Cocaine-induced supersensitivity and arrhythmogenesis

Hiroshi Inoue, Douglas P. Zipes

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

The mechanism of cocaine-related sudden death is unknown. To test whether cocaine potentiated changes in sinus cycle length, condaction in the atrioventricular node (AH interval) and ventricular effective refractory period induced by infused norepinephrine and ansae subclaviae stimulation, the dose-response curves of sinus cycle length, AH interval and ventricular effective refractory period to infused norepinephrine (0.01 to 0.21) μg/kg body weight per min) and the frequency-response curves to ansae subclaviae stimulation (1 to 4 Hz, 2 to 3 mA, 4 ms pulses) were determined before and after intravenous injection of cocaine (5 mg/kg) in 15 anesthetized open chest dogs. Cocaine potentiated shortening of sinus cycle length, AH interval and ventricular effective refractory period induced by norepinephrine infusion and shifted dose-response curves cf these variables to the left in eight dogs (supersensitivity). Cocaine did not affect frequency-response curves of sinus cycle length and AH interval to ansae subclaviae stimulation. Ansae subclaviae stimulation shortened the ventricular effective refractory period more after cocaine injection, but frequency-response curves were not shifted to the left in seven dogs (no supersensitivity). Cocaine did not enhance electrical induction of ventricular tachyarrhythmias in 15 dogs without acute myocardial infarction. Acute myocardial infarction was produced hy coronary artery ligation in another group of 21 dogs. Of 10 dogs with acute myocardial infarction, spontaneous or electrically induced ventricular tachycardia developed in 1 dog without drugs, in 3 dogs given, norepinephrine and in 7 dogs given norepinephrine and cocaine (p < 0.03 versus without drugs). Induction of ventricular tachyarrhythmia during ansae subclaviae stimulation was not enhanced by cocaine in an additional 11 dogs with acute myocardial infarction. It is concluded that cocaine produces increased shortening of the ventricular effective refractory period in response to infused norepinephrine, but not in response to ansae subclaviae stimulation. Cocaine potentiates the development of ventricular tachycardia in dogs treated with norepinephrine infusion after acute myocardial infarction.

Original languageEnglish
Pages (from-to)867-874
Number of pages8
JournalJournal of the American College of Cardiology
Volume11
Issue number4
DOIs
StatePublished - 1988

Fingerprint

Cocaine
Dogs
Norepinephrine
Myocardial Infarction
Ventricular Tachycardia
Tachycardia
Atrioventricular Node
Sudden Death
Intravenous Injections
Pharmaceutical Preparations
Ligation
Coronary Vessels
Thorax
Body Weight
Injections

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Cocaine-induced supersensitivity and arrhythmogenesis. / Inoue, Hiroshi; Zipes, Douglas P.

In: Journal of the American College of Cardiology, Vol. 11, No. 4, 1988, p. 867-874.

Research output: Contribution to journalArticle

Inoue, Hiroshi ; Zipes, Douglas P. / Cocaine-induced supersensitivity and arrhythmogenesis. In: Journal of the American College of Cardiology. 1988 ; Vol. 11, No. 4. pp. 867-874.
@article{d06506c5907141da9138cbbd9647dbe1,
title = "Cocaine-induced supersensitivity and arrhythmogenesis",
abstract = "The mechanism of cocaine-related sudden death is unknown. To test whether cocaine potentiated changes in sinus cycle length, condaction in the atrioventricular node (AH interval) and ventricular effective refractory period induced by infused norepinephrine and ansae subclaviae stimulation, the dose-response curves of sinus cycle length, AH interval and ventricular effective refractory period to infused norepinephrine (0.01 to 0.21) μg/kg body weight per min) and the frequency-response curves to ansae subclaviae stimulation (1 to 4 Hz, 2 to 3 mA, 4 ms pulses) were determined before and after intravenous injection of cocaine (5 mg/kg) in 15 anesthetized open chest dogs. Cocaine potentiated shortening of sinus cycle length, AH interval and ventricular effective refractory period induced by norepinephrine infusion and shifted dose-response curves cf these variables to the left in eight dogs (supersensitivity). Cocaine did not affect frequency-response curves of sinus cycle length and AH interval to ansae subclaviae stimulation. Ansae subclaviae stimulation shortened the ventricular effective refractory period more after cocaine injection, but frequency-response curves were not shifted to the left in seven dogs (no supersensitivity). Cocaine did not enhance electrical induction of ventricular tachyarrhythmias in 15 dogs without acute myocardial infarction. Acute myocardial infarction was produced hy coronary artery ligation in another group of 21 dogs. Of 10 dogs with acute myocardial infarction, spontaneous or electrically induced ventricular tachycardia developed in 1 dog without drugs, in 3 dogs given, norepinephrine and in 7 dogs given norepinephrine and cocaine (p < 0.03 versus without drugs). Induction of ventricular tachyarrhythmia during ansae subclaviae stimulation was not enhanced by cocaine in an additional 11 dogs with acute myocardial infarction. It is concluded that cocaine produces increased shortening of the ventricular effective refractory period in response to infused norepinephrine, but not in response to ansae subclaviae stimulation. Cocaine potentiates the development of ventricular tachycardia in dogs treated with norepinephrine infusion after acute myocardial infarction.",
author = "Hiroshi Inoue and Zipes, {Douglas P.}",
year = "1988",
doi = "10.1016/0735-1097(88)90224-0",
language = "English",
volume = "11",
pages = "867--874",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "4",

}

TY - JOUR

T1 - Cocaine-induced supersensitivity and arrhythmogenesis

AU - Inoue, Hiroshi

AU - Zipes, Douglas P.

