Abstract
Arterial thrombosis and especially coronary thrombosis are known complications of cocaine abuse. We report three cases of severe life-threatening coronary arterial thrombosis manifesting as acute coronary syndromes. Thrombosis occurred predominantly in the proximal coronary tree with spontaneous distal embolization. The thrombotic occlusions were frequently not superimposed on flow-limiting atherosclerotic lesions. Treatment of these patients with thrombolytic, antithrombotic and anti-platelet therapy resulted in thrombus and symptom resolution. While stenting these vessels can be successfully executed and may be required in some cases of ST-elevation myocardial infarction, it may expose these patients to the risk of stent thrombosis, which is reported to be significantly higher than the risk of the general population.
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Case 1
A 45-year-old male without significant medical history presented with substernal chest pain associated with shortness of breath starting 1 h prior to admission. The patient was a chronic cocaine user, and his last cocaine use occurred 1 h prior to chest pain onset. Patient was noted to be diaphoretic and in moderate distress. His initial blood pressure 145/90, pulse 85, respirations 20. Cardiac examination was unremarkable. Admission electrocardiogram (ECG) revealed ST-segment elevations V1-6, II, III, and aVF and ST depression in aVL. The patient was taken emergently to the cardiac catheterization laboratory. Coronary angiogram revealed a 98% thrombotic stenosis of the distal left main artery and ostial left anterior descending (LAD) artery as well as a thrombotic occlusion of the distal LAD ( Fig. 1 ). The right coronary artery (RCA) was disease free. In view hypotension (systolic blood pressure dropped to 85 mmHg), intra-aortic balloon counterpulsation was initiated; a temporary transvenous pacemaker lead was also positioned at the right ventricular apex. LAD and circumflex were wired by a 0.014” BMW wires (Abbott, Santa Clara, CA, USA). Aspiration thrombectomy of the distal LAD using an Export catheter (Medtronic, Minneapolis, MN, USA) was attempted but resulted in ventricular fibrillation treated by defibrillation. Subsequently 40 U of intracoronary tissue plasminogen activator (t-PA) was given. The distal LAD occlusion resolved. The patient also received aspirin, plavix, heparin drip and eptifibatide drip. After t-PA, the distal LAD lesion resolved however the ostial LAD lesion persisted and was treated by a Liberte 4/18 mm (Boston Scientific, Galway, Ireland) bare metal stent ( Fig. 2 ). Post-percutaneous coronary intervention (PCI) ECG revealed complete ST-elevation resolution. The patient had an uneventful course and was discharged on Day 2 post myocardial infarction (MI) in stable condition. Creatinine phosphokinase (CPK) and Troponin I peaked at 2431 U/l and 149 ng/ml, respectively. His discharge echocardiogram revealed left ventricular ejection fraction (LVEF) of 60% with apical hypokinesis.
