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Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation

Identifieur interne : 000178 ( Main/Corpus ); précédent : 000177; suivant : 000179

Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation

Auteurs : Pablo Denes ; James M. Cummings ; Ross Simpson ; Delon Wu ; Fernando Amat-Y-Leon ; Ramesh Dhingra ; Kenneth M. Rosen

Source :

RBID : ISTEX:5839A092A7D8A71CBCDC2C1F9EC5B97C8BEBADBB

Abstract

Electrophysiologic effects of intravenous propranolol, 0.1 mg/kg, were evaluated in 18 patients with anomalous pathways utilizing intracardiac stimulation and recording. Fourteen patients had Wolff-Parkinson-White syndrome and four had concealed ventricular preexcitation. Anomalous pathway effective refractory period could be measured during the control period and after propranolol administration in nine patients and was 304 ± 7.5 (mean ± standard error of the mean) and 304 ± 8.3 msec, respectively (difference not significant). Ventricular paced 1:1 ventriculoatrial (V-A) conduction (reflecting retrograde anomalous pathway conduction) measured in 12 patients was intact during both the control period and after propranolol at rates of 170 to 200/min. Sustained paroxysmal supraventricular tachycardia was induced in 14 patients during the control period and in 10 after propranolol (in 4 of whom the tachycardia could not be sustained because of atrioventricular [A-V] nodal refractoriness). Mean cycle length of tachycardia in these 10 patients was 328 ± 18 (control) and 352 ± 19 msec (propranolol) (P < 0.01). The increase in tachycardia cycle length reflected an increase in A-V nodal conduction time (A-H interval).In conclusion: (1) Propranolol has an insignificant effect on both anterograde and retrograde anomalous pathway properties. (2) In most cases, propranolol does not interfere with induction of sustained circus movement tachycardia. However, it does produce a statistically significant but slight slowing of the rate of tachycardia. (3) In a minority of cases, propranolol inhibits induction of sustained paroxysmal supraventricular tachycardia by increasing A-V nodal refractoriness.

