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Ann Thorac Surg 2001;71:340-341
© 2001 The Society of Thoracic Surgeons


Case report

Cocaine abuse and coronary artery dissection

Khalid E. Eskander, MDa, Neil S. Brass, MDb, Elliot T. Gelfand, MDa

a Division of Cardiothoracic Surgery, University of Alberta, Edmonton, Alberta, Canada
b Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada

Accepted for publication March 3, 2000.

Address reprint requests to Dr Gelfand, 3H2.11 Walter Mackenzie Health Sciences Center, University of Alberta Hospitals, 8440–112 St, Edmonton, Alberta, Canada T6G 2B7
e-mail: egelfand{at}cha.ab.ca


    Abstract
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 Abstract
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A 33-year-old man with a history of recent cocaine use presented with dissection of the left main coronary artery extending distally to involve the left anterior descending (LAD) and circumflex arteries. He required emergency four-vessel aortocoronary bypass, which was uncomplicated.


    Introduction
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Cocaine abuse in North America is recognized as a growing problem. Cocaine is associated with many cardiovascular complications, including myocardial infarction, arrhythmias, and aortic dissection [15]. We describe the successful management of a patient with coronary artery dissection and resultant myocardial infarction induced by cocaine.

A previously healthy 33-year-old man presented to a local hospital with episodic visceral chest pain. Initial electrocardiograms and cardiac enzymes were normal; however, repeat studies the following day showed anterior T-wave inversion and mild elevation of creatinine kinase with a positive myocardial fraction. He stabilized initially on a regimen of aspirin, ß-blocker, and intravenous heparin. The following day he had a further episode of chest pain with transient pseudonormalization of his T-wave changes. He was transferred to a tertiary care center for further evaluation and treatment.

He had a 10-pack-year history of smoking and mild hyperlipidemia. He admitted to prior use of cocaine but initially denied any recent use. He remained pain free for 48 hours. Treadmill testing produced ST elevation over the anterior precordial leads associated with mild chest discomfort. Twenty-four hours later he had a spontaneous episode of chest pain requiring readmission to the coronary care unit and administration of intravenous nitrates. Left ventriculography showed marked anterolateral and apical hypokinesis. Coronary angiography revealed a dissection originating in the left main stem coronary artery and extending distally along the left anterior descending (LAD) artery to the origin of the second diagonal branch and circumferentially involving the origin of the circumflex (Fig 1). The remainder of the vessels were otherwise angiographically normal. At that point, on repeated questioning, he admitted to inhaling cocaine the evening prior to his presentation to hospital.



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Fig 1. Coronary arteriogram showing dissection of the left anterior descending artery.

 
The patient was referred for emergency bypass surgery. At operation the anterior and apical portions of the left ventricle had reduced contractility, and a hematoma was present over the proximal LAD. A four-vessel coronary bypass was performed, with the left internal thoracic artery to the LAD, and saphenous vein grafts to the first diagonal, ramus intermedius, and to the distal portion of the circumflex. He was weaned from cardiopulmonary bypass easily, was extubated the same evening, and was discharged on the fourth postoperative day. A stress test done 2 months postoperatively was normal.


    Comment
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The majority of the reported effects due to both acute and chronic cocaine cardiotoxicity have been attributed to its two major pharmacologic effects of increasing sympathetic stimulation and reducing sodium transport [1]. Cocaine-induced myocardial infarction is thought to be due to a number of effects of excessive sympathetic stimulation, including increasing myocardial work with oxygen demand exceeding supply, coronary vasospasm, and thrombosis [2]. It was noted that infarction may develop from hours to days after the last dose of cocaine. The increased sympathetic action of cocaine is due to its ability to block epinephrine and norepinephrine reuptake at the presynaptic level, as well as causing leakage of the neurotransmitters into the synaptic space. The accumulation of neurotransmitter acts to increase the heart rate and blood pressure while simultaneously inducing vasoconstriction. Sustained marked hypertension resulting from intense sympathetic stimulation has been proposed as a mechanism to explain aortic dissection and rupture following cocaine use [3, 4].

We believe that we are reporting only the second case of cocaine-induced isolated coronary artery dissection and the first to involve the LAD. Jaffe and associates [4] discussed a 27-year-old man who suffered extensive dissection of the right coronary artery following cocaine use. Cohle and associates [5] also reported cocaine induced aortic dissection extending to involve the left main coronary artery and into the LAD, the diagonal, and the circumflex. In this instance, the coronary artery dissection was secondary to the aortic dissection.

Spontaneous coronary dissection generally occurs in women and is most often idiopathic although it does occur in Marfan’s syndrome or with chest trauma, coronary angiography and angioplasty, and operation [6, 7]. It is unlikely that our case is due to a spontaneous dissection. We speculate that the coronary dissection in this young man was a direct consequence of his cocaine use and that the stuttering chest pain during the course of his hospitalization can be attributed to propagation of the dissection and resultant myocardial ischemia without infarction.

In the setting of recent cocaine use and ongoing ischemic chest pain, unstable angina, or myocardial infarction, especially in young patients, and in the absence of the usual risk factors for coronary disease, one should entertain a high index of suspicion for coronary artery dissection. Prompt angiography and surgical correction are recommended.


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 Abstract
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 Comment
 References
 

  1. Kloner R.A., Hale S., Alker K., Rezkalla S. The effects of acute and chronic cocaine use on the heart. Circulation 1992;85:407-419.
  2. Benowitz N.L. Clinical pharmacology and toxicology of cocaine. Pharmacol Toxicol 1993;72:3-12.
  3. Adkins M.S., Gaines W.E., Anderson W.A., Laub G.W., Fernandez J., McGrath L.B. Chronic type A aortic dissection: an unusual complication of cocaine inhalation. Ann Thorac Surg 1993;56:977-979.
  4. Jaffe B.D., Broderick T.M., Leier C.V. Cocaine-induced coronary artery dissection. N Engl J Med 1994;330:510-511.
  5. Cohle S.D., Lie J.T. Dissection of the aorta and coronary arteries associated with acute cocaine intoxication. Arch Pathol Lab Med 1992;116:1239-1241.
  6. Davies M.J., Treasure T., Richardson P.D. The pathogenesis of spontaneous arterial dissection. Heart 1996;75:434-435.
  7. Thayer J.O., Healy R.W., Maggs P.R. Spontaneous coronary artery dissection. Ann Thorac Surg 1987;44:97-102.



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This Article
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Khalid E. Eskander
Elliot T. Gelfand
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Right arrow Articles by Eskander, K. E.
Right arrow Articles by Gelfand, E. T.
Related Collections
Right arrow Cardiac - pharmacology
Right arrow Coronary disease


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