Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation
Identifieur interne : 000317 ( Main/Corpus ); précédent : 000316; suivant : 000318Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation
Auteurs : Shinichi Niwano ; Masayuki Yamaura ; Takashi Washizuka ; Yasutaka Tanabe ; Hiroshi Furushima ; Koji Taneda ; Yoshifusa AizawaSource :
- Pacing and Clinical Electrophysiology [ 0147-8389 ] ; 1998-10.
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Abstract
The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.
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DOI: 10.1111/j.1540-8159.1998.tb00011.x
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Japan</mods:affiliation></affiliation></author><author><name sortKey="Washizuka, Takashi" sort="Washizuka, Takashi" uniqKey="Washizuka T" first="Takashi" last="Washizuka">Takashi Washizuka</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Tanabe, Yasutaka" sort="Tanabe, Yasutaka" uniqKey="Tanabe Y" first="Yasutaka" last="Tanabe">Yasutaka Tanabe</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Furushima, Hiroshi" sort="Furushima, Hiroshi" uniqKey="Furushima H" first="Hiroshi" last="Furushima">Hiroshi Furushima</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. 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Japan</mods:affiliation></affiliation></author><author><name sortKey="Yamaura, Masayuki" sort="Yamaura, Masayuki" uniqKey="Yamaura M" first="Masayuki" last="Yamaura">Masayuki Yamaura</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Washizuka, Takashi" sort="Washizuka, Takashi" uniqKey="Washizuka T" first="Takashi" last="Washizuka">Takashi Washizuka</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Tanabe, Yasutaka" sort="Tanabe, Yasutaka" uniqKey="Tanabe Y" first="Yasutaka" last="Tanabe">Yasutaka Tanabe</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Furushima, Hiroshi" sort="Furushima, Hiroshi" uniqKey="Furushima H" first="Hiroshi" last="Furushima">Hiroshi Furushima</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Taneda, Koji" sort="Taneda, Koji" uniqKey="Taneda K" first="Koji" last="Taneda">Koji Taneda</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author><author><name sortKey="Aizawa, Yoshifusa" sort="Aizawa, Yoshifusa" uniqKey="Aizawa Y" first="Yoshifusa" last="Aizawa">Yoshifusa Aizawa</name><affiliation><mods:affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Pacing and Clinical Electrophysiology</title><idno type="ISSN">0147-8389</idno><idno type="eISSN">1540-8159</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1998-10">1998-10</date><biblScope unit="volume">21</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1918">1918</biblScope><biblScope unit="page" to="1926">1926</biblScope></imprint><idno type="ISSN">0147-8389</idno></series><idno type="istex">BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4</idno><idno type="DOI">10.1111/j.1540-8159.1998.tb00011.x</idno><idno type="ArticleID">PACE1918</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0147-8389</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>arrhythmogenicity</term><term>atrial pacin</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>SHINICHI NIWANO</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item><json:item><name>MASAYUKI YAMAURA</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item><json:item><name>TAKASHI WASHIZUKA</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item><json:item><name>YASUTAKA TANABE</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item><json:item><name>HIROSHI FURUSHIMA</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item><json:item><name>KOJI TANEDA</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item><json:item><name>YOSHIFUSA AIZAWA</name><affiliations><json:string>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>arrhythmogenicity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>atrial pacin</value></json:item></subject><articleId><json:string>PACE1918</json:string></articleId><language><json:string>eng</json:string></language><abstract>The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.</abstract><qualityIndicators><score>9.199</score><pdfVersion>1.6</pdfVersion><pdfPageSize>567 x 785 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>2</keywordCount><abstractCharCount>2598</abstractCharCount><pdfWordCount>4699</pdfWordCount><pdfCharCount>27638</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>466</abstractWordCount></qualityIndicators><title>Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation</title><genre><json:string>article</json:string></genre><host><volume>21</volume><publisherId><json:string>PACE</json:string></publisherId><pages><total>9</total><last>1926</last><first>1918</first></pages><issn><json:string>0147-8389</json:string></issn><issue>10</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.tb00011.x</json:string></doi><id>BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation</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">Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation</title><author><persName><forename type="first">SHINICHI</forename><surname>NIWANO</surname></persName><note type="correspondence"><p>Correspondence: Address for reprints: Shinichi Niwano, M.D., First Department of Internal Medicine, Niigata University School of Medicine, 1–754 Asahi‐machi Niigata, 951 Japan. Fax: 81‐25‐223‐0856; e‐mail:</p></note><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation></author><author><persName><forename