A previously healthy 24-year-old black man was transferred to our cardiac care unit from a nearby hospital after presenting with acute-onset, “crushing,” mid-sternal chest pain. His symptoms had begun while he was seated at his workstation after having exercised for 2 hours on the morning of presentation; he had stopped exercising approximately 30 minutes before the onset of his symptoms. His chest pain was accompanied by shortness of breath, anxiousness, diaphoresis, and 4 episodes of emesis. He had no history of diabetes, hypertension, hyperlipidemia, or cigarette smoking, but was an infrequent cigar smoker (approximately 3 cigars per year). He had no family history of early coronary artery disease or sudden death. He denied use of cocaine, amphetamines, hormones, steroids, alcohol, or other recreational drugs.
The patient described an exercise regimen consisting of weight-training and aerobic activity 5 times a week, for 2 hours each time; 2 times per week, before exercise, he ingested 1 capsule of Nutrex Lipo-6x® (Nutrex Research, Inc.; Oviedo, Fla). Although he admitted to prior use of other weight-loss products (Hydroxycut®, Stacker 2®, and Stacker 3®), he denied the use of any of these products since beginning Nutrex Lipo-6x, approximately 3 weeks before presentation. On the morning of presentation, the patient had taken 1 Nutrex Lipo-6x capsule, along with a caffeine-containing energy drink, and then had engaged in his usual exercise routine. He denied ever having exceeded the manufacturer's recommended dose (as indicated on the product label).
Physical examination revealed a well-developed young man in moderate distress. He was afebrile. His blood pressure was 141/81 mmHg, his heart rate was 62 beats/min, and his respiratory rate was 16 breaths/min. He had no jugular venous distention, and his lungs were clear to auscultation in all fields. His chest was not tender to palpation. Cardiac auscultation revealed an S4
gallop with a normal S1
. The electrocardiogram revealed sinus bradycardia with 3-to 6-mm ST-segment elevations in leads II, III, aVF, and V3
(). Initial laboratory studies, within 4 hours of the onset of his symptoms, were remarkable for a white blood cell count of 17,100 cells/mm3
, a creatine kinase level of 409 U/L, a creatine kinase MB fraction of 2.4 ng/mL, and a troponin I level of 0.04 ng/mL. He had been given aspirin, subcutaneous enoxaparin, sublingual nitroglycerin, and intravenous morphine at presentation, which did not relieve his chest pain or ST elevation.
Fig. 1. Patient's electrocardiogram at presentation reveals sinus bradycardia with 3-to 6-mm ST-segment elevations in leads II, III, aVF, and V3 through V6.
The patient was taken for emergent cardiac angiography within 1 hour of presentation, which revealed nonocclusive thrombus in the proximal left anterior descending coronary artery (LAD) and total thrombotic occlusion of the distal LAD (). Eptifibatide was started as a bolus, followed by an infusion. A Pronto® V3 thrombus extraction catheter (Vascular Solutions, Inc.; Minneapolis, Minn) was passed through the thrombus 4 times, thereby extracting a large amount of thrombotic material. Follow-up angiography revealed resolution of the proximal LAD thrombus, but the distal LAD remained occluded due to a large residual thrombus burden. A 3 × 12-mm Maverick® balloon catheter (Boston Scientific Corporation; Natick, Mass) was then inflated to 6 atm on 3 occasions, but this had no effect on the distal LAD occlusive thrombus. The balloon was then inflated to 2 atm, and the thrombus was moved as far distally as possible, into the apical LAD. Follow-up angiography revealed a persistent thrombotic occlusion of the apical LAD, but the remainder of the coronary artery system was without disease (). At the conclusion of the case, the patient was pain free, with significant improvement of his ST elevations.
Fig. 2. Coronary angiogram at presentation (right anterior oblique cranial view) reveals nonocclusive thrombus (arrowhead) in the proximal left anterior descending coronary artery (LAD) and total thrombotic occlusion (arrow) of the distal LAD.
Fig. 3. Coronary angiogram after percutaneous coronary intervention (right anterior oblique cranial view) reveals resolution of the proximal left anterior descending coronary artery (LAD) thrombus (arrowhead). A persistent total occlusion of the distal (more ...)
The patient was then transported to the cardiac care unit, pain free and in a hemodynamically stable condition; the eptifibatide infusion was continued (for a total of 18 hr), and an unfractionated-heparin infusion was added. An angiotensin-converting enzyme inhibitor, a β-blocker, aspirin, and an HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitor were also initiated. The patient met the diagnostic criteria for a myocardial infarction with a peak troponin I level of 56 ng/mL and a peak creatine kinase level of 2,160 U/L (MB fraction, 245 ng/mL). These peak values were obtained approximately 24 hours after the initial laboratory studies. His hospital course was unremarkable except for transient pericarditis, which was successfully treated with higher-dose aspirin therapy. Transthoracic echocardiography performed before his discharge from the hospital revealed overall preserved left ventricular systolic function with left ventricular ejection fraction visually estimated to be 0.55 to 0.60, severe apical hypokinesis, and a small pericardial effusion. Spontaneous echocardiographic contrast was present in the apex, without evidence of thrombus. Additional laboratory assessment included a lipid profile and evaluation for a hypercoagulable state, the results of which were within normal limits. The incidental finding of hemoglobin C trait, which is not known to be associated an increased risk of thrombosis, was discovered in the course of the patient's extensive laboratory evaluation. He was discharged from the hospital on warfarin therapy (thromboembolic prophylaxis in consideration of his apical myocardial infarction), aspirin, metoprolol tartrate, lisinopril, and atorvastatin. At follow-up, the patient had returned to full activities and had remained asymptomatic. Follow-up echocardiography revealed normal left ventricular function, with resolution of his apical hypokinesis.