Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway
Identifieur interne : 000169 ( Main/Corpus ); précédent : 000168; suivant : 000170Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway
Auteurs : Bo Sang Kwon ; Eun Jung Bae ; Gi Beom Kim ; Chung Il Noh ; Jung Yun Choi ; Yong Soo YunSource :
- Journal of Cardiovascular Electrophysiology [ 1045-3873 ] ; 2010-03.
English descriptors
- KwdEn :
Abstract
LV Dysfunction in WPW Syndrome. Introduction: Echocardiographic studies have shown that some patients with Wolff‐Parkinson‐White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction. Methods: Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 ± 4.2 years) were retrospectively analyzed. Results: The left ventricular ejection fraction (LVEF) of patients with septal APs (53 ± 11%) was significantly lower than that of patients with right (62 ± 5%) or left (61 ± 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 ± 4% and 42 ± 5%, respectively) and an increased LV end diastolic dimension (P < 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 ± 18 ms and 113 ± 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal‐to‐posterior wall motion delay, from 154 ± 91 ms to 33 ± 17 ms) and interventricular septal thinning (from 3.0 ± 0.5 mm to 5.3 ± 2.6 mm), and a significant increase in LVEF (from 42 ± 5% to 67 ± 8%; P = 0.001). Conclusion: The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function. (J Cardiovasc Electrophysiol, Vol. 21, pp. 290–295, March 2010)
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DOI: 10.1111/j.1540-8167.2009.01612.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title><author><name sortKey="Kwon, Bo Sang" sort="Kwon, Bo Sang" uniqKey="Kwon B" first="Bo Sang" last="Kwon">Bo Sang Kwon</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Bae, Eun Jung" sort="Bae, Eun Jung" uniqKey="Bae E" first="Eun Jung" last="Bae">Eun Jung Bae</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Gi Beom" sort="Kim, Gi Beom" uniqKey="Kim G" first="Gi Beom" last="Kim">Gi Beom Kim</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Noh, Chung Il" sort="Noh, Chung Il" uniqKey="Noh C" first="Chung Il" last="Noh">Chung Il Noh</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Choi, Jung Yun" sort="Choi, Jung Yun" uniqKey="Choi J" first="Jung Yun" last="Choi">Jung Yun Choi</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yun, Yong Soo" sort="Yun, Yong Soo" uniqKey="Yun Y" first="Yong Soo" last="Yun">Yong Soo Yun</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno 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Bae</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Gi Beom" sort="Kim, Gi Beom" uniqKey="Kim G" first="Gi Beom" last="Kim">Gi Beom Kim</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Noh, Chung Il" sort="Noh, Chung Il" uniqKey="Noh C" first="Chung Il" last="Noh">Chung Il Noh</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Choi, Jung Yun" sort="Choi, Jung Yun" uniqKey="Choi J" first="Jung Yun" last="Choi">Jung Yun Choi</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yun, Yong Soo" sort="Yun, Yong Soo" uniqKey="Yun Y" first="Yong Soo" last="Yun">Yong Soo Yun</name><affiliation><mods:affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</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="2010-03">2010-03</date><biblScope unit="volume">21</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="290">290</biblScope><biblScope unit="page" to="295">295</biblScope></imprint><idno type="ISSN">1045-3873</idno></series><idno type="istex">9567517CEB2B4F36498AA91E9569A7D846BE3E56</idno><idno type="DOI">10.1111/j.1540-8167.2009.01612.x</idno><idno type="ArticleID">JCE1612</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>cardiomyopathy</term><term>catheter ablation</term><term>resynchronization</term><term>septal dyskinesia</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">LV Dysfunction in WPW Syndrome. Introduction: Echocardiographic studies have shown that some patients with Wolff‐Parkinson‐White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction. Methods: Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 ± 4.2 years) were retrospectively analyzed. Results: The left ventricular ejection fraction (LVEF) of patients with septal APs (53 ± 11%) was significantly lower than that of patients with right (62 ± 5%) or left (61 ± 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 ± 4% and 42 ± 5%, respectively) and an increased LV end diastolic dimension (P < 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 ± 18 ms and 113 ± 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal‐to‐posterior wall motion delay, from 154 ± 91 ms to 33 ± 17 ms) and interventricular septal thinning (from 3.0 ± 0.5 mm to 5.3 ± 2.6 mm), and a significant increase in LVEF (from 42 ± 5% to 67 ± 8%; P = 0.001). Conclusion: The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function. (J Cardiovasc Electrophysiol, Vol. 21, pp. 290–295, March 2010)</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>BO SANG KWON M.D.</name><affiliations><json:string>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</json:string></affiliations></json:item><json:item><name>EUN JUNG BAE M.D.</name><affiliations><json:string>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</json:string></affiliations></json:item><json:item><name>GI BEOM KIM M.D.</name><affiliations><json:string>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</json:string></affiliations></json:item><json:item><name>CHUNG IL NOH M.D.</name><affiliations><json:string>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</json:string></affiliations></json:item><json:item><name>JUNG YUN CHOI M.D.</name><affiliations><json:string>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</json:string></affiliations></json:item><json:item><name>YONG SOO YUN M.D.