Effects of lidocaine and propranolol on the normal and anomalous pathways in patients with preexcitation
Identifieur interne : 000839 ( Main/Corpus ); précédent : 000838; suivant : 000840Effects of lidocaine and propranolol on the normal and anomalous pathways in patients with preexcitation
Auteurs : Kenneth M. Rosen ; Christa Barwolf ; Ali Ehsani ; Shahbudin H. RahimtoolaSource :
- The American Journal of Cardiology [ 0002-9149 ] ; 1972.
Abstract
Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction.Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal.Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes.In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. Both drugs could affect reentrant tachycardia in patients with this syndrome by causing depression of part of the circus pathway.
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DOI: 10.1016/0002-9149(72)90003-3
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Rosen</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</mods:affiliation></affiliation></author><author><name sortKey="Barwolf, Christa" sort="Barwolf, Christa" uniqKey="Barwolf C" first="Christa" last="Barwolf">Christa Barwolf</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</mods:affiliation></affiliation></author><author><name sortKey="Ehsani, Ali" sort="Ehsani, Ali" uniqKey="Ehsani A" first="Ali" last="Ehsani">Ali Ehsani</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</mods:affiliation></affiliation></author><author><name sortKey="Rahimtoola, Shahbudin H" sort="Rahimtoola, Shahbudin H" uniqKey="Rahimtoola S" first="Shahbudin H." last="Rahimtoola">Shahbudin H. 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Rosen</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</mods:affiliation></affiliation></author><author><name sortKey="Barwolf, Christa" sort="Barwolf, Christa" uniqKey="Barwolf C" first="Christa" last="Barwolf">Christa Barwolf</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</mods:affiliation></affiliation></author><author><name sortKey="Ehsani, Ali" sort="Ehsani, Ali" uniqKey="Ehsani A" first="Ali" last="Ehsani">Ali Ehsani</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</mods:affiliation></affiliation></author><author><name sortKey="Rahimtoola, Shahbudin H" sort="Rahimtoola, Shahbudin H" uniqKey="Rahimtoola S" first="Shahbudin H." last="Rahimtoola">Shahbudin H. Rahimtoola</name><affiliation><mods:affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</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="1972">1972</date><biblScope unit="volume">30</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="801">801</biblScope><biblScope unit="page" to="809">809</biblScope></imprint><idno type="ISSN">0002-9149</idno></series><idno type="istex">A0D3437EE3039FA57A29365F1D6706027782ECE7</idno><idno type="DOI">10.1016/0002-9149(72)90003-3</idno><idno type="PII">0002-9149(72)90003-3</idno><idno type="ArticleID">72900033</idno></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">Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction.Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal.Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes.In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. Both drugs could affect reentrant tachycardia in patients with this syndrome by causing depression of part of the circus pathway.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Kenneth M. Rosen MD, FACC</name><affiliations><json:string>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</json:string></affiliations></json:item><json:item><name>Christa Barwolf MD</name><affiliations><json:string>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</json:string></affiliations></json:item><json:item><name>Ali Ehsani MD</name><affiliations><json:string>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</json:string></affiliations></json:item><json:item><name>Shahbudin H. Rahimtoola MB, FRCP, FACC</name><affiliations><json:string>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</json:string></affiliations></json:item></author><articleId><json:string>72900033</json:string></articleId><language><json:string>eng</json:string></language><abstract>Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction.Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal.Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes.In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. 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Rosen, MD, Department of Medicine, University of Illinois Hospital, PO Box 6998, Chicago, Ill. 60680.</note><affiliation>Address for reprints: Kenneth M. Rosen, MD, Department of Medicine, University of Illinois Hospital, PO Box 6998, Chicago, Ill. 60680.</affiliation><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation></author><author><persName><forename type="first">Christa</forename><surname>Barwolf</surname></persName><roleName type="degree">MD</roleName><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation></author><author><persName><forename type="first">Ali</forename><surname>Ehsani</surname></persName><roleName type="degree">MD</roleName><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation></author><author><persName><forename type="first">Shahbudin H.