Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs

H. Inoue, B. F. Waller, D. P. Zipes

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Abstract

The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 μg/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 ± 2.3 minutes or degenerated into ventricular fibrillation after 7.0 ± 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100% ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25% phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100% ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82%) of 11 dogs receiving phenol, 7 (88%) of 8 dogs receiving 100% ethyl alcohol occlusively, 6 (75%) of 8 dogs receiving 100% ethyl alcohol nonocclusively and 6 (67%) of 9 dogs receiving 50% ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25% ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53%) of 15 and 3 (60%) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p < 0.05) immediately after injection of 100% ethyl alcohol in seven dogs. Pathologic examination revealed that transmural myocardial necrosis (involvement greater than the inner one-half of the left ventricular wall) was present in 35 of 41 dogs receiving phenol or alcohol and nontransmural necrosis was present in the remaining 6 dogs. Fibrin or thrombus, or both, was present in the diagonal coronary branch in 6 dogs and adventitial hemorrhage was present in 8 of 41 dogs. It is concluded that intracoronary injection of 25% phenol or 50 to 100% ethyl alcohol ablates aconitine-induced ventricular tachycardia. Although myocardial necrosis results, this approach may be useful in selected instances, particularly with drugs that may be less necrotizing or more specific for the arrhythmogenic site or that can be injected with greater accuracy into smaller coronary arteries supplying the arrhythmogenic area.

Original languageEnglish
Pages (from-to)1342-1349
Number of pages8
JournalJournal of the American College of Cardiology
Volume10
Issue number6
StatePublished - 1987

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Aconitine
Ventricular Tachycardia
Phenol
Ethanol
Dogs
Injections
Coronary Vessels
Necrosis
Sodium Chloride
Adventitia
Ventricular Fibrillation

ASJC Scopus subject areas

  • Nursing(all)

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Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs. / Inoue, H.; Waller, B. F.; Zipes, D. P.

In: Journal of the American College of Cardiology, Vol. 10, No. 6, 1987, p. 1342-1349.

Research output: Contribution to journalArticle

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title = "Intracoronary ethyl alcohol or phenol injection ablates aconitine-induced ventricular tachycardia in dogs",
abstract = "The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 μg/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 ± 2.3 minutes or degenerated into ventricular fibrillation after 7.0 ± 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100{\%} ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25{\%} phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100{\%} ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82{\%}) of 11 dogs receiving phenol, 7 (88{\%}) of 8 dogs receiving 100{\%} ethyl alcohol occlusively, 6 (75{\%}) of 8 dogs receiving 100{\%} ethyl alcohol nonocclusively and 6 (67{\%}) of 9 dogs receiving 50{\%} ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25{\%} ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53{\%}) of 15 and 3 (60{\%}) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p < 0.05) immediately after injection of 100{\%} ethyl alcohol in seven dogs. Pathologic examination revealed that transmural myocardial necrosis (involvement greater than the inner one-half of the left ventricular wall) was present in 35 of 41 dogs receiving phenol or alcohol and nontransmural necrosis was present in the remaining 6 dogs. Fibrin or thrombus, or both, was present in the diagonal coronary branch in 6 dogs and adventitial hemorrhage was present in 8 of 41 dogs. It is concluded that intracoronary injection of 25{\%} phenol or 50 to 100{\%} ethyl alcohol ablates aconitine-induced ventricular tachycardia. Although myocardial necrosis results, this approach may be useful in selected instances, particularly with drugs that may be less necrotizing or more specific for the arrhythmogenic site or that can be injected with greater accuracy into smaller coronary arteries supplying the arrhythmogenic area.",
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N2 - The hypothesis whether localized ventricular tachycardia could be ablated by myocardial necrosis induced with chemical agents injected into a coronary artery was tested. In 59 anesthetized dogs, a diagonal branch of the left anterior descending coronary artery was cannulated either occlusively or nonocclusively. Localized ventricular tachycardia was induced by injecting approximately 0.01 ml of 30 μg/ml of aconitine solution into the left ventricular wall perfused by the cannulated diagonal branch in 54 dogs. In eight untreated control dogs, aconitine-induced ventricular tachycardia lasted 10.2 ± 2.3 minutes or degenerated into ventricular fibrillation after 7.0 ± 4.0 minutes. In the remaining 46 dogs, 1 ml of saline solution, 25, 50 or 100% ethyl alcohol or 0.94 ml (mean [range 0.4 to 2.0]) of 25% phenol at room temperature was injected into the occluded coronary artery and 1 ml of 100% ethyl alcohol at body temperature was injected into the nonoccluded coronary artery. Ventricular tachycardia was eliminated in 9 (82%) of 11 dogs receiving phenol, 7 (88%) of 8 dogs receiving 100% ethyl alcohol occlusively, 6 (75%) of 8 dogs receiving 100% ethyl alcohol nonocclusively and 6 (67%) of 9 dogs receiving 50% ethyl alcohol for an entire follow-up period of 10 to 60 minutes. However, saline solution and 25% ethyl alcohol suppressed ventricular tachycardia only transiently in 8 (53%) of 15 and 3 (60%) of 5 dogs, respectively. Left ventricular end-diastolic pressure rose from 8.0 to 11.2 mm Hg (p < 0.05) immediately after injection of 100% ethyl alcohol in seven dogs. Pathologic examination revealed that transmural myocardial necrosis (involvement greater than the inner one-half of the left ventricular wall) was present in 35 of 41 dogs receiving phenol or alcohol and nontransmural necrosis was present in the remaining 6 dogs. Fibrin or thrombus, or both, was present in the diagonal coronary branch in 6 dogs and adventitial hemorrhage was present in 8 of 41 dogs. It is concluded that intracoronary injection of 25% phenol or 50 to 100% ethyl alcohol ablates aconitine-induced ventricular tachycardia. Although myocardial necrosis results, this approach may be useful in selected instances, particularly with drugs that may be less necrotizing or more specific for the arrhythmogenic site or that can be injected with greater accuracy into smaller coronary arteries supplying the arrhythmogenic area.

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