In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation
Identifieur interne : 000417 ( Istex/Corpus ); précédent : 000416; suivant : 000418In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation
Auteurs : Timothy A. Simmers ; Fred H. M. Wittkampf ; Richard N. W. Hauer ; Etienne O. Robles De MedinaSource :
- Pacing and Clinical Electrophysiology [ 0147-8389 ] ; 1994-03.
English descriptors
Abstract
While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed‐chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm3 after 5 seconds pulse duration to a maximum 388 mm3 and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short‘test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.
Url:
DOI: 10.1111/j.1540-8159.1994.tb01421.x
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ISTEX:0E115073020E969778DBC9BD14616C08AAD3C835Le document en format XML
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Wittkampf</name><affiliation><mods:affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Hauer, Richard N W" sort="Hauer, Richard N W" uniqKey="Hauer R" first="Richard N. W." last="Hauer">Richard N. W. Hauer</name><affiliation><mods:affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="De Medina, Etienne O Robles" sort="De Medina, Etienne O Robles" uniqKey="De Medina E" first="Etienne O. Robles" last="De Medina">Etienne O. 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Simmers</name><affiliation><mods:affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Address for reprints; Timothy A. Simmers, M.D., Dept. of Cardiology, Heart‐Lung Institute, E03.406, University Hospital Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Fax: 011‐31‐30‐542155.</mods:affiliation></affiliation></author><author><name sortKey="Wittkampf, Fred H M" sort="Wittkampf, Fred H M" uniqKey="Wittkampf F" first="Fred H. M." last="Wittkampf">Fred H. M. Wittkampf</name><affiliation><mods:affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Hauer, Richard N W" sort="Hauer, Richard N W" uniqKey="Hauer R" first="Richard N. 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Robles De Medina</name><affiliation><mods:affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</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="1994-03">1994-03</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="523">523</biblScope><biblScope unit="page" to="531">531</biblScope></imprint><idno type="ISSN">0147-8389</idno></series><idno type="istex">0E115073020E969778DBC9BD14616C08AAD3C835</idno><idno type="DOI">10.1111/j.1540-8159.1994.tb01421.x</idno><idno type="ArticleID">PACE523</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0147-8389</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>catheter ablation</term><term>radiofrequency</term><term>ventricular tachycardia</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed‐chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm3 after 5 seconds pulse duration to a maximum 388 mm3 and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short‘test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>TIMOTHY A. SIMMERS</name><affiliations><json:string>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</json:string><json:string>Address for reprints; Timothy A. Simmers, M.D., Dept. of Cardiology, Heart‐Lung Institute, E03.406, University Hospital Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Fax: 011‐31‐30‐542155.</json:string></affiliations></json:item><json:item><name>FRED H.M. WITTKAMPF</name><affiliations><json:string>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</json:string></affiliations></json:item><json:item><name>RICHARD N.W. HAUER</name><affiliations><json:string>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</json:string></affiliations></json:item><json:item><name>ETIENNE O. ROBLES DE MEDINA</name><affiliations><json:string>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</json:string></affiliations></json:item></author><subject><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>radiofrequency</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ventricular tachycardia</value></json:item></subject><articleId><json:string>PACE523</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed‐chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm3 after 5 seconds pulse duration to a maximum 388 mm3 and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short‘test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.</abstract><qualityIndicators><score>8.711</score><pdfVersion>1.6</pdfVersion><pdfPageSize>576 x 791 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1690</abstractCharCount><pdfWordCount>4211</pdfWordCount><pdfCharCount>27082</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>259</abstractWordCount></qualityIndicators><title>In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation</title><genre><json:string>article</json:string></genre><host><volume>17</volume><publisherId><json:string>PACE</json:string></publisherId><pages><total>9</total><last>531</last><first>523</first></pages><issn><json:string>0147-8389</json:string></issn><issue>3</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><categories><wos><json:string>science</json:string><json:string>engineering, biomedical</json:string><json:string>cardiac & cardiovascular systems</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>cardiovascular system & hematology</json:string></scienceMetrix></categories><publicationDate>1994</publicationDate><copyrightDate>1994</copyrightDate><doi><json:string>10.1111/j.1540-8159.1994.tb01421.x</json:string></doi><id>0E115073020E969778DBC9BD14616C08AAD3C835</id><score>0.16389732</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/0E115073020E969778DBC9BD14616C08AAD3C835/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/0E115073020E969778DBC9BD14616C08AAD3C835/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/0E115073020E969778DBC9BD14616C08AAD3C835/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1994</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation</title><author xml:id="author-1"><persName><forename type="first">TIMOTHY A.</forename><surname>SIMMERS</surname></persName><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</affiliation><affiliation>Address for reprints; Timothy A. Simmers, M.D., Dept. of Cardiology, Heart‐Lung Institute, E03.406, University Hospital Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Fax: 011‐31‐30‐542155.</affiliation></author><author xml:id="author-2"><persName><forename type="first">FRED H.M.</forename><surname>WITTKAMPF</surname></persName><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</affiliation></author><author xml:id="author-3"><persName><forename type="first">RICHARD N.W.