Management of Dissection and Other <br />
Complications:<br />
<br />
Spontaneous Coronary Artery Dissection in a Young Woman Precipitated by R

Spontaneous coronary artery dissection (SCAD) is a relatively rare entity that has been associated with a high morbidity and mortality.1 Although a precise definition for SCAD has not been universally accepted,2 it has generally been defined as the occurrence of a coronary dissection in the absence of trauma, aortic dissection or iatrogenic causes such as coronary angiography or angioplasty.3,4 Cases of SCAD are often associated with one of several different clinical profiles and/or precipitating events. Most cases have been described in young, otherwise healthy women who are often pregnant or in the puerperium1,4–6 and are free of demonstrable coronary atherosclerosis.3 Cases have also been reported in patients with cystic medial necrosis,3 sarcoidosis1 and Marfans syndrome.1 Joffe7 reported a case of SCAD that was precipitated by the illicit use of cocaine. Although SCAD usually occurs as a truly spontaneous event without any identifiable precipitating cause,3 it has also been associated with hemodynamically significant activities such as aerobic exercise1,3,8,9 and weight lifting.10 We report a case of acute myocardial infarction due to spontaneous coronary artery dissection in the setting of forceful retching. To our knowledge, this is the first reported case of such an association. Case Report. A 31-year-old Caucasian female with no previously defined cardiac disease presented with an acute myocardial infarction. She had been in her usual state of good health; 2 days prior to presentation, she became inebriated during an alcoholic binge. She became nauseous with repeated, very forceful retching that went on for 4 hours before she lost consciousness. She awoke several hours later with chest, left shoulder and left arm discomfort. Symptoms waxed and waned for 48 hours, at which time she presented to the local emergency room. Her electrocardiogram revealed ST-segment elevation in leads I, II, aVL and V1 through V6 consistent with an acute anterior wall myocardial infarction. She denied doing any strenuous exercise or exertion, suffering trauma or using illicit drugs. She was not pregnant or in the puerperium. She took no prescribed or nonprescription medications and she specifically denied the use of oral contraceptive agents. Her past medical history was unremarkable. Her only cardiac risk factor was cigarette smoking. She did not have hypertension, diabetes or hyperlipidemia and there was no family history of coronary artery disease. There was no history of alcohol abuse. The physical examination revealed her to be in mild distress due to ongoing chest discomfort. Her blood pressure was 90/60 mmHg and her heart rate was 100 beats/minute. The cardiopulmonary examination was otherwise unremarkable. There was no physical evidence for trauma or connective tissue disease. An echocardiogram revealed akinesis of the anterior wall, the anterior septum and the apex with a left ventricular ejection fraction (LVEF) of 45%. There was no pericardial effusion. Her chest x-ray was normal. Laboratory investigation revealed no evidence for a hypercoagulable state or for collagen vascular disease. Her anticardiolipin antibody assay, antinuclear factor, protein C, protein S, complete blood count and coagulation profile were all within normal limits. Her cardiac enzymes, which were first drawn 48 hours after symptoms began, were elevated with a creatinine kinase (CK) of 195 U/L (normal, 24–173 U/L), a CK-MB of 13.4 ng/ml (normal,

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