Recurrent coronary vasoconstriction caused by intranasal cocaine

Possible role for metabolites

Walter C. Brogan, Richard A. Lange, D. Brent Glamann, L. David Hillis

Research output: Contribution to journalArticle

Abstract

Objective: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. Design: Randomized, double-blind, controlled clinical trial. Setting: Cardiac catheterization laboratory of a large teaching hospital. Patients: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. Measurements: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. Results: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 ± 1.6 mm (mean ± SD) at baseline to 2.0 ± 1.4 mm at 30 minutes (P <0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 ± 1.6 mm) (P > 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 ± 1.4 mm, P <0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. Conclusion: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.

Original languageEnglish (US)
Pages (from-to)556-561
Number of pages6
JournalAnnals of Internal Medicine
Volume116
Issue number7
StatePublished - Apr 1 1992
Externally publishedYes

Fingerprint

Vasoconstriction
Cocaine
Catheterization
Intranasal Administration
Controlled Clinical Trials
Cardiac Catheterization
Chest Pain
Teaching Hospitals
Coronary Vessels
Body Weight
Control Groups

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Brogan, W. C., Lange, R. A., Glamann, D. B., & Hillis, L. D. (1992). Recurrent coronary vasoconstriction caused by intranasal cocaine: Possible role for metabolites. Annals of Internal Medicine, 116(7), 556-561.

Recurrent coronary vasoconstriction caused by intranasal cocaine : Possible role for metabolites. / Brogan, Walter C.; Lange, Richard A.; Glamann, D. Brent; Hillis, L. David.

In: Annals of Internal Medicine, Vol. 116, No. 7, 01.04.1992, p. 556-561.

Research output: Contribution to journalArticle

Brogan, WC, Lange, RA, Glamann, DB & Hillis, LD 1992, 'Recurrent coronary vasoconstriction caused by intranasal cocaine: Possible role for metabolites', Annals of Internal Medicine, vol. 116, no. 7, pp. 556-561.
Brogan, Walter C. ; Lange, Richard A. ; Glamann, D. Brent ; Hillis, L. David. / Recurrent coronary vasoconstriction caused by intranasal cocaine : Possible role for metabolites. In: Annals of Internal Medicine. 1992 ; Vol. 116, No. 7. pp. 556-561.
@article{240d25402bb8407cbbd0b5c3d8b26955,
title = "Recurrent coronary vasoconstriction caused by intranasal cocaine: Possible role for metabolites",
abstract = "Objective: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. Design: Randomized, double-blind, controlled clinical trial. Setting: Cardiac catheterization laboratory of a large teaching hospital. Patients: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. Measurements: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. Results: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 ± 1.6 mm (mean ± SD) at baseline to 2.0 ± 1.4 mm at 30 minutes (P <0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 ± 1.6 mm) (P > 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 ± 1.4 mm, P <0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. Conclusion: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.",
author = "Brogan, {Walter C.} and Lange, {Richard A.} and Glamann, {D. Brent} and Hillis, {L. David}",
year = "1992",
month = "4",
day = "1",
language = "English (US)",
volume = "116",
pages = "556--561",
journal = "Annals of Internal Medicine",
issn = "0003-4819",
publisher = "American College of Physicians",
number = "7",

}

TY - JOUR

T1 - Recurrent coronary vasoconstriction caused by intranasal cocaine

T2 - Possible role for metabolites

AU - Brogan, Walter C.

AU - Lange, Richard A.

AU - Glamann, D. Brent

AU - Hillis, L. David

PY - 1992/4/1

Y1 - 1992/4/1

N2 - Objective: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. Design: Randomized, double-blind, controlled clinical trial. Setting: Cardiac catheterization laboratory of a large teaching hospital. Patients: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. Measurements: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. Results: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 ± 1.6 mm (mean ± SD) at baseline to 2.0 ± 1.4 mm at 30 minutes (P <0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 ± 1.6 mm) (P > 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 ± 1.4 mm, P <0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. Conclusion: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.

AB - Objective: To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. Design: Randomized, double-blind, controlled clinical trial. Setting: Cardiac catheterization laboratory of a large teaching hospital. Patients: Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. Measurements: At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. Results: In response to cocaine, proximal coronary arterial diameter decreased from 2.4 ± 1.6 mm (mean ± SD) at baseline to 2.0 ± 1.4 mm at 30 minutes (P <0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 ± 1.6 mm) (P > 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 ± 1.4 mm, P <0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. Conclusion: Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.

UR - http://www.scopus.com/inward/record.url?scp=0026535146&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026535146&partnerID=8YFLogxK

M3 - Article

VL - 116

SP - 556

EP - 561

JO - Annals of Internal Medicine

JF - Annals of Internal Medicine

SN - 0003-4819

IS - 7

ER -