Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node
Identifieur interne : 001630 ( Istex/Corpus ); précédent : 001629; suivant : 001631Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node
Auteurs : Arjun D. Sharma ; George J. KleinSource :
- The American Journal of Cardiology [ 0002-9149 ] ; 1988.
Abstract
A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 ± 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 ± 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p < 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 ±0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p < 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.
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DOI: 10.1016/0002-9149(88)90939-3
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Klein</name><affiliation><mods:affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8C70017D257EA6C4A28430F2F21D4C09818A8EC9</idno><date when="1988" year="1988">1988</date><idno type="doi">10.1016/0002-9149(88)90939-3</idno><idno type="url">https://api-v5.istex.fr/document/8C70017D257EA6C4A28430F2F21D4C09818A8EC9/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001630</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001630</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node</title><author><name sortKey="Sharma, Arjun D" sort="Sharma, Arjun D" uniqKey="Sharma A" first="Arjun D." last="Sharma">Arjun D. Sharma</name><affiliation><mods:affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</mods:affiliation></affiliation></author><author><name sortKey="Klein, George J" sort="Klein, George J" uniqKey="Klein G" first="George J." last="Klein">George J. Klein</name><affiliation><mods:affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The American Journal of Cardiology</title><title level="j" type="abbrev">AJC</title><idno type="ISSN">0002-9149</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988">1988</date><biblScope unit="volume">61</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="330">330</biblScope><biblScope unit="page" to="335">335</biblScope></imprint><idno type="ISSN">0002-9149</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-9149</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 ± 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 ± 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p < 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 ±0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p < 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Arjun D. Sharma MD</name><affiliations><json:string>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</json:string></affiliations></json:item><json:item><name>George J. Klein MD</name><affiliations><json:string>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Arrhythmias and conduction disturbances</value></json:item></subject><articleId><json:string>88909393</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 ± 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 ± 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p > 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 ±0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p > 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. 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Sharma, MD, University Hospital, Box 5339, Station A, London, Ontario, Canada N6A 5A5.</note><note type="biography">Dr. Sharma is an Ontario Ministry of Health Career Scientist.</note><affiliation>Address for reprints: A.D. Sharma, MD, University Hospital, Box 5339, Station A, London, Ontario, Canada N6A 5A5.</affiliation><affiliation>Dr. Sharma is an Ontario Ministry of Health Career Scientist.</affiliation><affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</affiliation></author><author xml:id="author-0001"><persName><forename type="first">George J.</forename><surname>Klein</surname></persName><roleName type="degree">MD</roleName><note type="biography">Dr. Klein is a Research Associate of the Heart and Stroke Foundation of Ontario, Ontario, Canada.</note><affiliation>Dr. Klein is a Research Associate of the Heart and Stroke Foundation of Ontario, Ontario, Canada.</affiliation><affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</affiliation></author><idno type="istex">8C70017D257EA6C4A28430F2F21D4C09818A8EC9</idno><idno type="DOI">10.1016/0002-9149(88)90939-3</idno><idno type="PII">0002-9149(88)90939-3</idno><idno type="ArticleID">88909393</idno></analytic><monogr><title level="j">The American Journal of Cardiology</title><title level="j" type="abbrev">AJC</title><idno type="pISSN">0002-9149</idno><idno type="PII">S0002-9149(00)X0759-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988"></date><biblScope unit="volume">61</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="330">330</biblScope><biblScope unit="page" to="335">335</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 ± 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 ± 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p < 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 ±0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p < 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.</p></abstract><textClass><keywords scheme="keyword"><list><head>article-category</head><item><term>Arrhythmias and conduction disturbances</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1988">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/8C70017D257EA6C4A28430F2F21D4C09818A8EC9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AJC</jid><aid>88909393</aid><ce:pii>0002-9149(88)90939-3</ce:pii><ce:doi>10.1016/0002-9149(88)90939-3</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright><ce:doctopics><ce:doctopic><ce:text>Arrhythmias and conduction disturbances</ce:text></ce:doctopic></ce:doctopics></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This study was supported by grants in aid from the Medical Research Council of Canada and the Heart and Stroke Foundation of Ontario.</ce:note-para></ce:article-footnote><ce:title>Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node</ce:title><ce:author-group><ce:author><ce:given-name>Arjun D.</ce:given-name><ce:surname>Sharma</ce:surname><ce:degrees>MD</ce:degrees><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>George J.</ce:given-name><ce:surname>Klein</ce:surname><ce:degrees>MD</ce:degrees><ce:cross-ref refid="FN2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address for reprints: A.D. Sharma, MD, University Hospital, Box 5339, Station A, London, Ontario, Canada N6A 5A5.</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>Dr. Sharma is an Ontario Ministry of Health Career Scientist.</ce:note-para></ce:footnote><ce:footnote id="FN2"><ce:label>2</ce:label><ce:note-para>Dr. Klein is a Research Associate of the Heart and Stroke Foundation of Ontario, Ontario, Canada.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="20" month="7" year="1987"></ce:date-received><ce:date-accepted day="1" month="10" year="1987"></ce:date-accepted><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 ± 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 ± 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC<ce:inf loc="post">50</ce:inf> of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p < 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 ±0.97 mg and the EC<ce:inf loc="post">50</ce:inf> was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p < 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC<ce:inf loc="post">50</ce:inf>. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node</title></titleInfo><name type="personal"><namePart type="given">Arjun D.</namePart><namePart type="family">Sharma</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</affiliation><description>Address for reprints: A.D. Sharma, MD, University Hospital, Box 5339, Station A, London, Ontario, Canada N6A 5A5.</description><description>Dr. Sharma is an Ontario Ministry of Health Career Scientist.</description><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">MD</namePart><affiliation>From the University Hospital, Robarts Research Institute, University of Western Ontario, London, Canada</affiliation><description>Dr. Klein is a Research Associate of the Heart and Stroke Foundation of Ontario, Ontario, Canada.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1988</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 ± 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 ± 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p < 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 ±0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p < 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.</abstract><note>This study was supported by grants in aid from the Medical Research Council of Canada and the Heart and Stroke Foundation of Ontario.</note><subject><genre>article-category</genre><topic>Arrhythmias and conduction disturbances</topic></subject><relatedItem type="host"><titleInfo><title>The American Journal of Cardiology</title></titleInfo><titleInfo type="abbreviated"><title>AJC</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19880201</dateIssued></originInfo><identifier type="ISSN">0002-9149</identifier><identifier type="PII">S0002-9149(00)X0759-X</identifier><part><date>19880201</date><detail type="volume"><number>61</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue pages"><start>A2</start><end>A82</end></extent><extent unit="issue pages"><start>201</start><end>412</end></extent><extent unit="pages"><start>330</start><end>335</end></extent></part></relatedItem><identifier type="istex">8C70017D257EA6C4A28430F2F21D4C09818A8EC9</identifier><identifier type="DOI">10.1016/0002-9149(88)90939-3</identifier><identifier type="PII">0002-9149(88)90939-3</identifier><identifier type="ArticleID">88909393</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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