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Ann Thorac Surg 2001;71:340-341
© 2001 The Society of Thoracic Surgeons
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, 8440112 St, Edmonton, Alberta, Canada T6G 2B7
e-mail: egelfand{at}cha.ab.ca
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| Introduction |
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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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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 Marfans 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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