</forename><surname>Rahimtoola</surname></persName><roleName type="degree">MB, FRCP, FACC</roleName><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation></author></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)X0343-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1972"></date><biblScope unit="volume">30</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="801">801</biblScope><biblScope unit="page" to="809">809</biblScope></imprint></monogr><idno type="istex">A0D3437EE3039FA57A29365F1D6706027782ECE7</idno><idno type="DOI">10.1016/0002-9149(72)90003-3</idno><idno type="PII">0002-9149(72)90003-3</idno><idno type="ArticleID">72900033</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1972</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction.Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal.Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes.In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. Both drugs could affect reentrant tachycardia in patients with this syndrome by causing depression of part of the circus pathway.</p></abstract></profileDesc><revisionDesc><change when="1972-07-12">Registration</change><change when="1972">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></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>72900033</aid><ce:pii>0002-9149(72)90003-3</ce:pii><ce:doi>10.1016/0002-9149(72)90003-3</ce:doi><ce:copyright type="unknown" year="1972"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This study was supported in part by Contract NIH 71-2478, Myocardial Infarction Program, National Heart and Lung Institute, National Institutes of Health, Department of Health, Education and Welfare.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Clinical study</ce:textfn></ce:dochead><ce:title>Effects of lidocaine and propranolol on the normal and anomalous pathways in patients with preexcitation</ce:title><ce:author-group><ce:author><ce:given-name>Kenneth M.</ce:given-name><ce:surname>Rosen</ce:surname><ce:degrees>MD, FACC</ce:degrees><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup loc="post">1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Christa</ce:given-name><ce:surname>Barwolf</ce:surname><ce:degrees>MD</ce:degrees><ce:cross-ref refid="AFF1"><ce:sup loc="post">1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ali</ce:given-name><ce:surname>Ehsani</ce:surname><ce:degrees>MD</ce:degrees><ce:cross-ref refid="AFF1"><ce:sup loc="post">1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Shahbudin H.</ce:given-name><ce:surname>Rahimtoola</ce:surname><ce:degrees>MB, FRCP, FACC</ce:degrees><ce:cross-ref refid="AFF1"><ce:sup loc="post">1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup loc="post">2</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>1</ce:label><ce:textfn>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>2</ce:label><ce:textfn>From the Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago, III, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address for reprints: Kenneth M. Rosen, MD, Department of Medicine, University of Illinois Hospital, PO Box 6998, Chicago, Ill. 60680.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="20" month="3" year="1972"></ce:date-received><ce:date-accepted day="12" month="7" year="1972"></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">Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction.</ce:simple-para><ce:simple-para view="all" id="simple-para.0015">Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal.</ce:simple-para><ce:simple-para view="all" id="simple-para.0020">Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes.</ce:simple-para><ce:simple-para view="all" id="simple-para.0025">In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. Both drugs could affect reentrant tachycardia in patients with this syndrome by causing depression of part of the circus pathway.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effects of lidocaine and propranolol on the normal and anomalous pathways in patients with preexcitation</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Effects of lidocaine and propranolol on the normal and anomalous pathways in patients with preexcitation</title></titleInfo><name type="personal"><namePart type="given">Kenneth M.</namePart><namePart type="family">Rosen</namePart><namePart type="termsOfAddress">MD, FACC</namePart><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation><description>Address for reprints: Kenneth M. Rosen, MD, Department of Medicine, University of Illinois Hospital, PO Box 6998, Chicago, Ill. 60680.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christa</namePart><namePart type="family">Barwolf</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ali</namePart><namePart type="family">Ehsani</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shahbudin H.