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
Hauptverfasser: HANDLIN, LARRY R., BRODINE, WILLIAM N., GIBBS, HARRY, VACEK, JAMES L.
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container_end_page 869
container_issue 6
container_start_page 864
container_title Pacing and clinical electrophysiology
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creator HANDLIN, LARRY R.
BRODINE, WILLIAM N.
GIBBS, HARRY
VACEK, JAMES L.
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 &gt; 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. 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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 &gt; 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. 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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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