Clinical electrophysiologic effects of tocainide
The electrophysiologic properties of tocainide were evaluated by electrophysiologic studies in 11 patients before, during and after a constant intravenous infusion of the drug for 15 minutes. Peak plasma tocainide concentrations averaged 11.0 +/- 1.7 microgram/ml (SEM), range 3.7 to 22.7. AH, HV, QR...
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Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1978-04, Vol.57 (4), p.685-691 |
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description | The electrophysiologic properties of tocainide were evaluated by electrophysiologic studies in 11 patients before, during and after a constant intravenous infusion of the drug for 15 minutes. Peak plasma tocainide concentrations averaged 11.0 +/- 1.7 microgram/ml (SEM), range 3.7 to 22.7. AH, HV, QRS, QTc and RR intervals were measured every 5 minutes during sinus and atrial-paced rhythms and showed small changes which were not statistically significant for HV and QRS. Mild shortening of RR was significant (P less than 0.05) at 15 minutes only. AH tended to increase slightly for spontaneous (but not paced) rhythm, becoming significant at 15 minutes only (P less than 0.05). QTc decreased slightly, a change which was significant (P less than 0.05) for paced but not spontaneous rhythm. A progressive rise in mean arterial pressure occurred during infusion and persisted through 30 minutes (P less than 0.001). Comparison of electrophysiologic studies at 0 and 30 minutes showed decreased in mean effective refractory periods of atrium, A-V node, and right ventricle by 17, 22, and 23 msec, respectively (P less than 0.05, 0.01, 0.01). Functional refractory period of the A-V node showed an average decrease which was not significant. Sinus node recovery time and Wenckebach cycle length were unchanged. The drug was well tolerated in all 11 patients. Hypotension in a twelfth patient may or may not have been drug related. These results obtained at therapeutic plasma concentrations suggest qualitative similarities between the conduction system effects of tocainide and those published for lidocaine. |
doi_str_mv | 10.1161/01.CIR.57.4.685 |
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Peak plasma tocainide concentrations averaged 11.0 +/- 1.7 microgram/ml (SEM), range 3.7 to 22.7. AH, HV, QRS, QTc and RR intervals were measured every 5 minutes during sinus and atrial-paced rhythms and showed small changes which were not statistically significant for HV and QRS. Mild shortening of RR was significant (P less than 0.05) at 15 minutes only. AH tended to increase slightly for spontaneous (but not paced) rhythm, becoming significant at 15 minutes only (P less than 0.05). QTc decreased slightly, a change which was significant (P less than 0.05) for paced but not spontaneous rhythm. A progressive rise in mean arterial pressure occurred during infusion and persisted through 30 minutes (P less than 0.001). Comparison of electrophysiologic studies at 0 and 30 minutes showed decreased in mean effective refractory periods of atrium, A-V node, and right ventricle by 17, 22, and 23 msec, respectively (P less than 0.05, 0.01, 0.01). Functional refractory period of the A-V node showed an average decrease which was not significant. Sinus node recovery time and Wenckebach cycle length were unchanged. The drug was well tolerated in all 11 patients. Hypotension in a twelfth patient may or may not have been drug related. These results obtained at therapeutic plasma concentrations suggest qualitative similarities between the conduction system effects of tocainide and those published for lidocaine.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.57.4.685</identifier><identifier>PMID: 630677</identifier><language>eng</language><publisher>United States</publisher><subject>Aged ; Anilides - therapeutic use ; Anti-Arrhythmia Agents - blood ; Anti-Arrhythmia Agents - therapeutic use ; Blood Pressure ; Cardiac Catheterization ; Electrophysiology ; Female ; Heart Conduction System - drug effects ; Heart Conduction System - physiopathology ; Humans ; Lidocaine - therapeutic use ; Male ; Middle Aged ; Myocardial Contraction - drug effects</subject><ispartof>Circulation (New York, N.Y.), 1978-04, Vol.57 (4), p.685-691</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-e8b4f38ebdc4de00d3493234a9d062a5692878a81f726e098f6103d0e29cb8f83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/630677$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Anderson, J L</creatorcontrib><creatorcontrib>Mason, J W</creatorcontrib><creatorcontrib>Winkle, R A</creatorcontrib><creatorcontrib>Meffin, P J</creatorcontrib><creatorcontrib>Fowles, R E</creatorcontrib><creatorcontrib>Peters, L</creatorcontrib><creatorcontrib>Harrison, D C</creatorcontrib><title>Clinical electrophysiologic effects of tocainide</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The electrophysiologic properties of tocainide were evaluated by electrophysiologic studies in 11 patients before, during and after a constant intravenous infusion of the drug for 15 minutes. Peak plasma tocainide concentrations averaged 11.0 +/- 1.7 microgram/ml (SEM), range 3.7 to 22.7. AH, HV, QRS, QTc and RR intervals were measured every 5 minutes during sinus and atrial-paced rhythms and showed small changes which were not statistically significant for HV and QRS. Mild shortening of RR was significant (P less than 0.05) at 15 minutes only. AH tended to increase slightly for spontaneous (but not paced) rhythm, becoming significant at 15 minutes only (P less than 0.05). QTc decreased slightly, a change which was significant (P less than 0.05) for paced but not spontaneous rhythm. A progressive rise in mean arterial pressure occurred during infusion and persisted through 30 minutes (P less than 0.001). Comparison of electrophysiologic studies at 0 and 30 minutes showed decreased in mean effective refractory periods of atrium, A-V node, and right ventricle by 17, 22, and 23 msec, respectively (P less than 0.05, 0.01, 0.01). Functional refractory period of the A-V node showed an average decrease which was not significant. Sinus node recovery time and Wenckebach cycle length were unchanged. The drug was well tolerated in all 11 patients. Hypotension in a twelfth patient may or may not have been drug related. These results obtained at therapeutic plasma concentrations suggest qualitative similarities between the conduction system effects of tocainide and those published for lidocaine.