Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: A case report
Summary Intravenous amiodarone (AMD) induces multiple antiarrhythmic effects via blocking of Na+ , Ca2+ , and IKr channels, and β receptors. A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occ...
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| Veröffentlicht in: | Journal of cardiology 2009-12, Vol.54 (3), p.460-465 |
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| creator | Yoshioka, Koichiro, MD, PhD, FJCC Amino, Mari, MD, PhD Matsuzaki, Atsushi, MD Shima, Makiyoshi, MD Fujii, Toshiharu, MD Kanda, Shigetaka, MD Deguchi, Yoshiaki, MD Kodama, Itsuo, MD, PhD Tanabe, Teruhisa, MD, PhD, FJCC |
| description | Summary Intravenous amiodarone (AMD) induces multiple antiarrhythmic effects via blocking of Na+ , Ca2+ , and IKr channels, and β receptors. A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occurred 5 h after AMD administration. AMD was withdrawn at 24 h because of prolonged QTc interval (716 ms), which persisted for a further 48 h (661 ms). Ventricular premature contraction (VPC) was significantly decreased at 7 h; however, VPC increased again after discontinuing AMD. Depolarization changes induced by the Na+ -channel blocking action of AMD were analyzed. There was increasing filtered QRS-duration and duration of low-amplitude signals at voltage |
| doi_str_mv | 10.1016/j.jjcc.2009.02.002 |
| format | Article |
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A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occurred 5 h after AMD administration. AMD was withdrawn at 24 h because of prolonged QTc interval (716 ms), which persisted for a further 48 h (661 ms). Ventricular premature contraction (VPC) was significantly decreased at 7 h; however, VPC increased again after discontinuing AMD. Depolarization changes induced by the Na+ -channel blocking action of AMD were analyzed. There was increasing filtered QRS-duration and duration of low-amplitude signals at voltage <40 μV, and decreasing root-mean-square voltage of signals in the last 40 ms of ventricular late potentials (LPs) within 7 h. However after stopping AMD, LPs were reversed. The blood concentration of AMD reached the effective level within 10 min but decreased immediately to an ineffective level. Onset and disappearance of the VPC-inhibiting effect corresponded to the depressive effect on depolarization but not with the increase in the prolonged repolarization effect and blood concentration. Even if the QT interval is sufficiently prolonged, the Na+ -channel blocking action is required for AMD to induce the antiarrhythmic effect.</description><identifier>ISSN: 0914-5087</identifier><identifier>EISSN: 1876-4738</identifier><identifier>DOI: 10.1016/j.jjcc.2009.02.002</identifier><identifier>PMID: 19944322</identifier><language>eng</language><publisher>Netherlands: Elsevier Ltd</publisher><subject>Amiodarone - administration & dosage ; Amiodarone - blood ; Amiodarone - pharmacology ; Anti-Arrhythmia Agents - administration & dosage ; Anti-Arrhythmia Agents - blood ; Anti-Arrhythmia Agents - pharmacology ; Cardiopulmonary Resuscitation ; Cardiovascular ; Depolarization ; Depression, Chemical ; Electrocardiography, Ambulatory ; Humans ; Infusions, Intravenous ; Intravenous amiodarone ; Late potential ; Longitudinal Studies ; Male ; Middle Aged ; Repolarization ; Sodium Channel Blockers ; Tachycardia, Ventricular - physiopathology ; Tachycardia, Ventricular - therapy ; Time Factors ; Ventricular Function - drug effects</subject><ispartof>Journal of cardiology, 2009-12, Vol.54 (3), p.460-465</ispartof><rights>Japanese College of Cardiology</rights><rights>2009 Japanese College of Cardiology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-83df169271af3d3fa8b12fa96bb76607718f4dfe0ff041995d549b83fea1416b3</citedby><cites>FETCH-LOGICAL-c463t-83df169271af3d3fa8b12fa96bb76607718f4dfe0ff041995d549b83fea1416b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0914508709000641$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19944322$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshioka, Koichiro, MD, PhD, FJCC</creatorcontrib><creatorcontrib>Amino, Mari, MD, PhD</creatorcontrib><creatorcontrib>Matsuzaki, Atsushi, MD</creatorcontrib><creatorcontrib>Shima, Makiyoshi, MD</creatorcontrib><creatorcontrib>Fujii, Toshiharu, MD</creatorcontrib><creatorcontrib>Kanda, Shigetaka, MD</creatorcontrib><creatorcontrib>Deguchi, Yoshiaki, MD</creatorcontrib><creatorcontrib>Kodama, Itsuo, MD, PhD</creatorcontrib><creatorcontrib>Tanabe, Teruhisa, MD, PhD, FJCC</creatorcontrib><title>Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: