Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation
Identifieur interne : 000071 ( Main/Corpus ); précédent : 000070; suivant : 000072Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation
Auteurs : Yuji Muraoka ; Shinji Karakawa ; Togo Yamagata ; Hideo Matsuura ; Goro KajiyamaSource :
- Pacing and Clinical Electrophysiology [ 0147-8389 ] ; 1998-02.
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- KwdEn :
Abstract
The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty‐four patients with Wolff‐Parkinson‐White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF‐AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo‐AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo‐AF group (83.3%‐5.6%, P < 0.0001), while it was unchanged in the RF‐AF group (83.3%‐75%). In preablation studies, the effective refractory periods of the atrium in the RF‐AF group and the Cryo‐AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo‐AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo‐AF group, but not in the RF‐AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.
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DOI: 10.1111/j.1540-8159.1998.tb00069.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title><author><name sortKey="Muraoka, Yuji" sort="Muraoka, Yuji" uniqKey="Muraoka Y" first="Yuji" last="Muraoka">Yuji Muraoka</name><affiliation><mods:affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</mods:affiliation></affiliation></author><author><name sortKey="Karakawa, Shinji" sort="Karakawa, Shinji" uniqKey="Karakawa S" first="Shinji" last="Karakawa">Shinji Karakawa</name><affiliation><mods:affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yamagata, Togo" sort="Yamagata, Togo" uniqKey="Yamagata T" first="Togo" last="Yamagata">Togo Yamagata</name><affiliation><mods:affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</mods:affiliation></affiliation></author><author><name sortKey="Matsuura, Hideo" sort="Matsuura, Hideo" uniqKey="Matsuura H" first="Hideo" last="Matsuura">Hideo Matsuura</name><affiliation><mods:affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kajiyama, Goro" sort="Kajiyama, Goro" uniqKey="Kajiyama G" first="Goro" last="Kajiyama">Goro Kajiyama</name><affiliation><mods:affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, 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type="istex">E96520E2521424CF6996A6151026471F784637E4</idno><idno type="DOI">10.1111/j.1540-8159.1998.tb00069.x</idno><idno type="ArticleID">PACE438</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0147-8389</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cryoablation</term><term>Wolff‐Parkinson‐White syndrome</term><term>atrial fibrillation</term><term>atrial vulnerability</term><term>catheter ablation</term><term>effective refractory period</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty‐four patients with Wolff‐Parkinson‐White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF‐AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo‐AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo‐AF group (83.3%‐5.6%, P < 0.0001), while it was unchanged in the RF‐AF group (83.3%‐75%). In preablation studies, the effective refractory periods of the atrium in the RF‐AF group and the Cryo‐AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo‐AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo‐AF group, but not in the RF‐AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>YUJI MURAOKA</name><affiliations><json:string>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</json:string></affiliations></json:item><json:item><name>SHINJI KARAKAWA</name><affiliations><json:string>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</json:string></affiliations></json:item><json:item><name>TOGO YAMAGATA</name><affiliations><json:string>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</json:string></affiliations></json:item><json:item><name>HIDEO MATSUURA</name><affiliations><json:string>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</json:string></affiliations></json:item><json:item><name>GORO KAJIYAMA</name><affiliations><json:string>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, 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>atrial vulnerability</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>Cryoablation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>effective refractory period</value></json:item></subject><articleId><json:string>PACE438</json:string></articleId><language><json:string>eng</json:string></language><abstract>The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty‐four patients with Wolff‐Parkinson‐White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF‐AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo‐AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo‐AF group (83.3%‐5.6%, P > 0.0001), while it was unchanged in the RF‐AF group (83.3%‐75%). In preablation studies, the effective refractory periods of the atrium in the RF‐AF group and the Cryo‐AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P > 0.0001). Following ablation, the effective refractory period for patients in the Cryo‐AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P > 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo‐AF group, but not in the RF‐AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.</abstract><qualityIndicators><score>8.838</score><pdfVersion>1.6</pdfVersion><pdfPageSize>564 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1999</abstractCharCount><pdfWordCount>4338</pdfWordCount><pdfCharCount>29594</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>292</abstractWordCount></qualityIndicators><title>Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title><genre><json:string>article</json:string></genre><host><volume>21</volume><publisherId><json:string>PACE</json:string></publisherId><pages><total>9</total><last>446</last><first>438</first></pages><issn><json:string>0147-8389</json:string></issn><issue>2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1540-8159</json:string></eissn><title>Pacing and Clinical Electrophysiology</title><doi><json:string>10.1111/(ISSN)1540-8159</json:string></doi></host><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1111/j.1540-8159.1998.tb00069.x</json:string></doi><id>E96520E2521424CF6996A6151026471F784637E4</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/E96520E2521424CF6996A6151026471F784637E4/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/E96520E2521424CF6996A6151026471F784637E4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/E96520E2521424CF6996A6151026471F784637E4/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title><author><persName><forename type="first">YUJI</forename><surname>MURAOKA</surname></persName><note type="correspondence"><p>Correspondence: Address for reprints: Yuji Muraoka, M.D., First Department of Internal Modiciiie, Hiroshima University School of Medirino, Kasumi 1–2–3. Minami‐ku, Hiroshima, 734, japan. Fax: 81‐82‐257‐5194.