Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease

Heikki V. Huikuri, Marilyn Cox, Alberto Interian, Kenneth M. Kessler, Frances Glicksman, Agustin Castellanos, Robert J Myerburg

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Abstract

The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed ≥1 membrane-active antiarrhythmic drug (mean 2.2 ± 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had ≥1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 ± 14 vs 86 ± 11 beats/min, p < 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 ± 14 to 80 ± 9 beats/min, p < 0.001) than in nonresponders (from 86 ± 11 to 74 ± 9 beats/min, p < 0.01) (p < 0.05 between the groups), despite equal plasma propranolol concentrations (84 ± 50 vs 88 ± 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had ≥1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after β blockade (p < 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 ± 38 vs 302 ± 66 ms, p < 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.

Original languageEnglish
Pages (from-to)1305-1309
Number of pages5
JournalThe American journal of cardiology
Volume64
Issue number19
DOIs
StatePublished - Dec 1 1989

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Tachycardia
Propranolol
Coronary Artery Disease
Ventricular Flutter
Heart Rate
Anti-Arrhythmia Agents
Ventricular Fibrillation
Membranes
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease. / Huikuri, Heikki V.; Cox, Marilyn; Interian, Alberto; Kessler, Kenneth M.; Glicksman, Frances; Castellanos, Agustin; Myerburg, Robert J.

In: The American journal of cardiology, Vol. 64, No. 19, 01.12.1989, p. 1305-1309.

Research output: Contribution to journalArticle

Huikuri, Heikki V. ; Cox, Marilyn ; Interian, Alberto ; Kessler, Kenneth M. ; Glicksman, Frances ; Castellanos, Agustin ; Myerburg, Robert J. / Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease. In: The American journal of cardiology. 1989 ; Vol. 64, No. 19. pp. 1305-1309.
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abstract = "The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed ≥1 membrane-active antiarrhythmic drug (mean 2.2 ± 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had ≥1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29{\%}) became noninducible (responders) and 17 patients (71{\%}) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 ± 14 vs 86 ± 11 beats/min, p < 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 ± 14 to 80 ± 9 beats/min, p < 0.001) than in nonresponders (from 86 ± 11 to 74 ± 9 beats/min, p < 0.01) (p < 0.05 between the groups), despite equal plasma propranolol concentrations (84 ± 50 vs 88 ± 43 ng/ml, difference not significant). Seven of 11 patients (64{\%}) who had ≥1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after β blockade (p < 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 ± 38 vs 302 ± 66 ms, p < 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.",
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