A case report</title><title>Journal of cardiology</title><addtitle>J Cardiol</addtitle><description>Summary Intravenous amiodarone (AMD) induces multiple antiarrhythmic effects via blocking of Na+ , Ca2+ , and IKr channels, and β receptors. A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occurred 5 h after AMD administration. AMD was withdrawn at 24 h because of prolonged QTc interval (716 ms), which persisted for a further 48 h (661 ms). Ventricular premature contraction (VPC) was significantly decreased at 7 h; however, VPC increased again after discontinuing AMD. Depolarization changes induced by the Na+ -channel blocking action of AMD were analyzed. There was increasing filtered QRS-duration and duration of low-amplitude signals at voltage <40 μV, and decreasing root-mean-square voltage of signals in the last 40 ms of ventricular late potentials (LPs) within 7 h. However after stopping AMD, LPs were reversed. The blood concentration of AMD reached the effective level within 10 min but decreased immediately to an ineffective level. Onset and disappearance of the VPC-inhibiting effect corresponded to the depressive effect on depolarization but not with the increase in the prolonged repolarization effect and blood concentration. Even if the QT interval is sufficiently prolonged, the Na+ -channel blocking action is required for AMD to induce the antiarrhythmic effect.</description><subject>Amiodarone - administration & dosage</subject><subject>Amiodarone - blood</subject><subject>Amiodarone - pharmacology</subject><subject>Anti-Arrhythmia Agents - administration & dosage</subject><subject>Anti-Arrhythmia Agents - blood</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Cardiopulmonary Resuscitation</subject><subject>Cardiovascular</subject><subject>Depolarization</subject><subject>Depression, Chemical</subject><subject>Electrocardiography, Ambulatory</subject><subject>Humans</subject><subject>Infusions, Intravenous</subject><subject>Intravenous amiodarone</subject><subject>Late potential</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Repolarization</subject><subject>Sodium Channel Blockers</subject><subject>Tachycardia, Ventricular - physiopathology</subject><subject>Tachycardia, Ventricular - therapy</subject><subject>Time Factors</subject><subject>Ventricular Function - drug effects</subject><issn>0914-5087</issn><issn>1876-4738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU-r1DAUxYMovvHpF3Ah2blqvUk6aSsiPB7-gwEX6jqkyY2mdpIxaQdG8LubvhkQXbhJyM05B-7vEPKUQc2AyRdjPY7G1Bygr4HXAPwe2bCulVXTiu4-2UDPmmoLXXtFHuU8AkjoO_mQXLG-bxrB-Yb82sXw1c-L9UFPVJfjlH2m0dH5G1KLh4Q5-yNSdA7NfPfjw5z0EUNcMtV7H61OMSCNYdXHSSf_U8--PHWwNP01eklvqNEZ78ZpfkweOD1lfHK5r8mXt28-376vdh_ffbi92VWmkWKuOmEdkz1vmXbCCqe7gXGnezkMrZTQtqxzjXUIzkFTdtvabdMPnXCoWcPkIK7J83PuIcUfC-ZZ7X02OE06YNlCtaLIoGW8KPlZaVLMOaFTh-T3Op0UA7VSV6NaqauVugKuCvVienaJX4Y92j-WC-YieHUWYFny6DGpbDwGg9anQlXZ6P-f__ofu5l88EZP3_GEeYxLKsVlxVQuBvVp7X2tHXoonTdM_AZqN6rn</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Yoshioka, Koichiro, MD, PhD, FJCC</creator><creator>Amino, Mari, MD, PhD</creator><creator>Matsuzaki, Atsushi, MD</creator><creator>Shima, Makiyoshi, MD</creator><creator>Fujii, Toshiharu, MD</creator><creator>Kanda, Shigetaka, MD</creator><creator>Deguchi, Yoshiaki, MD</creator><creator>Kodama, Itsuo, MD, PhD</creator><creator>Tanabe, Teruhisa, MD, PhD, FJCC</creator><general>Elsevier Ltd</general><scope>6I.