A 19-year-old African American man was brought to the emergency department (ED) by emergency medical services (EMS) after an episode of syncope earlier on the day of admission while playing basketball at his college. This occurred suddenly and was associated with a transient episode of lightheadedness, diaphoresis, and blurred vision. This was followed by lost consciousness for less than 10 seconds, with spontaneous recovery as witnessed by his friends on the sidelines. There was not any involuntary movement of the body, urinary or bowel incontinence, or postictal confusion as per the witnesses. After regaining consciousness, there was a complaint of nonradiating, substernal, burning chest pain with a "6 out of 10" intensity, which lasted approximately 20-30 minutes and was relieved with a nitroglycerin sublingual pill given by EMS. On arrival to the ED, the patient was asymptomatic. Blood pressure was 103/67 mmHg, heart rate 85 bpm and regular, afebrile oxygen saturation > 95% on room air, and respiratory rate 12 per minute. Physical examination findings revealed a supple neck with no jugular venous distention; no carotid bruits were audible. Cardiovascular examination revealed a regular heart rhythm with normal S1 and S2 and no significant audible murmurs, parasternal heave, or thrill. The lungs were clear to auscultation bilaterally. There was no pitting pedal edema, and all peripheral pulses were palpable. The abdomen was soft and nondistended; no focal neurological deficits were evident.
History was positive for two similar events in the past. The first episode occurred approximately 10 years ago in Nigeria while playing soccer, and another event occurred a year ago year while running a block to catch a bus. Medical attention was not sought on both occasions. Family history was negative for similar syncopal attacks, sudden cardiac arrest, or arrhythmias. Social history was positive for drinking heavy amounts of Vodka with friends occasionally on the weekends along with marijuana but negative for cigarette smoking or other illicit drug use.
Initial laboratory values in the ED showed hemoglobin of 12.3 gm %, serum creatinine of 1.4 mg/dl (normal reference range 0.50 to 1.20 mg/dl) and BUN of 24 mg/dl, elevated initial troponin I of 0.23 ng/ml (normal reference range 0.00 to 0.07 ng/ml), total creatinine kinase level of 585 units/liter (normal reference range: 49 to 397 U/l), and urine with 11-20 hyaline casts. Thyroid stimulating hormone, serum potassium, and serum magnesium were within normal limits. His chest X-ray did not reveal any acute cardiopulmonary process (Figure 1). His initial electrocardiogram (EKG) revealed significant 4 mm to 5 mm ST depression in the anterolateral leads but otherwise unremarkable (Figure 2). A repeat EKG done within 2 hours of the initial presentation showed reversal of ST depression (Figure 3). A repeat troponin done in 6 hours revealed staggering troponin I of 53.30 ng/ml. Immediate bedside echocardiogram showed a nondilated left ventricular cavity with normal LV wall thickness and a mildly diminished LV ejection fraction at 45-50% (Figure 4). In the emergency room, immediate treatment with 325 mg of Aspirin and therapeutic Lovenox (1 mg/kg) was given. Overnight, periodic 5-7-beat runs of nonsustained ventricular tachycardia on the cardiac monitor occurred. Cardiac tomography (CT) angiography of the heart revealed a common trunk for the right and left coronary arteries arising from the right coronary cusp. The right coronary artery had a normal course. The LMCA traveled posteriorly between the ascending aorta and pulmonary outflow tract before resuming its normal course.
The LMCA narrowed in its midportion as it passed between these two structures (Figures 5(a) and 5(b)). These findings were confirmed by cardiac catheterization which showed an anomalous origin of the LMCA, originating from the right sinus of Valsalva (Figures 6(a) and 6(b)). The LMCA narrowed in its midportion with over 60-70% luminal stenosis due to a stricture present between the ascending aorta and the left ventricular outflow track. Afterwards, medical stabilization was achieved and a transfer to a tertiary care center was carried out.
Upon arrival at the tertiary care center, a procedure was performed involving the unroofing of the anomalous aortic origin of the left main coronary artery, including retro pulmonary unroofing by a congenital cardiothoracic surgeon. Recovery was satisfactory after the surgery, and postoperative complications did not occur.