Comparison of the effects of intravenous and oral betaxolol on antegrade and retrograde conduction in patients with atrioventricular nodal reentrant and atrioventricular reentrant tachycardia.
Identifieur interne : 001942 ( Main/Corpus ); précédent : 001941; suivant : 001943Comparison of the effects of intravenous and oral betaxolol on antegrade and retrograde conduction in patients with atrioventricular nodal reentrant and atrioventricular reentrant tachycardia.
Auteurs : V. Kühlkamp ; O. Ickrath ; R. Haasis ; L. SeipelSource :
- European Heart Journal [ 0195-668X ] ; 1989-06.
Abstract
The electrophysiologic effects of intravenous (015 mg kg−1) and oral (20 mg day−1) betaxolol have been investigated in 11 patients with atrioventricular (A-V) nodal reentrant tachycardia and eight patients with orthodromic A-V reentrant tachycardia. Betaxolol significantly (P > 001) prolonged sinus cycle length, sinus node recovery time, intranodal conduction time, and the antegrade functional refractory period of the A-V node. When the effective refractory period of the A-V node could be determined it was increased by betaxolol, whereas no significant electrophysiologic effects were observed in the atrium, the ventricle or the accessory pathway. Intravenous betaxolol prevented tachycardia in 8 out of 11 patients with A-V nodal reentrant tachycardia, whereas oral betaxolol was effective in 10 patients, primarily by acting on the antegrade limb in two patients and on the retrograde limb in eight patients. In those with A-V reentrant tachycardia, intravenous betaxolol did not prevent tachycardia in any patient, while it was effective after oral treatment in two patients. When the tachycardia remained inducible, cycle length of the tachycardia increased in all patients, due to prolongation of the antegrade and retrograde conduction time in patients with A-V nodal reentrant tachycardia, and due to an increase in the antegrade conduction time, i.e. the A-V node, in the patients with A-V reentrant tachycardia. In conclusion, betaxolol proved to be effective in the treatment of supraventricular tachycardia; for chronic treatment, a single oral dose (20 mg) seems to suffice.
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DOI: 10.1093/oxfordjournals.eurheartj.a059518
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Kühlkamp</name><affiliation><mods:affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</mods:affiliation></affiliation></author><author><name sortKey="Ickrath, O" sort="Ickrath, O" uniqKey="Ickrath O" first="O." last="Ickrath">O. Ickrath</name><affiliation><mods:affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</mods:affiliation></affiliation></author><author><name sortKey="Haasis, R" sort="Haasis, R" uniqKey="Haasis R" first="R." last="Haasis">R. Haasis</name><affiliation><mods:affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</mods:affiliation></affiliation></author><author><name sortKey="Seipel, L" sort="Seipel, L" uniqKey="Seipel L" first="L." last="Seipel">L. Seipel</name><affiliation><mods:affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Heart Journal</title><idno type="ISSN">0195-668X</idno><idno type="eISSN">1522-9645</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="1989-06">1989-06</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="493">493</biblScope><biblScope unit="page" to="501">501</biblScope></imprint><idno type="ISSN">0195-668X</idno></series><idno type="istex">4FFFF3589F78E5E9785440829B26C7CB8C6A2A30</idno><idno type="DOI">10.1093/oxfordjournals.eurheartj.a059518</idno><idno type="ArticleID">10.6.493</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0195-668X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">The electrophysiologic effects of intravenous (015 mg kg−1) and oral (20 mg day−1) betaxolol have been investigated in 11 patients with atrioventricular (A-V) nodal reentrant tachycardia and eight patients with orthodromic A-V reentrant tachycardia. Betaxolol significantly (P > 001) prolonged sinus cycle length, sinus node recovery time, intranodal conduction time, and the antegrade functional refractory period of the A-V node. When the effective refractory period of the A-V node could be determined it was increased by betaxolol, whereas no significant electrophysiologic effects were observed in the atrium, the ventricle or the accessory pathway. Intravenous betaxolol prevented tachycardia in 8 out of 11 patients with A-V nodal reentrant tachycardia, whereas oral betaxolol was effective in 10 patients, primarily by acting on the antegrade limb in two patients and on the retrograde limb in eight patients. In those with A-V reentrant tachycardia, intravenous betaxolol did not prevent tachycardia in any patient, while it was effective after oral treatment in two patients. When the tachycardia remained inducible, cycle length of the tachycardia increased in all patients, due to prolongation of the antegrade and retrograde conduction time in patients with A-V nodal reentrant tachycardia, and due to an increase in the antegrade conduction time, i.e. the A-V node, in the patients with A-V reentrant tachycardia. In conclusion, betaxolol proved to be effective in the treatment of supraventricular tachycardia; for chronic treatment, a single oral dose (20 mg) seems to suffice.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>V. KÜHLKAMP</name><affiliations><json:string>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</json:string><json:string>Address for correspondence: Volker Kühlkamp, Medizinische Universitätsklinik Abteilung III, Otfried M¨ller Str.10, D-7400 T¨bingen, F.R.C.</json:string></affiliations></json:item><json:item><name>O. ICKRATH</name><affiliations><json:string>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</json:string></affiliations></json:item><json:item><name>R. HAASIS</name><affiliations><json:string>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</json:string></affiliations></json:item><json:item><name>L. SEIPEL</name><affiliations><json:string>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Articles</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Betaxolol</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>electrophysiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>A-V nodal reentrant tachycardia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>A-V reentrant tachycardia</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The electrophysiologic effects of intravenous (015 mg kg−1) and oral (20 mg day−1) betaxolol have been investigated in 11 patients with atrioventricular (A-V) nodal reentrant tachycardia and eight patients with orthodromic A-V reentrant tachycardia. Betaxolol significantly (P > 001) prolonged sinus cycle length, sinus node recovery time, intranodal conduction time, and