PY - 1988

Y1 - 1988

N2 - The mechanism of cocaine-related sudden death is unknown. To test whether cocaine potentiated changes in sinus cycle length, condaction in the atrioventricular node (AH interval) and ventricular effective refractory period induced by infused norepinephrine and ansae subclaviae stimulation, the dose-response curves of sinus cycle length, AH interval and ventricular effective refractory period to infused norepinephrine (0.01 to 0.21) μg/kg body weight per min) and the frequency-response curves to ansae subclaviae stimulation (1 to 4 Hz, 2 to 3 mA, 4 ms pulses) were determined before and after intravenous injection of cocaine (5 mg/kg) in 15 anesthetized open chest dogs. Cocaine potentiated shortening of sinus cycle length, AH interval and ventricular effective refractory period induced by norepinephrine infusion and shifted dose-response curves cf these variables to the left in eight dogs (supersensitivity). Cocaine did not affect frequency-response curves of sinus cycle length and AH interval to ansae subclaviae stimulation. Ansae subclaviae stimulation shortened the ventricular effective refractory period more after cocaine injection, but frequency-response curves were not shifted to the left in seven dogs (no supersensitivity). Cocaine did not enhance electrical induction of ventricular tachyarrhythmias in 15 dogs without acute myocardial infarction. Acute myocardial infarction was produced hy coronary artery ligation in another group of 21 dogs. Of 10 dogs with acute myocardial infarction, spontaneous or electrically induced ventricular tachycardia developed in 1 dog without drugs, in 3 dogs given, norepinephrine and in 7 dogs given norepinephrine and cocaine (p < 0.03 versus without drugs). Induction of ventricular tachyarrhythmia during ansae subclaviae stimulation was not enhanced by cocaine in an additional 11 dogs with acute myocardial infarction. It is concluded that cocaine produces increased shortening of the ventricular effective refractory period in response to infused norepinephrine, but not in response to ansae subclaviae stimulation. Cocaine potentiates the development of ventricular tachycardia in dogs treated with norepinephrine infusion after acute myocardial infarction.

AB - The mechanism of cocaine-related sudden death is unknown. To test whether cocaine potentiated changes in sinus cycle length, condaction in the atrioventricular node (AH interval) and ventricular effective refractory period induced by infused norepinephrine and ansae subclaviae stimulation, the dose-response curves of sinus cycle length, AH interval and ventricular effective refractory period to infused norepinephrine (0.01 to 0.21) μg/kg body weight per min) and the frequency-response curves to ansae subclaviae stimulation (1 to 4 Hz, 2 to 3 mA, 4 ms pulses) were determined before and after intravenous injection of cocaine (5 mg/kg) in 15 anesthetized open chest dogs. Cocaine potentiated shortening of sinus cycle length, AH interval and ventricular effective refractory period induced by norepinephrine infusion and shifted dose-response curves cf these variables to the left in eight dogs (supersensitivity). Cocaine did not affect frequency-response curves of sinus cycle length and AH interval to ansae subclaviae stimulation. Ansae subclaviae stimulation shortened the ventricular effective refractory period more after cocaine injection, but frequency-response curves were not shifted to the left in seven dogs (no supersensitivity). Cocaine did not enhance electrical induction of ventricular tachyarrhythmias in 15 dogs without acute myocardial infarction. Acute myocardial infarction was produced hy coronary artery ligation in another group of 21 dogs. Of 10 dogs with acute myocardial infarction, spontaneous or electrically induced ventricular tachycardia developed in 1 dog without drugs, in 3 dogs given, norepinephrine and in 7 dogs given norepinephrine and cocaine (p < 0.03 versus without drugs). Induction of ventricular tachyarrhythmia during ansae subclaviae stimulation was not enhanced by cocaine in an additional 11 dogs with acute myocardial infarction. It is concluded that cocaine produces increased shortening of the ventricular effective refractory period in response to infused norepinephrine, but not in response to ansae subclaviae stimulation. Cocaine potentiates the development of ventricular tachycardia in dogs treated with norepinephrine infusion after acute myocardial infarction.

UR - http://www.scopus.com/inward/record.url?scp=0023875586&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023875586&partnerID=8YFLogxK

U2 - 10.1016/0735-1097(88)90224-0

DO - 10.1016/0735-1097(88)90224-0

M3 - Article

C2 - 3351156

AN - SCOPUS:0023875586

VL - 11

SP - 867

EP - 874

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 4

ER -