Url:
DOI: 10.1016/0002-9149(78)90858-5

Links to Exploration step

ISTEX:5839A092A7D8A71CBCDC2C1F9EC5B97C8BEBADBB

Le document en format XML

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<ce:degrees>MD, FACC</ce:degrees>
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<ce:author>
<ce:given-name>Ross</ce:given-name>
<ce:surname>Simpson</ce:surname>
<ce:degrees>MD</ce:degrees>
</ce:author>
<ce:author>
<ce:given-name>Delon</ce:given-name>
<ce:surname>Wu</ce:surname>
<ce:degrees>MD, FACC</ce:degrees>
</ce:author>
<ce:author>
<ce:given-name>Fernando</ce:given-name>
<ce:surname>Amat-Y-leon</ce:surname>
<ce:degrees>MD, FACC</ce:degrees>
</ce:author>
<ce:author>
<ce:given-name>Ramesh</ce:given-name>
<ce:surname>Dhingra</ce:surname>
<ce:degrees>MD, FACC</ce:degrees>
</ce:author>
<ce:author>
<ce:given-name>Kenneth M.</ce:given-name>
<ce:surname>Rosen</ce:surname>
<ce:degrees>MD, FACC</ce:degrees>
</ce:author>
<ce:affiliation>
<ce:textfn>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</ce:textfn>
</ce:affiliation>
<ce:correspondence id="COR1">
<ce:label></ce:label>
<ce:text>Address for reprints: Pablo Denes, MD, Cardiology Section, University of Illinois Hospital, P.O. Box 6998, Chicago, Illinois 60680.</ce:text>
</ce:correspondence>
</ce:author-group>
<ce:date-received day="6" month="9" year="1977"></ce:date-received>
<ce:date-revised day="14" month="11" year="1977"></ce:date-revised>
<ce:date-accepted day="16" month="11" year="1977"></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">Electrophysiologic effects of intravenous propranolol, 0.1 mg/kg, were evaluated in 18 patients with anomalous pathways utilizing intracardiac stimulation and recording. Fourteen patients had Wolff-Parkinson-White syndrome and four had concealed ventricular preexcitation. Anomalous pathway effective refractory period could be measured during the control period and after propranolol administration in nine patients and was 304 ± 7.5 (mean ± standard error of the mean) and 304 ± 8.3 msec, respectively (difference not significant). Ventricular paced 1:1 ventriculoatrial (V-A) conduction (reflecting retrograde anomalous pathway conduction) measured in 12 patients was intact during both the control period and after propranolol at rates of 170 to 200/min. Sustained paroxysmal supraventricular tachycardia was induced in 14 patients during the control period and in 10 after propranolol (in 4 of whom the tachycardia could not be sustained because of atrioventricular [A-V] nodal refractoriness). Mean cycle length of tachycardia in these 10 patients was 328 ± 18 (control) and 352 ± 19 msec (propranolol) (
<ce:italic>P</ce:italic>
< 0.01). The increase in tachycardia cycle length reflected an increase in A-V nodal conduction time (A-H interval).</ce:simple-para>
<ce:simple-para view="all" id="simple-para.0015">In conclusion: (1) Propranolol has an insignificant effect on both anterograde and retrograde anomalous pathway properties. (2) In most cases, propranolol does not interfere with induction of sustained circus movement tachycardia. However, it does produce a statistically significant but slight slowing of the rate of tachycardia. (3) In a minority of cases, propranolol inhibits induction of sustained paroxysmal supraventricular tachycardia by increasing A-V nodal refractoriness.</ce:simple-para>
</ce:abstract-sec>
</ce:abstract>
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<title>Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation</title>
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<title>Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation</title>
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<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
<description>Address for reprints: Pablo Denes, MD, Cardiology Section, University of Illinois Hospital, P.O. Box 6998, Chicago, Illinois 60680.</description>
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<name type="personal">
<namePart type="given">James M.</namePart>
<namePart type="family">Cummings</namePart>
<namePart type="termsOfAddress">MD, FACC</namePart>
<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
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<roleTerm type="text">author</roleTerm>
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<name type="personal">
<namePart type="given">Ross</namePart>
<namePart type="family">Simpson</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
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<name type="personal">
<namePart type="given">Delon</namePart>
<namePart type="family">Wu</namePart>
<namePart type="termsOfAddress">MD, FACC</namePart>
<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
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</name>
<name type="personal">
<namePart type="given">Fernando</namePart>
<namePart type="family">Amat-Y-leon</namePart>
<namePart type="termsOfAddress">MD, FACC</namePart>
<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Ramesh</namePart>
<namePart type="family">Dhingra</namePart>
<namePart type="termsOfAddress">MD, FACC</namePart>
<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
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<namePart type="given">Kenneth M.</namePart>
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<namePart type="termsOfAddress">MD, FACC</namePart>
<affiliation>From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine and West Side Veterans' Administration Hospital, Division of Adult Cardiology, Chicago, Illinois USA</affiliation>
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<abstract lang="en">Electrophysiologic effects of intravenous propranolol, 0.1 mg/kg, were evaluated in 18 patients with anomalous pathways utilizing intracardiac stimulation and recording. Fourteen patients had Wolff-Parkinson-White syndrome and four had concealed ventricular preexcitation. Anomalous pathway effective refractory period could be measured during the control period and after propranolol administration in nine patients and was 304 ± 7.5 (mean ± standard error of the mean) and 304 ± 8.3 msec, respectively (difference not significant). Ventricular paced 1:1 ventriculoatrial (V-A) conduction (reflecting retrograde anomalous pathway conduction) measured in 12 patients was intact during both the control period and after propranolol at rates of 170 to 200/min. Sustained paroxysmal supraventricular tachycardia was induced in 14 patients during the control period and in 10 after propranolol (in 4 of whom the tachycardia could not be sustained because of atrioventricular [A-V] nodal refractoriness). Mean cycle length of tachycardia in these 10 patients was 328 ± 18 (control) and 352 ± 19 msec (propranolol) (P < 0.01). The increase in tachycardia cycle length reflected an increase in A-V nodal conduction time (A-H interval).In conclusion: (1) Propranolol has an insignificant effect on both anterograde and retrograde anomalous pathway properties. (2) In most cases, propranolol does not interfere with induction of sustained circus movement tachycardia. However, it does produce a statistically significant but slight slowing of the rate of tachycardia. (3) In a minority of cases, propranolol inhibits induction of sustained paroxysmal supraventricular tachycardia by increasing A-V nodal refractoriness.</abstract>
<note>This work was supported in part by Training Grant HL 05879-07 and Conduction Disease Grant PHS HL 18794-02 from the U.S. Public Health Service, Bethesda, Maryland.</note>
<note type="content">Section title: Clinical study</note>
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