</name><affiliations><json:string>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</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>septal dyskinesia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiomyopathy</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>resynchronization</value></json:item></subject><articleId><json:string>JCE1612</json:string></articleId><language><json:string>eng</json:string></language><abstract>LV Dysfunction in WPW Syndrome. Introduction: Echocardiographic studies have shown that some patients with Wolff‐Parkinson‐White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction. Methods: Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 ± 4.2 years) were retrospectively analyzed. Results: The left ventricular ejection fraction (LVEF) of patients with septal APs (53 ± 11%) was significantly lower than that of patients with right (62 ± 5%) or left (61 ± 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 ± 4% and 42 ± 5%, respectively) and an increased LV end diastolic dimension (P > 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 ± 18 ms and 113 ± 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal‐to‐posterior wall motion delay, from 154 ± 91 ms to 33 ± 17 ms) and interventricular septal thinning (from 3.0 ± 0.5 mm to 5.3 ± 2.6 mm), and a significant increase in LVEF (from 42 ± 5% to 67 ± 8%; P = 0.001). Conclusion: The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function. (J Cardiovasc Electrophysiol, Vol. 21, pp. 290–295, March 2010)</abstract><qualityIndicators><score>7.159</score><pdfVersion>1.4</pdfVersion><pdfPageSize>594 x 783 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1844</abstractCharCount><pdfWordCount>3659</pdfWordCount><pdfCharCount>22981</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>297</abstractWordCount></qualityIndicators><title>Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title><genre><json:string>article</json:string></genre><host><volume>21</volume><publisherId><json:string>JCE</json:string></publisherId><pages><total>6</total><last>295</last><first>290</first></pages><issn><json:string>1045-3873</json:string></issn><issue>3</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1540-8167</json:string></eissn><title>Journal of Cardiovascular Electrophysiology</title><doi><json:string>10.1111/(ISSN)1540-8167</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1111/j.1540-8167.2009.01612.x</json:string></doi><id>9567517CEB2B4F36498AA91E9569A7D846BE3E56</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9567517CEB2B4F36498AA91E9569A7D846BE3E56/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9567517CEB2B4F36498AA91E9569A7D846BE3E56/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9567517CEB2B4F36498AA91E9569A7D846BE3E56/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Inc</publisher><pubPlace>Malden, USA</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title><author><persName><forename type="first">BO SANG</forename><surname>KWON</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation></author><author><persName><forename type="first">EUN JUNG</forename><surname>BAE</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation></author><author><persName><forename type="first">GI BEOM</forename><surname>KIM</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation></author><author><persName><forename type="first">CHUNG IL</forename><surname>NOH</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation></author><author><persName><forename type="first">JUNG YUN</forename><surname>CHOI</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation></author><author><persName><forename type="first">YONG SOO</forename><surname>YUN</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</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="2010-03"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="290">290</biblScope><biblScope unit="page" to="295">295</biblScope></imprint></monogr><idno type="istex">9567517CEB2B4F36498AA91E9569A7D846BE3E56</idno><idno type="DOI">10.1111/j.1540-8167.2009.01612.x</idno><idno type="ArticleID">JCE1612</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>LV Dysfunction in WPW Syndrome. Introduction: Echocardiographic studies have shown that some patients with Wolff‐Parkinson‐White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction. Methods: Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 ± 4.2 years) were retrospectively analyzed. Results: The left ventricular ejection fraction (LVEF) of patients with septal APs (53 ± 11%) was significantly lower than that of patients with right (62 ± 5%) or left (61 ± 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 ± 4% and 42 ± 5%, respectively) and an increased LV end diastolic dimension (P < 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 ± 18 ms and 113 ± 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal‐to‐posterior wall motion delay, from 154 ± 91 ms to 33 ± 17 ms) and interventricular septal thinning (from 3.0 ± 0.5 mm to 5.3 ± 2.6 mm), and a significant increase in LVEF (from 42 ± 5% to 67 ± 8%; P = 0.001). Conclusion: The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function. (J Cardiovasc Electrophysiol, Vol. 21, pp. 290–295, March 2010)</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Wolff‐Parkinson‐White syndrome</term></item><item><term>septal dyskinesia</term></item><item><term>cardiomyopathy</term></item><item><term>catheter ablation</term></item><item><term>resynchronization</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9567517CEB2B4F36498AA91E9569A7D846BE3E56/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="03003"><doi origin="wiley">10.1111/jce.2010.21.issue-3</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2010-03">March 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="10" status="forIssue"><doi origin="wiley">10.1111/j.1540-8167.2009.01612.x</doi><idGroup><id type="unit" value="JCE1612"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title><title type="tocHeading2"><i>Clinical</i></title></titleGroup><copyright>© 2009 Wiley Periodicals, Inc.