(Chest. 2000;117:275-277.)
© 2000
American College of Chest Physicians
Cocaine-Induced Bradyarrhythmia*
An Unsuspected Cause of Syncope
Victor J. Castro, MD and
Robert Nacht, MD
*
From the State University of New York Health Science Center at Brooklyn, Brooklyn, NY.
Correspondence to: Victor J. Castro, 130 Retreat Ave #C3, Hartford, CT 01606
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Abstract
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Cocaine
use is associated with adverse events in nearly every organ system.
Cardiovascular complications include hemorrhagic and ischemic stroke,
aortic dissection, cardiomyopathy, accelerated coronary artery disease,
myocardial infarction, and sudden cardiac death. Syncope may be the
presenting symptom in these conditions. However, cocaine-induced
bradyarrhythmias have been scarcely mentioned. As this case
exemplifies, clinicians should be aware of this association when they
evaluate syncope, especially in young patients.
Key Words: bradyarrhythmia • cocaine • syncope
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Introduction
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Syncope is a common symptom representing approximately 5%
of hospital admitting diagnoses. Syncope may be caused by a wide
diversity of disorders accounting for the variable prognosis, ranging
from a benign episode to sudden cardiac death. Cocaine use, although
prevalent in inner cities, is not routinely considered as a cause.
Adverse events have been reported in nearly every organ system with
cocaine use. Cardiovascular complications include endocarditis,
hemorrhagic and ischemic stroke, aortic dissection, accelerated
coronary artery disease, myocardial infarction, and sudden cardiac
death.1
Syncope may be the presenting symptom in these
conditions. However cocaine-induced bradyarrhythmias have been scarcely
mentioned.
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Case Presentation
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A 36-year-old black woman with apparently no
significant medical history was brought by ambulance after a syncopal
episode. The patient denied chest pain, palpitations, dyspnea,
previous syncope, medication, or drug use. On physical
examination, the patient was afebrile, with vital signs as follows:
BP, 110/70 mm Hg; heart rate, 46 beats/min; and respiratory rate,
12 breaths/min. There was no jugular venous distention nor were
any carotid bruits heard. The chest was clear, and heart sounds were
normal without rubs, gallops, or murmurs. A neurologic examination
revealed no focal deficits. The initial rhythm strip and ECG showed
sinus arrest with junctional escape rhythm at 43 beats/min (Fig 1)
.
Ancillary data including CBC count, serum chemistries, cardiac
enzymes, chest radiograph, and head CT scan were normal. The results of
toxicology were positive for cocaine. The patient admitted to cocaine
use 1 h prior to admission. Telemetry and repeat ECG revealed a
return to sinus rhythm 8 h later (Fig 2)
.\
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Discussion
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Syncope is a sudden temporary loss of consciousness and
postural tone with a spontaneous recovery not requiring electrical or
chemical cardioversion. Syncope is not uncommon in healthy young
adults. Its incidence increases with age and is associated with a high
recurrence rate. Etiology can be classified into five major categories:
neurologic, metabolic, psychiatric, cardiac mechanical disease, and
cardiac arrhythmia. Cardiovascular disorders are the most frequent and
important etiologic category, associated with the highest 1-year
mortality rate.2
3
4
Cocaine use has been associated with
multiple cardiac alterations. Autopsy findings include accelerated
coronary artery disease, myocardial infarction, myocardial band
necrosis, myocarditis, and dilated cardiomyopathy. Coronary spasm,
transient hypercoagulability and increased myocardial oxygen demand can
cause myocardial infarction even in the absence of significant coronary
artery disease. Tachyarrhythmias and sudden cardiac death may occur
secondary to ischemia, myocarditis, concomitant drug use, neurohormonal
activation, and transient electrophysiologic abnormalities.
