Effect of Isoproterenol on Accessory Pathways Without Overt Retrograde Conduction
Identifieur interne : 000158 ( Istex/Corpus ); précédent : 000157; suivant : 000159Effect of Isoproterenol on Accessory Pathways Without Overt Retrograde Conduction
Auteurs : Huagui G. Li ; Raymond Yee ; George J. KleinSource :
- Journal of Cardiovascular Electrophysiology [ 1045-3873 ] ; 1995-03.
English descriptors
Abstract
Effect of Isoproterenol on Accessory Pathways. Introduction: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP). Methods and Results: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug‐free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom. Conclusions: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.
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DOI: 10.1111/j.1540-8167.1995.tb00768.x
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ISTEX:4C5F8EA5E155985A3E82BC53456D01C810FB67D6Le document en format XML
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Introduction: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP). Methods and Results: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug‐free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom. Conclusions: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>HUAGUI G. LI M.D.</name><affiliations><json:string>Department of Medicine, University of Western Ontario, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>RAYMOND YEE M.D.</name><affiliations><json:string>Department of Medicine, University of Western Ontario, London, Ontario, Canada</json:string></affiliations></json:item><json:item><name>GEORGE J. KLEIN M.D.</name><affiliations><json:string>Department of Medicine, University of Western Ontario, London, Ontario, Canada</json:string><json:string>Address for correspondence: George J. Klein, M.D., University Hospital, 339 Windermere Road, London, Ontario. N6A 5A5 Canada. Fax:519‐434‐3278.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>isoproterenol</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>retrograde accessory pathway conduction</value></json:item></subject><articleId><json:string>JCE170</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Effect of Isoproterenol on Accessory Pathways. Introduction: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP). Methods and Results: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug‐free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P > 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom. Conclusions: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. 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Klein, M.D., University Hospital, 339 Windermere Road, London, Ontario. N6A 5A5 Canada. Fax:519‐434‐3278.</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 Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1995-03"></date><biblScope unit="volume">6</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="170">170</biblScope><biblScope unit="page" to="173">173</biblScope></imprint></monogr><idno type="istex">4C5F8EA5E155985A3E82BC53456D01C810FB67D6</idno><idno type="DOI">10.1111/j.1540-8167.1995.tb00768.x</idno><idno type="ArticleID">JCE170</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Effect of Isoproterenol on Accessory Pathways. Introduction: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP). Methods and Results: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug‐free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom. Conclusions: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>isoproterenol</term></item><item><term>retrograde accessory pathway conduction</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/4C5F8EA5E155985A3E82BC53456D01C810FB67D6/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)1540-8167</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.1995.6.issue-3</doi><numberingGroup><numbering type="journalVolume" number="6">6</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="1995-03">March 1995</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0017000" status="forIssue"><doi origin="wiley">10.1111/j.1540-8167.1995.tb00768.x</doi><idGroup><id type="unit" value="JCE170"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title><title type="tocHeading2"><!--WileyML 3Gv2 convertor changed from tocHeading1 to tocHeading2-->Clinical</title></titleGroup><eventGroup><event type="firstOnline" date="2007-04-29"></event><event type="publishedOnlineFinalForm" date="2007-04-29"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-10"></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="170">170</numbering><numbering type="pageLast" number="173">173</numbering></numberingGroup><correspondenceTo>Address for correspondence: George J. Klein, M.D., University Hospital, 339 Windermere Road, London, Ontario. N6A 5A5 Canada. Fax:519‐434‐3278.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCE.JCE170.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 1 December 1994; Accepted for publication 23 February 1995</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="8"></count><count type="linksCrossRef" number="4"></count></countGroup><titleGroup><title type="main">Effect of Isoproterenol on Accessory Pathways Without Overt Retrograde Conduction</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>HUAGUI G.</givenNames><familyName>LI</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>RAYMOND</givenNames><familyName>YEE</familyName><degrees>M.D.</degrees></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1" corresponding="yes"><personName><givenNames>GEORGE J.</givenNames><familyName>KLEIN</familyName><degrees>M.D.</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Department of Medicine, University of Western Ontario, London, Ontario, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">isoproterenol</keyword><keyword xml:id="k2">retrograde accessory pathway conduction</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Effect of Isoproterenol on Accessory Pathways. <i>Introduction</i>: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP).</p><p> <i>Methods and Results</i>: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug‐free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom.</p><p> <i>Conclusions</i>: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p>Dr. H.G. Li is a Research Fellowship recipient of the Heart and Stroke Foundation of Ontario. Dr. G.J. Klein is a Distinguished Research Professor of the Heart and Stroke Foundation of Ontario. This study was supported in part by the Heart and Stroke Foundation of Ontario.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effect of Isoproterenol on Accessory Pathways Without Overt Retrograde Conduction</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effect of Isoproterenol on Accessory Pathways Without Overt Retrograde Conduction</title></titleInfo><name type="personal"><namePart type="given">HUAGUI G.</namePart><namePart type="family">LI</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RAYMOND</namePart><namePart type="family">YEE</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GEORGE J.</namePart><namePart type="family">KLEIN</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Medicine, University of Western Ontario, London, Ontario, Canada</affiliation><affiliation>Address for correspondence: George J. 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Introduction: Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP). Methods and Results: To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug‐free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom. Conclusions: We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.</abstract><subject lang="en"><genre>keywords</genre><topic>isoproterenol</topic><topic>retrograde accessory pathway conduction</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>1995</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>170</start><end>173</end><total>4</total></extent></part></relatedItem><identifier type="istex">4C5F8EA5E155985A3E82BC53456D01C810FB67D6</identifier><identifier type="DOI">10.1111/j.1540-8167.1995.tb00768.x</identifier><identifier type="ArticleID">JCE170</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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