</forename><surname>HAUER</surname></persName><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</affiliation></author><author xml:id="author-4"><persName><forename type="first">ETIENNE O. ROBLES</forename><surname>DE MEDINA</surname></persName><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</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="1994-03"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="523">523</biblScope><biblScope unit="page" to="531">531</biblScope></imprint></monogr><idno type="istex">0E115073020E969778DBC9BD14616C08AAD3C835</idno><idno type="DOI">10.1111/j.1540-8159.1994.tb01421.x</idno><idno type="ArticleID">PACE523</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed‐chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm3 after 5 seconds pulse duration to a maximum 388 mm3 and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short‘test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>catheter ablation</term></item><item><term>radiofrequency</term></item><item><term>ventricular tachycardia</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/0E115073020E969778DBC9BD14616C08AAD3C835/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="03003"><doi origin="wiley">10.1111/pace.1994.17.issue-3</doi><numberingGroup><numbering type="journalVolume" number="17">17</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="1994-03">March 1994</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0052300" status="forIssue"><doi origin="wiley">10.1111/j.1540-8159.1994.tb01421.x</doi><idGroup><id type="unit" value="PACE523"></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:2.3.5 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-07"></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="523">523</numbering><numbering type="pageLast" number="531">531</numbering></numberingGroup><correspondenceTo>Address for reprints; Timothy A. Simmers, M.D., Dept. of Cardiology, Heart‐Lung Institute, E03.406, University Hospital Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Fax: 011‐31‐30‐542155.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PACE.PACE523.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="referenceTotal" number="37"></count><count type="linksCrossRef" number="5"></count></countGroup><titleGroup><title type="main">In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>TIMOTHY A.</givenNames><familyName>SIMMERS</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>FRED H.M.</givenNames><familyName>WITTKAMPF</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>RICHARD N.W.</givenNames><familyName>HAUER</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>ETIENNE O. ROBLES</givenNames><familyNamePrefix>DE</familyNamePrefix><familyName>MEDINA</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="NL"><unparsedAffiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">catheter ablation</keyword><keyword xml:id="k2">radiofrequency</keyword><keyword xml:id="k3">ventricular tachycardia</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed‐chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm<sup>3</sup> after 5 seconds pulse duration to a maximum 388 mm<sup>3</sup> and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short‘test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>Parts of this study were presented at the 14th congress of the European Society of Cardiology, September 1992, Barcelona, Spain as well as al the Ventricuiar Arrhythmias, State of the Art' workshop, |une 1993, Gbttingen, Germany.</p></note><note xml:id="n-fnt-2" numbered="no"><p>Supported by The Netherlands Heart Foundation, grant 91.062, The Hague, and the Wijnand M. Pon Foundation, Leusden, The Netherlands.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>In Vivo Ventricular Lesion Growth in Radiofrequency Catheter Ablation</title></titleInfo><name type="personal"><namePart type="given">TIMOTHY A.</namePart><namePart type="family">SIMMERS</namePart><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</affiliation><affiliation>Address for reprints; Timothy A. Simmers, M.D., Dept. of Cardiology, Heart‐Lung Institute, E03.406, University Hospital Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands. Fax: 011‐31‐30‐542155.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">FRED H.M.</namePart><namePart type="family">WITTKAMPF</namePart><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RICHARD N.W.</namePart><namePart type="family">HAUER</namePart><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ETIENNE O. ROBLES</namePart><namePart type="family">DE MEDINA</namePart><affiliation>Heart‐Lung Institute, University Hospital and University of Utrecht and the Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands</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">1994-03</dateIssued><copyrightDate encoding="w3cdtf">1994</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">37</extent></physicalDescription><abstract lang="en">While radiofrequency catheter ablation has proved highly effective in the treafment of various supravenfricular tQchyarrhythmias, resulls in the trentment of ventricular tachycardia invite improvement. Knowledge of lesion growth in vivo might improve understanding of this discrepancy. So far only information from in vitro and in vivo studies using a small 2 mm tip eiectrode is available. Growlh of ventricular radiofrequency lesions created with a 4 mm ahlalion electrode was studied in 11 closed‐chest dogs. Endocardia] ablations were performed at 31 left and 35 right ventricuiar sites at a power setting of 25 Watts and 5, 10, 20, 30 or 60 seconds pulse duration. Macroscopic and histopathologic lesion examination were performed after one week survival. Mean lesion volume increased from 52 mm3 after 5 seconds pulse duration to a maximum 388 mm3 and approximately 7 mm depth after 30 seconds. Lesions were prolate spheroid in form, with a sparing of subendocardial myocardium and maximum lesion diameter at some millimeters depth. Results indicate that catheter positioning at no more tlian 7 mm from the target is required for successful ablation. Due to lesion geometry, subendocardial targets demand even more exact catheter positioning, while subepicardial substrates may not be ammenable to ablation if ventricular wall thickness exceeds 7 mm at the ablation site. Repeated pulses at adjacent sites may be required for ablation of extended arrhytbmogenic areas. Volume at 5 seconds was only approximately 15% of mature lesions. Therefore, the use of a short‘test pulse after careful mapping may be useful to pinpoint the most appropriate site for ablation in discrete pathways.</abstract><subject lang="en"><genre>keywords</genre><topic>catheter ablation</topic><topic>radiofrequency</topic><topic>ventricular tachycardia</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>1994</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>523</start><end>531</end><total>9</total></extent></part></relatedItem><identifier type="istex">0E115073020E969778DBC9BD14616C08AAD3C835</identifier><identifier type="DOI">10.1111/j.1540-8159.1994.tb01421.x</identifier><identifier type="ArticleID">PACE523</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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