the antegrade functional refractory period of the A-V node. When the effective refractory period of the A-V node could be determined it was increased by betaxolol, whereas no significant electrophysiologic effects were observed in the atrium, the ventricle or the accessory pathway. Intravenous betaxolol prevented tachycardia in 8 out of 11 patients with A-V nodal reentrant tachycardia, whereas oral betaxolol was effective in 10 patients, primarily by acting on the antegrade limb in two patients and on the retrograde limb in eight patients. In those with A-V reentrant tachycardia, intravenous betaxolol did not prevent tachycardia in any patient, while it was effective after oral treatment in two patients. When the tachycardia remained inducible, cycle length of the tachycardia increased in all patients, due to prolongation of the antegrade and retrograde conduction time in patients with A-V nodal reentrant tachycardia, and due to an increase in the antegrade conduction time, i.e. the A-V node, in the patients with A-V reentrant tachycardia. 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Betaxolol significantly (P > 001) prolonged sinus cycle length, sinus node recovery time, intranodal conduction time, and the antegrade functional refractory period of the A-V node. When the effective refractory period of the A-V node could be determined it was increased by betaxolol, whereas no significant electrophysiologic effects were observed in the atrium, the ventricle or the accessory pathway. Intravenous betaxolol prevented tachycardia in 8 out of 11 patients with A-V nodal reentrant tachycardia, whereas oral betaxolol was effective in 10 patients, primarily by acting on the antegrade limb in two patients and on the retrograde limb in eight patients. In those with A-V reentrant tachycardia, intravenous betaxolol did not prevent tachycardia in any patient, while it was effective after oral treatment in two patients. When the tachycardia remained inducible, cycle length of the tachycardia increased in all patients, due to prolongation of the antegrade and retrograde conduction time in patients with A-V nodal reentrant tachycardia, and due to an increase in the antegrade conduction time, i.e. the A-V node, in the patients with A-V reentrant tachycardia. 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Betaxolol significantly (P > 001) prolonged sinus cycle length, sinus node recovery time, intranodal conduction time, and the antegrade functional refractory period of the A-V node. When the effective refractory period of the A-V node could be determined it was increased by betaxolol, whereas no significant electrophysiologic effects were observed in the atrium, the ventricle or the accessory pathway. Intravenous betaxolol prevented tachycardia in 8 out of 11 patients with A-V nodal reentrant tachycardia, whereas oral betaxolol was effective in 10 patients, primarily by acting on the antegrade limb in two patients and on the retrograde limb in eight patients. In those with A-V reentrant tachycardia, intravenous betaxolol did not prevent tachycardia in any patient, while it was effective after oral treatment in two patients. When the tachycardia remained inducible, cycle length of the tachycardia increased in all patients, due to prolongation of the antegrade and retrograde conduction time in patients with A-V nodal reentrant tachycardia, and due to an increase in the antegrade conduction time, i.e. the A-V node, in the patients with A-V reentrant tachycardia. In conclusion, betaxolol proved to be effective in the treatment of supraventricular tachycardia; for chronic treatment, a single oral dose (20 mg) seems to suffice.</p></abstract><kwd-group><kwd>Betaxolol</kwd><kwd>electrophysiology</kwd><kwd>A-V nodal reentrant tachycardia</kwd><kwd>A-V reentrant tachycardia</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Comparison of the effects of intravenous and oral betaxolol on antegrade and retrograde conduction in patients with atrioventricular nodal reentrant and atrioventricular reentrant tachycardia.</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Comparison of the effects of intravenous and oral betaxolol on antegrade and retrograde conduction in patients with atrioventricular nodal reentrant and atrioventricular reentrant tachycardia.</title></titleInfo><name type="personal"><namePart type="given">V.</namePart><namePart type="family">KÜHLKAMP</namePart><affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O.</namePart><namePart type="family">ICKRATH</namePart><affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">HAASIS</namePart><affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">SEIPEL</namePart><affiliation>Medizinische Universitatsklinik Abteilung III, Tubingen, FRG</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><subject><topic>Articles</topic></subject><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">1989-06</dateIssued><copyrightDate encoding="w3cdtf">1989</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>The electrophysiologic effects of intravenous (015 mg kg−1) and oral (20 mg day−1) betaxolol have been investigated in 11 patients with atrioventricular (A-V) nodal reentrant tachycardia and eight patients with orthodromic A-V reentrant tachycardia. Betaxolol significantly (P > 001) prolonged sinus cycle length, sinus node recovery time, intranodal conduction time, and the antegrade functional refractory period of the A-V node. When the effective refractory period of the A-V node could be determined it was increased by betaxolol, whereas no significant electrophysiologic effects were observed in the atrium, the ventricle or the accessory pathway. Intravenous betaxolol prevented tachycardia in 8 out of 11 patients with A-V nodal reentrant tachycardia, whereas oral betaxolol was effective in 10 patients, primarily by acting on the antegrade limb in two patients and on the retrograde limb in eight patients. In those with A-V reentrant tachycardia, intravenous betaxolol did not prevent tachycardia in any patient, while it was effective after oral treatment in two patients. When the tachycardia remained inducible, cycle length of the tachycardia increased in all patients, due to prolongation of the antegrade and retrograde conduction time in patients with A-V nodal reentrant tachycardia, and due to an increase in the antegrade conduction time, i.e. the A-V node, in the patients with A-V reentrant tachycardia. 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|clé= ISTEX:4FFFF3589F78E5E9785440829B26C7CB8C6A2A30
|texte= Comparison of the effects of intravenous and oral betaxolol on antegrade and retrograde conduction in patients with atrioventricular nodal reentrant and atrioventricular reentrant tachycardia.
}}
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