Slowing of Ventricular Tachycardia as a Possible Endpoint for Serial Drug Testing at Electrophysiological Study
Certain patients who cannot be rendered noninducible by serial drug testing during electrophysiology study demonstrate significant slowing of their ventricular tachycardia rate with selected agents. We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could...
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Veröffentlicht in: | Pacing and clinical electrophysiology 1992-06, Vol.15 (6), p.864-869 |
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description | Certain patients who cannot be rendered noninducible by serial drug testing during electrophysiology study demonstrate significant slowing of their ventricular tachycardia rate with selected agents. We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could be considered an acceptable endpoint for treatment. This group consisted of 14 males and 5 females (mean age 63 ± 9) with a mean ejection fraction of 28 ± 13% and inducible sustained ventricular tachycardia. Sixteen patients had known coronary artery disease and 13 had prior myocardial infarction. The other three patients had idiopathic cardiomyopathy. Serial drug testing during an electrophysiology protocol that used up to three extrastimuli at two or three cycle lengths at two right ventricular sites was used to select a medication regimen that provided optimal ventricular tachycardia slowing without limiting side effects. Five patients were treated with amiodarone, three with Ic agents fall with ejection fraction > 30%), and the remainder with la and Ib agents alone or in combination. Mean initial ventricular tachycardia rate was 219 ± 26 beats/mm with posttreafment ventricular tachycardia rate 137 ±17 fmean initial cycle length 278 ± 35 msec, posttreatment 443 ± 53 msec). Two groups were identified, those who had recurrent (although well‐tolerated) ventricular tachycardia (group 1, n = 6, mean time to recurrence = 15 months), and those who did not (group II, n = 11, mean follow‐up 22 months). Overall sudden death rate was 5%, while total mortality was 11% (all mortality in group I). No factor such as sex, age, drug type, ejection fraction, presence of coronary artery disease or aneurysm, or ventricular tachycardia morphology was significantly different between the groups. Conclusions: Significant ventricular tachycardia slowing by selected drug therapy at electrophysiology study is an acceptable therapeutic endpoint for certain patients, with a low rate of subsequent sudden death. However, recurrence, even if well tolerated, may be a marker for need for nonmedical therapy such as a device or surgery. |
doi_str_mv | 10.1111/j.1540-8159.1992.tb03076.x |
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We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could be considered an acceptable endpoint for treatment. This group consisted of 14 males and 5 females (mean age 63 ± 9) with a mean ejection fraction of 28 ± 13% and inducible sustained ventricular tachycardia. Sixteen patients had known coronary artery disease and 13 had prior myocardial infarction. The other three patients had idiopathic cardiomyopathy. Serial drug testing during an electrophysiology protocol that used up to three extrastimuli at two or three cycle lengths at two right ventricular sites was used to select a medication regimen that provided optimal ventricular tachycardia slowing without limiting side effects. Five patients were treated with amiodarone, three with Ic agents fall with ejection fraction > 30%), and the remainder with la and Ib agents alone or in combination. Mean initial ventricular tachycardia rate was 219 ± 26 beats/mm with posttreafment ventricular tachycardia rate 137 ±17 fmean initial cycle length 278 ± 35 msec, posttreatment 443 ± 53 msec). Two groups were identified, those who had recurrent (although well‐tolerated) ventricular tachycardia (group 1, n = 6, mean time to recurrence = 15 months), and those who did not (group II, n = 11, mean follow‐up 22 months). Overall sudden death rate was 5%, while total mortality was 11% (all mortality in group I). No factor such as sex, age, drug type, ejection fraction, presence of coronary artery disease or aneurysm, or ventricular tachycardia morphology was significantly different between the groups. Conclusions: Significant ventricular tachycardia slowing by selected drug therapy at electrophysiology study is an acceptable therapeutic endpoint for certain patients, with a low rate of subsequent sudden death. However, recurrence, even if well tolerated, may be a marker for need for nonmedical therapy such as a device or surgery.