</p></note><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation></author><author><persName><forename type="first">SHINJI</forename><surname>KARAKAWA</surname></persName><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation></author><author><persName><forename type="first">TOGO</forename><surname>YAMAGATA</surname></persName><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation></author><author><persName><forename type="first">HIDEO</forename><surname>MATSUURA</surname></persName><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation></author><author><persName><forename type="first">GORO</forename><surname>KAJIYAMA</surname></persName><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation></author></analytic><monogr><title level="j">Pacing and Clinical Electrophysiology</title><idno type="pISSN">0147-8389</idno><idno type="eISSN">1540-8159</idno><idno type="DOI">10.1111/(ISSN)1540-8159</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-02"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="438">438</biblScope><biblScope unit="page" to="446">446</biblScope></imprint></monogr><idno type="istex">E96520E2521424CF6996A6151026471F784637E4</idno><idno type="DOI">10.1111/j.1540-8159.1998.tb00069.x</idno><idno type="ArticleID">PACE438</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty‐four patients with Wolff‐Parkinson‐White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF‐AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo‐AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo‐AF group (83.3%‐5.6%, P < 0.0001), while it was unchanged in the RF‐AF group (83.3%‐75%). In preablation studies, the effective refractory periods of the atrium in the RF‐AF group and the Cryo‐AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo‐AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo‐AF group, but not in the RF‐AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.</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>atrial vulnerability</term></item><item><term>catheter ablation</term></item><item><term>Cryoablation</term></item><item><term>effective refractory period</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-02">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E96520E2521424CF6996A6151026471F784637E4/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)1540-8159</doi><issn type="print">0147-8389</issn><issn type="electronic">1540-8159</issn><idGroup><id type="product" value="PACE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="PACING CLINICAL ELECTROPHYSIOLOGY">Pacing and Clinical Electrophysiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="02002"><doi origin="wiley">10.1111/pace.1998.21.issue-2</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="1998-02">February 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0043800" status="forIssue"><doi origin="wiley">10.1111/j.1540-8159.1998.tb00069.x</doi><idGroup><id type="unit" value="PACE438"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><eventGroup><event type="firstOnline" date="2006-06-30"></event><event type="publishedOnlineFinalForm" date="2006-06-30"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="438">438</numbering><numbering type="pageLast" number="446">446</numbering></numberingGroup><correspondenceTo>Address for reprints: Yuji Muraoka, M.D., First Department of Internal Modiciiie, Hiroshima University School of Medirino, Kasumi 1–2–3. Minami‐ku, Hiroshima, 734, japan. Fax: 81‐82‐257‐5194.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PACE.PACE438.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received June 6, 1996; revised November 22, 1996: accepted December 12, 1996.</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="23"></count><count type="linksCrossRef" number="6"></count></countGroup><titleGroup><title type="main"><b>Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome:</b> Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>YUJI</givenNames><familyName>MURAOKA</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>SHINJI</givenNames><familyName>KARAKAWA</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>TOGO</givenNames><familyName>YAMAGATA</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>HIDEO</givenNames><familyName>MATSUURA</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>GORO</givenNames><familyName>KAJIYAMA</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, 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">atrial vulnerability</keyword><keyword xml:id="k4">catheter ablation</keyword><keyword xml:id="k5">Cryoablation</keyword><keyword xml:id="k6">effective refractory period</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty‐four patients with Wolff‐Parkinson‐White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF‐AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo‐AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo‐AF group (83.3%‐5.6%, P < 0.0001), while it was unchanged in the RF‐AF group (83.3%‐75%). In preablation studies, the effective refractory periods of the atrium in the RF‐AF group and the Cryo‐AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo‐AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo‐AF group, but not in the RF‐AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation</title></titleInfo><name type="personal"><namePart type="given">YUJI</namePart><namePart type="family">MURAOKA</namePart><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation><description>Correspondence: Address for reprints: Yuji Muraoka, M.D., First Department of Internal Modiciiie, Hiroshima University School of Medirino, Kasumi 1–2–3. Minami‐ku, Hiroshima, 734, japan. Fax: 81‐82‐257‐5194.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SHINJI</namePart><namePart type="family">KARAKAWA</namePart><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TOGO</namePart><namePart type="family">YAMAGATA</namePart><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HIDEO</namePart><namePart type="family">MATSUURA</namePart><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GORO</namePart><namePart type="family">KAJIYAMA</namePart><affiliation>First Department of Internal Medicine, Hiroshima University School of Medicine, Kasnmi 1–2–3, Minami‐ku, Hiroshima, Japan</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">1998-02</dateIssued><edition>Received June 6, 1996; revised November 22, 1996: accepted December 12, 1996.</edition><copyrightDate encoding="w3cdtf">1998</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">23</extent></physicalDescription><abstract lang="en">The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty‐four patients with Wolff‐Parkinson‐White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF‐AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo‐AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo‐AF group (83.3%‐5.6%, P < 0.0001), while it was unchanged in the RF‐AF group (83.3%‐75%). In preablation studies, the effective refractory periods of the atrium in the RF‐AF group and the Cryo‐AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo‐AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo‐AF group, but not in the RF‐AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff‐Parkinson‐White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.</abstract><subject lang="en"><genre>Keywords</genre><topic>Wolff‐Parkinson‐White syndrome</topic><topic>atrial fibrillation</topic><topic>atrial vulnerability</topic><topic>catheter ablation</topic><topic>Cryoablation</topic><topic>effective refractory period</topic></subject><relatedItem type="host"><titleInfo><title>Pacing and Clinical Electrophysiology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0147-8389</identifier><identifier type="eISSN">1540-8159</identifier><identifier type="DOI">10.1111/(ISSN)1540-8159</identifier><identifier type="PublisherID">PACE</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>438</start><end>446</end><total>9</total></extent></part></relatedItem><identifier type="istex">E96520E2521424CF6996A6151026471F784637E4</identifier><identifier type="DOI">10.1111/j.1540-8159.1998.tb00069.x</identifier><identifier type="ArticleID">PACE438</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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