</namePart><namePart type="family">Rahimtoola</namePart><namePart type="termsOfAddress">MB, FRCP, FACC</namePart><affiliation>From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital, Chicago, III, USA</affiliation><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">1972</dateIssued><dateValid encoding="w3cdtf">1972-07-12</dateValid><copyrightDate encoding="w3cdtf">1972</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">Eleven patients with preexcitation were studied by techniques of His bundle recording and atrial pacing. The P-delta interval was used as a measure of anomalous pathway conduction time and P-H interval, a measure of atrioventricular (A-V) nodal conduction time. In 4 patients, anomalous pathway conduction failed with atrial pacing at a critical paced rate, resulting in normalization of conduction.Lidocaine, 50 to 100 mg intravenously, produced a depressant effect on the anomalous pathway in 4 of 6 patients, as manifested by a decrease in the pacing rate producing failure of preexcitation. Anomalous pathway effective refractory period, measured in 2 patients, was prolonged in 1 after administration of lidocaine. The effects of lidocaine on the normal pathway appeared to be minimal.Propranolol, 5 mg intravenously, produced no apparent effect on anomalous pathway conduction in 8 of 9 patients. In 1 patient, the pacing rate producing QRS normalization was slightly decreased. The effective refractory period of the anomalous pathway was unchanged in 2 patients after administration of this drug. Propranolol depressed the normal pathway (in 6 patients whose H potentials were visualized at equivalent paced rates) as manifested by P-H prolongation or decrease in the pacing rate producing block proximal to H, or both. An additional effect related to depression of the normal pathway was the accentuation of preexcitation in patients with fusion QRS complexes.In summary, lidocaine depressed anomalous pathway conduction, whereas propranolol depressed A-V nodal conduction in patients with preexcitation. Both drugs could affect reentrant tachycardia in patients with this syndrome by causing depression of part of the circus pathway.</abstract><note>This study was supported in part by Contract NIH 71-2478, Myocardial Infarction Program, National Heart and Lung Institute, National Institutes of Health, Department of Health, Education and Welfare.</note><note type="content">Section title: Clinical study</note><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">197212</dateIssued></originInfo><identifier type="ISSN">0002-9149</identifier><identifier type="PII">S0002-9149(00)X0343-8</identifier><part><date>197212</date><detail type="volume"><number>30</number><caption>vol.</caption></detail><detail type="issue"><number>8</number><caption>no.</caption></detail><extent unit="issue pages"><start>A1</start><end>A32</end></extent><extent unit="issue pages"><start>A33</start><end>A58</end></extent><extent unit="issue pages"><start>791</start><end>942</end></extent><extent unit="pages"><start>801</start><end>809</end></extent></part></relatedItem><identifier type="istex">A0D3437EE3039FA57A29365F1D6706027782ECE7</identifier><identifier type="DOI">10.1016/0002-9149(72)90003-3</identifier><identifier type="PII">0002-9149(72)90003-3</identifier><identifier type="ArticleID">72900033</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/A0D3437EE3039FA57A29365F1D6706027782ECE7/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><analytic><title level="a" type="main">808 Ferrer Ml: New concepts relating to the pre-excitation syn-drome</title></analytic><monogr><title level="j">JAMA</title><imprint><biblScope unit="volume">201</biblScope><biblScope unit="page" from="162" to="63"></biblScope><date type="published" when="1967"></date></imprint></monogr></biblStruct><biblStruct><monogr><title level="m" type="main">Anatomic considerations of anomalous A-V path-ways. In, Mechanisms and Therapy of Cardiac Arrhythmias (Dreifus LS, Likoff W, ed)</title><author><persName><surname>Lev</surname></persName></author><imprint><date type="published" when="1966"></date><biblScope unit="page" from="665" to="670"></biblScope><pubPlace>New York, Grune & Stratton</pubPlace></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Pre-excitation revisited</title><author><persName><forename type="middle">D</forename><surname>Durrer</surname></persName></author><author><persName><surname>Schuilenburg Rm</surname></persName></author><author><persName><surname>Hjj</surname></persName></author></analytic><monogr><title level="j">Amer J Cardiol</title><imprint><biblScope unit="volume">25</biblScope><biblScope unit="page" from="690" to="697"></biblScope></imprint></monogr></biblStruct></listBibl></back></text></istex:refBibTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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