Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome
Identifieur interne : 001877 ( Main/Exploration ); précédent : 001876; suivant : 001878Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome
Auteurs : Takashi Hamada [Japon] ; Tatsuro Hiraki [Japon] ; Hisao Ikeda [Japon] ; Ichiro Kubara [Japon] ; Teruhisa Yoshida [Japon] ; Masanobu Ohga [Japon] ; Tsutomu Imaizumi [Japon]Source :
- 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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last="Ohga">Masanobu Ohga</name></author><author><name sortKey="Imaizumi, Tsutomu" sort="Imaizumi, Tsutomu" uniqKey="Imaizumi T" first="Tsutomu" last="Imaizumi">Tsutomu Imaizumi</name></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 type="wicri:Area/Main/Corpus">000525</idno><idno type="wicri:Area/Main/Curation">000455</idno><idno type="wicri:Area/Main/Exploration">001877</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome</title><author><name sortKey="Hamada, Takashi" sort="Hamada, Takashi" uniqKey="Hamada T" first="Takashi" last="Hamada">Takashi Hamada</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author><author><name sortKey="Hiraki, Tatsuro" sort="Hiraki, Tatsuro" uniqKey="Hiraki T" first="Tatsuro" last="Hiraki">Tatsuro Hiraki</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author><author><name sortKey="Ikeda, Hisao" sort="Ikeda, Hisao" uniqKey="Ikeda H" first="Hisao" last="Ikeda">Hisao Ikeda</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author><author><name sortKey="Kubara, Ichiro" sort="Kubara, Ichiro" uniqKey="Kubara I" first="Ichiro" last="Kubara">Ichiro Kubara</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author><author><name sortKey="Yoshida, Teruhisa" sort="Yoshida, Teruhisa" uniqKey="Yoshida T" first="Teruhisa" last="Yoshida">Teruhisa Yoshida</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author><author><name sortKey="Ohga, Masanobu" sort="Ohga, Masanobu" uniqKey="Ohga M" first="Masanobu" last="Ohga">Masanobu Ohga</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author><author><name sortKey="Imaizumi, Tsutomu" sort="Imaizumi, Tsutomu" uniqKey="Imaizumi T" first="Tsutomu" last="Imaizumi">Tsutomu Imaizumi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>*Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Kurume</wicri:regionArea><wicri:noRegion>Kurume</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Cardiovascular Electrophysiology</title><idno type="ISSN">1045-3873</idno><idno 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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><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Hamada, Takashi" sort="Hamada, Takashi" uniqKey="Hamada T" first="Takashi" last="Hamada">Takashi Hamada</name></noRegion><name sortKey="Hiraki, Tatsuro" sort="Hiraki, Tatsuro" uniqKey="Hiraki T" first="Tatsuro" last="Hiraki">Tatsuro Hiraki</name><name sortKey="Ikeda, Hisao" sort="Ikeda, Hisao" uniqKey="Ikeda H" first="Hisao" last="Ikeda">Hisao Ikeda</name><name sortKey="Imaizumi, Tsutomu" sort="Imaizumi, Tsutomu" uniqKey="Imaizumi T" first="Tsutomu" last="Imaizumi">Tsutomu Imaizumi</name><name sortKey="Kubara, Ichiro" sort="Kubara, Ichiro" uniqKey="Kubara I" first="Ichiro" last="Kubara">Ichiro Kubara</name><name sortKey="Ohga, Masanobu" sort="Ohga, Masanobu" uniqKey="Ohga M" first="Masanobu" last="Ohga">Masanobu Ohga</name><name sortKey="Yoshida, Teruhisa" sort="Yoshida, Teruhisa" uniqKey="Yoshida T" first="Teruhisa" last="Yoshida">Teruhisa Yoshida</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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