Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome
Identifieur interne : 000010 ( Main/Corpus ); précédent : 000009; suivant : 000011Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome
Auteurs : Leonard S. Dreifus ; Hein J. Wellens ; Yoshio Watanabe ; Dimitrios Kimbiris ; Raymond TruexSource :
- The American Journal of Cardiology [ 0002-9149 ] ; 1976.
Abstract
Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.
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DOI: 10.1016/0002-9149(76)90141-7
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U.S.A.</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="1976">1976</date><biblScope unit="volume">38</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="149">149</biblScope><biblScope unit="page" to="156">156</biblScope></imprint><idno type="ISSN">0002-9149</idno></series><idno type="istex">C1D406C73404537CE52FEEC4621903EF0008FFF6</idno><idno type="DOI">10.1016/0002-9149(76)90141-7</idno><idno type="PII">0002-9149(76)90141-7</idno><idno type="ArticleID">76901417</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">Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Leonard S. Dreifus MD, FACC</name><affiliations><json:string>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.From the University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, The Netherlands</json:string></affiliations></json:item><json:item><name>Hein J. Wellens MD, FACC</name><affiliations><json:string>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</json:string></affiliations></json:item><json:item><name>Yoshio Watanabe MD, FACC</name><affiliations><json:string>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</json:string></affiliations></json:item><json:item><name>Dimitrios Kimbiris MD, FACC</name><affiliations><json:string>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</json:string></affiliations></json:item><json:item><name>Raymond Truex PhD</name><affiliations><json:string>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</json:string></affiliations></json:item></author><articleId><json:string>76901417</json:string></articleId><language><json:string>eng</json:string></language><abstract>Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. 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Dreifus, MD, The Lankenau Hospital, Lancaster and City Line Ave., Philadelphia, Pa. 19151.</note><affiliation>Address for reprints: Leonard S. Dreifus, MD, The Lankenau Hospital, Lancaster and City Line Ave., Philadelphia, Pa. 19151.</affiliation><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.From the University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, The Netherlands</affiliation></author><author><persName><forename type="first">Hein J.</forename><surname>Wellens</surname></persName><roleName type="degree">MD, FACC</roleName><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</affiliation></author><author><persName><forename type="first">Yoshio</forename><surname>Watanabe</surname></persName><roleName type="degree">MD, FACC</roleName><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</affiliation></author><author><persName><forename type="first">Dimitrios</forename><surname>Kimbiris</surname></persName><roleName type="degree">MD, FACC</roleName><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</affiliation></author><author><persName><forename type="first">Raymond</forename><surname>Truex</surname></persName><roleName type="degree">PhD</roleName><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</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)X0426-2</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1976"></date><biblScope unit="volume">38</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="149">149</biblScope><biblScope unit="page" to="156">156</biblScope></imprint></monogr><idno type="istex">C1D406C73404537CE52FEEC4621903EF0008FFF6</idno><idno type="DOI">10.1016/0002-9149(76)90141-7</idno><idno type="PII">0002-9149(76)90141-7</idno><idno type="ArticleID">76901417</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1976</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.</p></abstract></profileDesc><revisionDesc><change when="1976-01-22">Registration</change><change when="1976-01-21">Modified</change><change when="1976">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>76901417</aid><ce:pii>0002-9149(76)90141-7</ce:pii><ce:doi>10.1016/0002-9149(76)90141-7</ce:doi><ce:copyright type="unknown" year="1976"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This study was supported in part by Grant HL-07047 from the National Institutes of Health, Bethesda, Md.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Clinical study</ce:textfn></ce:dochead><ce:title>Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome</ce:title><ce:author-group><ce:author><ce:given-name>Leonard S.</ce:given-name><ce:surname>Dreifus</ce:surname><ce:degrees>MD, FACC</ce:degrees><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Hein J.