Prolongation of PR, QRS, and QT intervals, ventricular effective
refractory period, as well as class 1 antiarrhythmic type effects have
been noted.5
6
7
At the cellular level, cocaine may cause
early afterdepolarizations.8
Arrhythmias are a common cause of syncope. Either extreme of
ventricular rate—bradycardia or tachycardia—can depress cardiac
output to the point of critical hypotension with cerebral hypoperfusion
and syncope. Also, a neurocardiogenic reaction may be precipitated by
the arrhythmia. Marked sinus bradycardia, sinoatrial exit block or
sinus pause, high-grade AV block, supraventricular tachycardia,
and ventricular tachycardia/ventricular fibrillation are common
syncope-producing arrhythmias. Cocaine use as the etiology for
bradyarrhythmias has been barely mentioned or considered in the
differential diagnosis.9
10
The mechanism remains
unclear. In older noncocaine-user patients, primary
degenerative disease of the sinus node and the conduction
system is the most common cause of sinoatrial disease and
high-grade AV block. This is unlikely to be present in young cocaine
users. Experimental studies have shown cocaine to depress sinus node
automaticity and block conduction at the AV node,11
prolonging AH and HV intervals.12
Localized spasm
involving the sinoatrial artery, inferior myocardial infarction, vagal
stimulation during nasal inhalation, overdrive suppression after
supraventricular tachycardia, and a direct toxic effect
may all contribute. With increasing cocaine use and more
potent "crack" cocaine, physicians will be more frequently
encountering cocaine-induced complications. Patients may
present even with delayed toxicity, due to an active metabolite
with long half-life.13
As this case exemplifies,
clinicians should be aware of this association when they evaluate
syncope, especially in young patients. If not correctly diagnosed,
unrecognized and/or recurrent use may lead to life-threatening
complications.
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Footnotes
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Presented in part as an abstract at the Annual Scientific Meeting of
the ACP-ASIM, May 15, 1999.
Received for publication May 4, 1999.
Accepted for publication August 9, 1999.
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References
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-
Mouhaffel, AH, Madu, EC, Satmary, WA, et al (1995) Cardiovascular complications of cocaine. Chest 107,1426-1434[Free Full Text]
-
Kapoor, W, Karpf, M, Wiend, S, et al (1983) A prospective evaluation and follow-up of patients with syncope. N Engl J Med 309,197-204[Abstract]
-
Kapoor, W (1990) Evaluation and outcome of patients with syncope. Medicine 69,160-175[Medline]
-
Silverstein, MD, Singer, DE, Mulley, A, et al (1982) Patients with syncope admitted to medical intensive care units. JAMA 248,1185-1189[Abstract]
-
Hale, SL, Lehmann, MH, Kloner, RA (1989) Electrical abnormalities after acute administration of cocaine in the rat. Am J Cardiol 63,1529-1530[CrossRef][ISI][Medline]
-
Kloner, RA, Hale, S, Alker, K, et al (1992) The effects of acute and chronic cocaine use on the heart. Circulation 85,407-419[Abstract/Free Full Text]
-
Clarkson, CW, Chang, C, Stolfi, A, et al (1993) Electrophysiological effects of high cocaine concentrations on intact canine heart: evidence for modulation by both heart rate and autonomic nervous system. Circulation 87,950-962[Abstract/Free Full Text]
-
Kimura, S, Basset, AL, Xi, H, et al (1992) Early afterdepolarizations and triggered activity induced by cocaine: a possible mechanism of cocaine arrhythmogenesis. Circulation 85,2227-2235[Abstract/Free Full Text]
-
Om, A, Ellenbogen, K, Vetrovec, G (1992) Cocaine-induced bradyarrhythmias. Am Heart J 124,232-234[CrossRef][ISI][Medline]
-
Castro V. Cocaine-induced bradyarrhythmia: an unsuspected cause of syncope. Abstract presented at: Scientific Meeting of ACP-ASIM; May 15, 1999; NY
-
Przywara, DA, Dambach, GE (1989) Direct actions of cocaine on cardiac cellular electrical activity. Circ Res 65,185-192[Abstract/Free Full Text]
-
Tracy, C, Bachenheimer, L, Solomon, A, et al (1989) Evidence that cocaine slows cardiac conduction by an action on both AV node and His-Purkinje tissue in the dog [abstract]. J Am Coll Cardiol 13,79A
-
Chokshi, SK, Gal, D, Isner, JM (1989) Vasospasm caused by cocaine metabolite: a possible explanation for delayed onset of cocaine-related cardiovascular toxicity [abstract]. Circulation 80(II),351
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TOP
Abstract
Introduction