</description><subject>Aged</subject><subject>Anilides - therapeutic use</subject><subject>Anti-Arrhythmia Agents - blood</subject><subject>Anti-Arrhythmia Agents - therapeutic use</subject><subject>Blood Pressure</subject><subject>Cardiac Catheterization</subject><subject>Electrophysiology</subject><subject>Female</subject><subject>Heart Conduction System - drug effects</subject><subject>Heart Conduction System - physiopathology</subject><subject>Humans</subject><subject>Lidocaine - therapeutic use</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Contraction - drug effects</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1978</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kElPwzAQRi3EVgpnLhxy4pZ0vMTLEUUslSohIThbjjOGoLQucXrov8eoFafRjN73SfMIuaVQUSrpAmjVLN-qWlWikro-ITNaM1GKmptTMgMAUyrO2CW5Suk7r5Kr-oKcSw5SqRmBZug3vXdDgQP6aYzbr33q4xA_e19gCPmWihiKKXqXwQ6vyVlwQ8Kb45yTj6fH9-alXL0-L5uHVem5YlOJuhWBa2w7LzoE6LgwnHHhTAeSuVoappV2mgbFJILRQVLgHSAzvtVB8zm5P_Rux_izwzTZdZ88DoPbYNwlq7nmJn-WwcUB9GNMacRgt2O_duPeUrB_iixQmxXZWllhs6KcuDtW79o1dv_8wQn_BbZnYKY</recordid><startdate>197804</startdate><enddate>197804</enddate><creator>Anderson, J L</creator><creator>Mason, J W</creator><creator>Winkle, R A</creator><creator>Meffin, P J</creator><creator>Fowles, R E</creator><creator>Peters, L</creator><creator>Harrison, D C</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>197804</creationdate><title>Clinical electrophysiologic effects of tocainide</title><author>Anderson, J L ; Mason, J W ; Winkle, R A ; Meffin, P J ; Fowles, R E ; Peters, L ; Harrison, D C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-e8b4f38ebdc4de00d3493234a9d062a5692878a81f726e098f6103d0e29cb8f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1978</creationdate><topic>Aged</topic><topic>Anilides - therapeutic use</topic><topic>Anti-Arrhythmia Agents - blood</topic><topic>Anti-Arrhythmia Agents - therapeutic use</topic><topic>Blood Pressure</topic><topic>Cardiac Catheterization</topic><topic>Electrophysiology</topic><topic>Female</topic><topic>Heart Conduction System - drug effects</topic><topic>Heart Conduction System - physiopathology</topic><topic>Humans</topic><topic>Lidocaine - therapeutic use</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Contraction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Anderson, J L</creatorcontrib><creatorcontrib>Mason, J W</creatorcontrib><creatorcontrib>Winkle, R A</creatorcontrib><creatorcontrib>Meffin, P J</creatorcontrib><creatorcontrib>Fowles, R E</creatorcontrib><creatorcontrib>Peters, L</creatorcontrib><creatorcontrib>Harrison, D C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Anderson, J L</au><au>Mason, J W</au><au>Winkle, R A</au><au>Meffin, P J</au><au>Fowles, R E</au><au>Peters, L</au><au>Harrison, D C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical electrophysiologic effects of tocainide</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1978-04</date><risdate>1978</risdate><volume>57</volume><issue>4</issue><spage>685</spage><epage>691</epage><pages>685-691</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><abstract>The electrophysiologic properties of tocainide were evaluated by electrophysiologic studies in 11 patients before, during and after a constant intravenous infusion of the drug for 15 minutes. Peak plasma tocainide concentrations averaged 11.0 +/- 1.7 microgram/ml (SEM), range 3.7 to 22.7. AH, HV, QRS, QTc and RR intervals were measured every 5 minutes during sinus and atrial-paced rhythms and showed small changes which were not statistically significant for HV and QRS. Mild shortening of RR was significant (P less than 0.05) at 15 minutes only. AH tended to increase slightly for spontaneous (but not paced) rhythm, becoming significant at 15 minutes only (P less than 0.05). QTc decreased slightly, a change which was significant (P less than 0.05) for paced but not spontaneous rhythm. A progressive rise in mean arterial pressure occurred during infusion and persisted through 30 minutes (P less than 0.001). Comparison of electrophysiologic studies at 0 and 30 minutes showed decreased in mean effective refractory periods of atrium, A-V node, and right ventricle by 17, 22, and 23 msec, respectively (P less than 0.05, 0.01, 0.01). Functional refractory period of the A-V node showed an average decrease which was not significant. Sinus node recovery time and Wenckebach cycle length were unchanged. The drug was well tolerated in all 11 patients. Hypotension in a twelfth patient may or may not have been drug related. These results obtained at therapeutic plasma concentrations suggest qualitative similarities between the conduction system effects of tocainide and those published for lidocaine.</abstract><cop>United States</cop><pmid>630677</pmid><doi>10.1161/01.CIR.57.4.685</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Anilides - therapeutic use Anti-Arrhythmia Agents - blood Anti-Arrhythmia Agents - therapeutic use Blood Pressure Cardiac Catheterization Electrophysiology Female Heart Conduction System - drug effects Heart Conduction System - physiopathology Humans Lidocaine - therapeutic use Male Middle Aged Myocardial Contraction - drug effects |
title | Clinical electrophysiologic effects of tocainide |
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