</ce:given-name><ce:surname>Wellens</ce:surname><ce:degrees>MD, 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:author><ce:given-name>Yoshio</ce:given-name><ce:surname>Watanabe</ce:surname><ce:degrees>MD, 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:author><ce:given-name>Dimitrios</ce:given-name><ce:surname>Kimbiris</ce:surname><ce:degrees>MD, 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:author><ce:given-name>Raymond</ce:given-name><ce:surname>Truex</ce:surname><ce:degrees>PhD</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 Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>2</ce:label><ce:textfn>From the University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, The Netherlands</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address for reprints: Leonard S. Dreifus, MD, The Lankenau Hospital, Lancaster and City Line Ave., Philadelphia, Pa. 19151.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="6" month="11" year="1975"></ce:date-received><ce:date-revised day="21" month="1" year="1976"></ce:date-revised><ce:date-accepted day="22" month="1" year="1976"></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">Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.</ce:simple-para><ce:simple-para view="all" id="simple-para.0015">Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome</title></titleInfo><name type="personal"><namePart type="given">Leonard S.</namePart><namePart type="family">Dreifus</namePart><namePart type="termsOfAddress">MD, FACC</namePart><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.From the University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, The Netherlands</affiliation><description>Address for reprints: Leonard S. Dreifus, MD, The Lankenau Hospital, Lancaster and City Line Ave., Philadelphia, Pa. 19151.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hein J.</namePart><namePart type="family">Wellens</namePart><namePart type="termsOfAddress">MD, FACC</namePart><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshio</namePart><namePart type="family">Watanabe</namePart><namePart type="termsOfAddress">MD, FACC</namePart><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dimitrios</namePart><namePart type="family">Kimbiris</namePart><namePart type="termsOfAddress">MD, FACC</namePart><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Raymond</namePart><namePart type="family">Truex</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>From the Departments of Medicine, Hahnemann Medical College, and the Temple University School of Medicine, Philadelphia, Pa. U.S.A.</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">1976</dateIssued><dateValid encoding="w3cdtf">1976-01-22</dateValid><dateModified encoding="w3cdtf">1976-01-21</dateModified><copyrightDate encoding="w3cdtf">1976</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">Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.</abstract><note>This study was supported in part by Grant HL-07047 from the National Institutes of Health, Bethesda, Md.</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">197608</dateIssued></originInfo><identifier type="ISSN">0002-9149</identifier><identifier type="PII">S0002-9149(00)X0426-2</identifier><part><date>197608</date><detail type="volume"><number>38</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>A1</start><end>A40</end></extent><extent unit="issue pages"><start>A42</start><end>A60</end></extent><extent unit="issue pages"><start>A64</start><end>A70</end></extent><extent unit="issue pages"><start>A76</start><end>A89</end></extent><extent unit="issue pages"><start>141</start><end>280</end></extent><extent unit="pages"><start>149</start><end>156</end></extent></part></relatedItem><identifier type="istex">C1D406C73404537CE52FEEC4621903EF0008FFF6</identifier><identifier type="DOI">10.1016/0002-9149(76)90141-7</identifier><identifier type="PII">0002-9149(76)90141-7</identifier><identifier type="ArticleID">76901417</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/C1D406C73404537CE52FEEC4621903EF0008FFF6/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><monogr></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachy-cardia</title><author><persName><forename type="middle">L</forename><surname>Wolff</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Parkinson</surname></persName></author><author><persName><surname>White</surname></persName></author></analytic><monogr><title level="j">Am Heart J</title><imprint><biblScope unit="volume">5</biblScope><biblScope unit="page" from="685" to="704"></biblScope><date type="published" when="1930"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Epicardial excitation of the ventricles in a patient with Wolff-Parkinson-White syndrome (type B)</title><author><persName><forename type="middle">D</forename><surname>Durrer</surname></persName></author><author><persName><surname>Jp</surname></persName></author></analytic><monogr><title level="j">Circulation</title><imprint><biblScope unit="volume">35</biblScope><biblScope unit="page" from="15" to="21"></biblScope><date type="published" when="1967"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Atrioventricular and ventriculoatrial excitation in Wolff-Parkinson-White syndrome (type B): Temporary ablation at surgery Control of recurrent tachy-cardia of Wolff-Parkinson-White syndrome by surgical ligature of the A-V bundle His bundle recordings in patients with reciprocating tachycardias and Wolff-Parkinson-White syn-drome Symposium on electrophysiologic correlates of clinical arrhythmias. 3. 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