</description><identifier>ISSN: 0147-8389</identifier><identifier>EISSN: 1540-8159</identifier><identifier>DOI: 10.1111/j.1540-8159.1992.tb03076.x</identifier><identifier>PMID: 1376898</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Amiodarone - therapeutic use ; Anti-Arrhythmia Agents - therapeutic use ; antiarrhythmic therapy ; Cardiac Pacing, Artificial ; Death, Sudden, Cardiac - epidemiology ; electrophysiological testing ; Female ; Heart Conduction System - drug effects ; Heart Conduction System - physiopathology ; Heart Rate - drug effects ; Humans ; Male ; Middle Aged ; Recurrence ; Retrospective Studies ; Tachycardia - diagnosis ; Tachycardia - drug therapy ; Tachycardia - mortality ; ventricular tachycardia</subject><ispartof>Pacing and clinical electrophysiology, 1992-06, Vol.15 (6), p.864-869</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3234-be58caccef1fb739dba00e1f1cff003fd2e5a9ba7d069ac64f53f9cb114327f73</citedby><cites>FETCH-LOGICAL-c3234-be58caccef1fb739dba00e1f1cff003fd2e5a9ba7d069ac64f53f9cb114327f73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1540-8159.1992.tb03076.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1540-8159.1992.tb03076.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1376898$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HANDLIN, LARRY R.</creatorcontrib><creatorcontrib>BRODINE, WILLIAM N.</creatorcontrib><creatorcontrib>GIBBS, HARRY</creatorcontrib><creatorcontrib>VACEK, JAMES L.</creatorcontrib><title>Slowing of Ventricular Tachycardia as a Possible Endpoint for Serial Drug Testing at Electrophysiological Study</title><title>Pacing and clinical electrophysiology</title><addtitle>Pacing Clin Electrophysiol</addtitle><description>Certain patients who cannot be rendered noninducible by serial drug testing during electrophysiology study demonstrate significant slowing of their ventricular tachycardia rate with selected agents. We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could be considered an acceptable endpoint for treatment. This group consisted of 14 males and 5 females (mean age 63 ± 9) with a mean ejection fraction of 28 ± 13% and inducible sustained ventricular tachycardia. Sixteen patients had known coronary artery disease and 13 had prior myocardial infarction. The other three patients had idiopathic cardiomyopathy. Serial drug testing during an electrophysiology protocol that used up to three extrastimuli at two or three cycle lengths at two right ventricular sites was used to select a medication regimen that provided optimal ventricular tachycardia slowing without limiting side effects. Five patients were treated with amiodarone, three with Ic agents fall with ejection fraction > 30%), and the remainder with la and Ib agents alone or in combination. Mean initial ventricular tachycardia rate was 219 ± 26 beats/mm with posttreafment ventricular tachycardia rate 137 ±17 fmean initial cycle length 278 ± 35 msec, posttreatment 443 ± 53 msec). Two groups were identified, those who had recurrent (although well‐tolerated) ventricular tachycardia (group 1, n = 6, mean time to recurrence = 15 months), and those who did not (group II, n = 11, mean follow‐up 22 months). Overall sudden death rate was 5%, while total mortality was 11% (all mortality in group I). No factor such as sex, age, drug type, ejection fraction, presence of coronary artery disease or aneurysm, or ventricular tachycardia morphology was significantly different between the groups. Conclusions: Significant ventricular tachycardia slowing by selected drug therapy at electrophysiology study is an acceptable therapeutic endpoint for certain patients, with a low rate of subsequent sudden death. However, recurrence, even if well tolerated, may be a marker for need for nonmedical therapy such as a device or surgery.</description><subject>Amiodarone - therapeutic use</subject><subject>Anti-Arrhythmia Agents - therapeutic use</subject><subject>antiarrhythmic therapy</subject><subject>Cardiac Pacing, Artificial</subject><subject>Death, Sudden, Cardiac - epidemiology</subject><subject>electrophysiological testing</subject><subject>Female</subject><subject>Heart Conduction System - drug effects</subject><subject>Heart Conduction System - physiopathology</subject><subject>Heart Rate - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Recurrence</subject><subject>Retrospective Studies</subject><subject>Tachycardia - diagnosis</subject><subject>Tachycardia - drug therapy</subject><subject>Tachycardia - mortality</subject><subject>ventricular tachycardia</subject><issn>0147-8389</issn><issn>1540-8159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkEFP2zAYhi20CTrGT5hkcdgtmV3HccwFobawIQZI7TZpF8tx7OLixsVORPPvlygVnOeLD-_7Pf78AHCOUYr7822TYpqhpMCUp5jzadqUiCCWp_sjMHmLPoAJwhlLClLwE_Apxg1CKEcZPQbHmLC84MUE-KXzr7ZeQ2_gb103warWyQBXUj11SobKSigjlPDRx2hLp-Girnbe1g00PsClDlY6OA_tGq50bAaSbODCadUEv3vqovXOr63qS8umrbrP4KORLuqzw30Kfl0vVrPvyd3DzY_Z1V2iyJRkSalpoaRS2mBTMsKrUiKkscHKGISIqaaaSl5KVqGcS5VnhhLDVYlxRqbMMHIKvo7cXfAvbb-Z2NqotHOy1r6NghGEKKO8L16MRRX6HwZtxC7YrQydwEgMtsVGDErFoFQMtsXBttj3w18Or7TlVlfvo6PePr8c81frdPcfZPF4NVsUedYTkpFgY6P3bwQZnkXOCKPiz_2NmM9us5_X9K-4Jf8AxhuhtA</recordid><startdate>199206</startdate><enddate>199206</enddate><creator>HANDLIN, LARRY R.</creator><creator>BRODINE, WILLIAM N.</creator><creator>GIBBS, HARRY</creator><creator>VACEK, JAMES L.