type="first">MASAYUKI</forename><surname>YAMAURA</surname></persName><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation></author><author><persName><forename type="first">TAKASHI</forename><surname>WASHIZUKA</surname></persName><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation></author><author><persName><forename type="first">YASUTAKA</forename><surname>TANABE</surname></persName><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation></author><author><persName><forename type="first">HIROSHI</forename><surname>FURUSHIMA</surname></persName><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation></author><author><persName><forename type="first">KOJI</forename><surname>TANEDA</surname></persName><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation></author><author><persName><forename type="first">YOSHIFUSA</forename><surname>AIZAWA</surname></persName><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. 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="1998-10"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1918">1918</biblScope><biblScope unit="page" to="1926">1926</biblScope></imprint></monogr><idno type="istex">BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4</idno><idno type="DOI">10.1111/j.1540-8159.1998.tb00011.x</idno><idno type="ArticleID">PACE1918</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>arrhythmogenicity</term></item><item><term>atrial pacin</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1998-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4/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="10010"><doi origin="wiley">10.1111/pace.1998.21.issue-10</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue" number="10">10</numbering></numberingGroup><coverDate startDate="1998-10">October 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0191800" status="forIssue"><doi origin="wiley">10.1111/j.1540-8159.1998.tb00011.x</doi><idGroup><id type="unit" value="PACE1918"></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="1918">1918</numbering><numbering type="pageLast" number="1926">1926</numbering></numberingGroup><correspondenceTo>Address for reprints: Shinichi Niwano, M.D., First Department of Internal Medicine, Niigata University School of Medicine, 1–754 Asahi‐machi Niigata, 951 Japan. Fax: 81‐25‐223‐0856; e‐mail: <email>niwano@med.niigataiu.ac.jp</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PACE.PACE1918.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received September 9, 1997; Revised November 3, 1997; Accepted November 21, 1997</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="31"></count><count type="linksCrossRef" number="8"></count></countGroup><titleGroup><title type="main"><b>Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites:</b> Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>SHINICHI</givenNames><familyName>NIWANO</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>MASAYUKI</givenNames><familyName>YAMAURA</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>TAKASHI</givenNames><familyName>WASHIZUKA</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>YASUTAKA</givenNames><familyName>TANABE</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>HIROSHI</givenNames><familyName>FURUSHIMA</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>KOJI</givenNames><familyName>TANEDA</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>YOSHIFUSA</givenNames><familyName>AIZAWA</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">arrhythmogenicity</keyword><keyword xml:id="k2">atrial pacin</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation</title></titleInfo><name type="personal"><namePart type="given">SHINICHI</namePart><namePart type="family">NIWANO</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation><description>Correspondence: Address for reprints: Shinichi Niwano, M.D., First Department of Internal Medicine, Niigata University School of Medicine, 1–754 Asahi‐machi Niigata, 951 Japan. Fax: 81‐25‐223‐0856; e‐mail: </description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MASAYUKI</namePart><namePart type="family">YAMAURA</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">TAKASHI</namePart><namePart type="family">WASHIZUKA</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YASUTAKA</namePart><namePart type="family">TANABE</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HIROSHI</namePart><namePart type="family">FURUSHIMA</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">KOJI</namePart><namePart type="family">TANEDA</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YOSHIFUSA</namePart><namePart type="family">AIZAWA</namePart><affiliation>First Department of Internal Medicine, Niigata University School of Medicine, Niigata. 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">1998-10</dateIssued><edition>Received September 9, 1997; Revised November 3, 1997; Accepted November 21, 1997</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">31</extent></physicalDescription><abstract lang="en">The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.</abstract><subject lang="en"><genre>Keywords</genre><topic>arrhythmogenicity</topic><topic>atrial pacin</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>10</number></detail><extent unit="pages"><start>1918</start><end>1926</end><total>9</total></extent></part></relatedItem><identifier type="istex">BA43C1067AA2ED62D1C98DA27F9DA6A18BC61BB4</identifier><identifier type="DOI">10.1111/j.1540-8159.1998.tb00011.x</identifier><identifier type="ArticleID">PACE1918</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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