Abstract
A 38-year-old cocaine abuser was admitted to the Emergency Department with a one hour history of precordial chest pain associated with shortness of breath and extreme discomfort. On admission his blood pressure was 90/60 mmHg, the resting 12-lead ECG showed ventricular tachycardia at about 300 beats per minute, and oxygen saturation was 86% in room air. After electrical cardioversion, the 12-lead ECG revealed sinusal rhythm and a significative ST segment elevation in leads I, aVL and V1-V6, that was about 0.5 mV in leads I and aVL and more than 1 mV in leads V2, V3 and V4. Laboratory determinations showed elevated creatine-chinase MB (CK-MB) and troponin I. An emergency coronary angiogram was normal. Cocaine use is a major cause of acute myocardial infarction in patients with normal epicardial coronary arteries but the exact mechanism still remains unclear. We hypothesize a non-IgE mediated mast-cell activation, with a direct action played by cocaine, and consequent massive expression of several factors effecting the microcirculatory system, including pro-inflammatory cytokines and chemokines. Our hypothesis is supported by an elevated serum tryptase levels in the patient.