</scope><scope>AAFTH</scope><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>20091201</creationdate><title>Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: A case report</title><author>Yoshioka, Koichiro, MD, PhD, FJCC ; Amino, Mari, MD, PhD ; Matsuzaki, Atsushi, MD ; Shima, Makiyoshi, MD ; Fujii, Toshiharu, MD ; Kanda, Shigetaka, MD ; Deguchi, Yoshiaki, MD ; Kodama, Itsuo, MD, PhD ; Tanabe, Teruhisa, MD, PhD, FJCC</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-83df169271af3d3fa8b12fa96bb76607718f4dfe0ff041995d549b83fea1416b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Amiodarone - administration & dosage</topic><topic>Amiodarone - blood</topic><topic>Amiodarone - pharmacology</topic><topic>Anti-Arrhythmia Agents - administration & dosage</topic><topic>Anti-Arrhythmia Agents - blood</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Cardiopulmonary Resuscitation</topic><topic>Cardiovascular</topic><topic>Depolarization</topic><topic>Depression, Chemical</topic><topic>Electrocardiography, Ambulatory</topic><topic>Humans</topic><topic>Infusions, Intravenous</topic><topic>Intravenous amiodarone</topic><topic>Late potential</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Repolarization</topic><topic>Sodium Channel Blockers</topic><topic>Tachycardia, Ventricular - physiopathology</topic><topic>Tachycardia, Ventricular - therapy</topic><topic>Time Factors</topic><topic>Ventricular Function - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshioka, Koichiro, MD, PhD, FJCC</creatorcontrib><creatorcontrib>Amino, Mari, MD, PhD</creatorcontrib><creatorcontrib>Matsuzaki, Atsushi, MD</creatorcontrib><creatorcontrib>Shima, Makiyoshi, MD</creatorcontrib><creatorcontrib>Fujii, Toshiharu, MD</creatorcontrib><creatorcontrib>Kanda, Shigetaka, MD</creatorcontrib><creatorcontrib>Deguchi, Yoshiaki, MD</creatorcontrib><creatorcontrib>Kodama, Itsuo, MD, PhD</creatorcontrib><creatorcontrib>Tanabe, Teruhisa, MD, PhD, FJCC</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshioka, Koichiro, MD, PhD, FJCC</au><au>Amino, Mari, MD, PhD</au><au>Matsuzaki, Atsushi, MD</au><au>Shima, Makiyoshi, MD</au><au>Fujii, Toshiharu, MD</au><au>Kanda, Shigetaka, MD</au><au>Deguchi, Yoshiaki, MD</au><au>Kodama, Itsuo, MD, PhD</au><au>Tanabe, Teruhisa, MD, PhD, FJCC</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: A case report</atitle><jtitle>Journal of cardiology</jtitle><addtitle>J Cardiol</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>54</volume><issue>3</issue><spage>460</spage><epage>465</epage><pages>460-465</pages><issn>0914-5087</issn><eissn>1876-4738</eissn><abstract>Summary Intravenous amiodarone (AMD) induces multiple antiarrhythmic effects via blocking of Na+ , Ca2+ , and IKr channels, and β receptors. A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occurred 5 h after AMD administration. AMD was withdrawn at 24 h because of prolonged QTc interval (716 ms), which persisted for a further 48 h (661 ms). Ventricular premature contraction (VPC) was significantly decreased at 7 h; however, VPC increased again after discontinuing AMD. Depolarization changes induced by the Na+ -channel blocking action of AMD were analyzed. There was increasing filtered QRS-duration and duration of low-amplitude signals at voltage <40 μV, and decreasing root-mean-square voltage of signals in the last 40 ms of ventricular late potentials (LPs) within 7 h. However after stopping AMD, LPs were reversed. The blood concentration of AMD reached the effective level within 10 min but decreased immediately to an ineffective level. Onset and disappearance of the VPC-inhibiting effect corresponded to the depressive effect on depolarization but not with the increase in the prolonged repolarization effect and blood concentration. Even if the QT interval is sufficiently prolonged, the Na+ -channel blocking action is required for AMD to induce the antiarrhythmic effect.</abstract><cop>Netherlands</cop><pub>Elsevier Ltd</pub><pmid>19944322</pmid><doi>10.1016/j.jjcc.2009.02.002</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amiodarone - administration & dosage Amiodarone - blood Amiodarone - pharmacology Anti-Arrhythmia Agents - administration & dosage Anti-Arrhythmia Agents - blood Anti-Arrhythmia Agents - pharmacology Cardiopulmonary Resuscitation Cardiovascular Depolarization Depression, Chemical Electrocardiography, Ambulatory Humans Infusions, Intravenous Intravenous amiodarone Late potential Longitudinal Studies Male Middle Aged Repolarization Sodium Channel Blockers Tachycardia, Ventricular - physiopathology Tachycardia, Ventricular - therapy Time Factors Ventricular Function - drug effects |
| title | Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: A case report |
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