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0022300" status="forIssue"><doi origin="wiley">10.1046/j.1540-8167.2002.00223.x</doi><idGroup><id type="unit" value="JCE223"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© Futura Publishing Company, Inc. 2002</copyright><eventGroup><event type="firstOnline" date="2003-08-12"></event><event type="publishedOnlineFinalForm" date="2003-08-12"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:Header result:Header" 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="2014-10-23"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="223">223</numbering><numbering type="pageLast" number="229">229</numbering></numberingGroup><correspondenceTo>Address for correspondence: Tatsuro Hiraki, M.D., Ph.D., Department of Internal Medicine III, Kurume University School of Medicine, 67 Asahi‐machi, Kurume 830‐0011, Japan. Fax: 81‐942‐33‐6509; E‐mail: <email normalForm="thiraki@med.kurume-u.ac.jp">thiraki@med.kurume‐u.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCE.JCE223.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Manuscript received 5 October 2001; Accepted for publication 4 February 2002.</unparsedEditorialHistory><titleGroup><title type="main">Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>TAKASHI</givenNames><familyName>HAMADA</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>TATSURO</givenNames><familyName>HIRAKI</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>HISAO</givenNames><familyName>IKEDA</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>ICHIRO</givenNames><familyName>KUBARA</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>TERUHISA</givenNames><familyName>YOSHIDA</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>MASANOBU</givenNames><familyName>OHGA</familyName><degrees>M.D., Ph.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>TSUTOMU</givenNames><familyName>IMAIZUMI</familyName><degrees>M.D., Ph.D.</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Wolff‐Parkinson‐White syndrome</keyword><keyword xml:id="k2">atrial fibrillation</keyword><keyword xml:id="k3">catheter ablation</keyword><keyword xml:id="k4">recurrence</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p> <b>Atrial Fibrillation and WPW Syndrome.</b><i>Introduction:</i> Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff‐Parkinson‐White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs).</p><p> <i>Methods and Results:</i> We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (<span type="mathematics">n = 14</span>), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (<span type="mathematics">n = 10</span>). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (<span type="mathematics">P < 0.0001 and P < 0.0001, respectively</span>) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (<span type="mathematics">P < 0.0001</span>) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long‐term follow‐up (<span type="mathematics">17 ± 7 months</span>).</p><p> <i>Conclusion:</i> The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP‐dependent atrial vulnerability, and the other is intrinsic and AP‐independent atrial vulnerability.</p><!-- (J Cardiovasc Electrophysiol, Vol. 13, pp. 223–229, March 2002)
</abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>This study was supported by a Grant for Science Frontier Research Pro‐motion Centers from the Ministry of Education, Science, Sports and Culture, Japan.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome</title></titleInfo><name type="personal"><namePart type="given">TAKASHI</namePart><namePart type="family">HAMADA</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TATSURO</namePart><namePart type="family">HIRAKI</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HISAO</namePart><namePart type="family">IKEDA</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ICHIRO</namePart><namePart type="family">KUBARA</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TERUHISA</namePart><namePart type="family">YOSHIDA</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MASANOBU</namePart><namePart type="family">OHGA</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TSUTOMU</namePart><namePart type="family">IMAIZUMI</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Inc</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2002-03</dateIssued><edition>Manuscript received 5 October 2001; Accepted for publication 4 February 2002.</edition><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Atrial Fibrillation and WPW Syndrome. Introduction: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff‐Parkinson‐White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). Methods and Results: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long‐term follow‐up (17 ± 7 months). Conclusion: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP‐dependent atrial vulnerability, and the other is intrinsic and AP‐independent atrial vulnerability.</abstract><subject lang="en"><genre>Keywords</genre><topic>Wolff‐Parkinson‐White syndrome</topic><topic>atrial fibrillation</topic><topic>catheter ablation</topic><topic>recurrence</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>2002</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>223</start><end>229</end><total>7</total></extent></part></relatedItem><identifier type="istex">07856F7CAABB980894830A85F063623FC87FA87B</identifier><identifier type="DOI">10.1046/j.1540-8167.2002.00223.x</identifier><identifier type="ArticleID">JCE223</identifier><accessCondition type="use and reproduction" contentType="copyright">© Futura Publishing Company, Inc. 2002</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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