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>199206</creationdate><title>Slowing of Ventricular Tachycardia as a Possible Endpoint for Serial Drug Testing at Electrophysiological Study</title><author>HANDLIN, LARRY R. ; BRODINE, WILLIAM N. ; GIBBS, HARRY ; VACEK, JAMES L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3234-be58caccef1fb739dba00e1f1cff003fd2e5a9ba7d069ac64f53f9cb114327f73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Amiodarone - therapeutic use</topic><topic>Anti-Arrhythmia Agents - therapeutic use</topic><topic>antiarrhythmic therapy</topic><topic>Cardiac Pacing, Artificial</topic><topic>Death, Sudden, Cardiac - epidemiology</topic><topic>electrophysiological testing</topic><topic>Female</topic><topic>Heart Conduction System - drug effects</topic><topic>Heart Conduction System - physiopathology</topic><topic>Heart Rate - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Recurrence</topic><topic>Retrospective Studies</topic><topic>Tachycardia - diagnosis</topic><topic>Tachycardia - drug therapy</topic><topic>Tachycardia - mortality</topic><topic>ventricular tachycardia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HANDLIN, LARRY R.</creatorcontrib><creatorcontrib>BRODINE, WILLIAM N.</creatorcontrib><creatorcontrib>GIBBS, HARRY</creatorcontrib><creatorcontrib>VACEK, JAMES L.</creatorcontrib><collection>Istex</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>Pacing and clinical electrophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HANDLIN, LARRY R.</au><au>BRODINE, WILLIAM N.</au><au>GIBBS, HARRY</au><au>VACEK, JAMES L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Slowing of Ventricular Tachycardia as a Possible Endpoint for Serial Drug Testing at Electrophysiological Study</atitle><jtitle>Pacing and clinical electrophysiology</jtitle><addtitle>Pacing Clin Electrophysiol</addtitle><date>1992-06</date><risdate>1992</risdate><volume>15</volume><issue>6</issue><spage>864</spage><epage>869</epage><pages>864-869</pages><issn>0147-8389</issn><eissn>1540-8159</eissn><abstract>Certain patients who cannot be rendered noninducible by serial drug testing during electrophysiology study demonstrate significant slowing of their ventricular tachycardia rate with selected agents. We evaluated the characteristics and outcome of 19 such patients to assess whether this slowing could be considered an acceptable endpoint for treatment. This group consisted of 14 males and 5 females (mean age 63 ± 9) with a mean ejection fraction of 28 ± 13% and inducible sustained ventricular tachycardia. Sixteen patients had known coronary artery disease and 13 had prior myocardial infarction. The other three patients had idiopathic cardiomyopathy. Serial drug testing during an electrophysiology protocol that used up to three extrastimuli at two or three cycle lengths at two right ventricular sites was used to select a medication regimen that provided optimal ventricular tachycardia slowing without limiting side effects. Five patients were treated with amiodarone, three with Ic agents fall with ejection fraction > 30%), and the remainder with la and Ib agents alone or in combination. Mean initial ventricular tachycardia rate was 219 ± 26 beats/mm with posttreafment ventricular tachycardia rate 137 ±17 fmean initial cycle length 278 ± 35 msec, posttreatment 443 ± 53 msec). Two groups were identified, those who had recurrent (although well‐tolerated) ventricular tachycardia (group 1, n = 6, mean time to recurrence = 15 months), and those who did not (group II, n = 11, mean follow‐up 22 months). Overall sudden death rate was 5%, while total mortality was 11% (all mortality in group I). No factor such as sex, age, drug type, ejection fraction, presence of coronary artery disease or aneurysm, or ventricular tachycardia morphology was significantly different between the groups. Conclusions: Significant ventricular tachycardia slowing by selected drug therapy at electrophysiology study is an acceptable therapeutic endpoint for certain patients, with a low rate of subsequent sudden death. However, recurrence, even if well tolerated, may be a marker for need for nonmedical therapy such as a device or surgery.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>1376898</pmid><doi>10.1111/j.1540-8159.1992.tb03076.x</doi><tpages>6</tpages></addata></record> |
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subjects | Amiodarone - therapeutic use Anti-Arrhythmia Agents - therapeutic use antiarrhythmic therapy Cardiac Pacing, Artificial Death, Sudden, Cardiac - epidemiology electrophysiological testing Female Heart Conduction System - drug effects Heart Conduction System - physiopathology Heart Rate - drug effects Humans Male Middle Aged Recurrence Retrospective Studies Tachycardia - diagnosis Tachycardia - drug therapy Tachycardia - mortality ventricular tachycardia |
title | Slowing of Ventricular Tachycardia as a Possible Endpoint for Serial Drug Testing at Electrophysiological Study |
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