</copyright><eventGroup><event type="firstOnline" date="2009-10-05"></event><event type="publishedOnlineFinalForm" date="2010-02-22"></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="290">290</numbering><numbering type="pageLast" number="295">295</numbering></numberingGroup><correspondenceTo>Address for correspondence: Eun Jung Bae, M.D., Seoul National University Children's Hospital, 101 Daehangno, Jongno‐gu, Seoul, Korea, 110‐744. Fax: +822‐743‐3455; E‐mail: <email>eunjbaek@snu.ac.kr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCE.JCE1612.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Manuscript received 21 May 2009; Revised manuscript received 28 July 2009; Accepted for publication 5 August 2009.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="1"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="21"></count><count type="linksCrossRef" number="26"></count></countGroup><titleGroup><title type="main">Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>BO SANG</givenNames><familyName>KWON</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>EUN JUNG</givenNames><familyName>BAE</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>GI BEOM</givenNames><familyName>KIM</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>CHUNG IL</givenNames><familyName>NOH</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>JUNG YUN</givenNames><familyName>CHOI</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>YONG SOO</givenNames><familyName>YUN</familyName><degrees>M.D.</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="KR"><unparsedAffiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1"><i>Wolff‐Parkinson‐White syndrome</i></keyword><keyword xml:id="k2"><i>septal dyskinesia</i></keyword><keyword xml:id="k3"><i>cardiomyopathy</i></keyword><keyword xml:id="k4"><i>catheter ablation</i></keyword><keyword xml:id="k5"><i>resynchronization</i></keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p> <b>LV Dysfunction in WPW Syndrome. <i>Introduction:</i></b> Echocardiographic studies have shown that some patients with Wolff‐Parkinson‐White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction.</p><p> <b><i>Methods:</i></b> Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 ± 4.2 years) were retrospectively analyzed.</p><p> <b><i>Results:</i></b> The left ventricular ejection fraction (LVEF) of patients with septal APs (53 ± 11%) was significantly lower than that of patients with right (62 ± 5%) or left (61 ± 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 ± 4% and 42 ± 5%, respectively) and an increased LV end diastolic dimension (P < 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 ± 18 ms and 113 ± 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal‐to‐posterior wall motion delay, from 154 ± 91 ms to 33 ± 17 ms) and interventricular septal thinning (from 3.0 ± 0.5 mm to 5.3 ± 2.6 mm), and a significant increase in LVEF (from 42 ± 5% to 67 ± 8%; P = 0.001).</p><p> <b><i>Conclusion:</i></b> The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function. <i>(J Cardiovasc Electrophysiol, Vol. 21, pp. 290–295, March 2010)</i></p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>No conflicts of interest were declared.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway</title></titleInfo><name type="personal"><namePart type="given">BO SANG</namePart><namePart type="family">KWON</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EUN JUNG</namePart><namePart type="family">BAE</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GI BEOM</namePart><namePart type="family">KIM</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CHUNG IL</namePart><namePart type="family">NOH</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JUNG YUN</namePart><namePart type="family">CHOI</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YONG SOO</namePart><namePart type="family">YUN</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea</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">2010-03</dateIssued><edition>Manuscript received 21 May 2009; Revised manuscript received 28 July 2009; Accepted for publication 5 August 2009.</edition><copyrightDate encoding="w3cdtf">2010</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">4</extent><extent unit="tables">1</extent><extent unit="references">21</extent></physicalDescription><abstract lang="en">LV Dysfunction in WPW Syndrome. Introduction: Echocardiographic studies have shown that some patients with Wolff‐Parkinson‐White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction. Methods: Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 ± 4.2 years) were retrospectively analyzed. Results: The left ventricular ejection fraction (LVEF) of patients with septal APs (53 ± 11%) was significantly lower than that of patients with right (62 ± 5%) or left (61 ± 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 ± 4% and 42 ± 5%, respectively) and an increased LV end diastolic dimension (P < 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 ± 18 ms and 113 ± 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal‐to‐posterior wall motion delay, from 154 ± 91 ms to 33 ± 17 ms) and interventricular septal thinning (from 3.0 ± 0.5 mm to 5.3 ± 2.6 mm), and a significant increase in LVEF (from 42 ± 5% to 67 ± 8%; P = 0.001). Conclusion: The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function. (J Cardiovasc Electrophysiol, Vol. 21, pp. 290–295, March 2010)</abstract><subject lang="en"><genre>Keywords</genre><topic>Wolff‐Parkinson‐White syndrome</topic><topic>septal dyskinesia</topic><topic>cardiomyopathy</topic><topic>catheter ablation</topic><topic>resynchronization</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>2010</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>290</start><end>295</end><total>6</total></extent></part></relatedItem><identifier type="istex">9567517CEB2B4F36498AA91E9569A7D846BE3E56</identifier><identifier type="DOI">10.1111/j.1540-8167.2009.01612.x</identifier><identifier type="ArticleID">JCE1612</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 Wiley Periodicals, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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