SOFT - TIAFT 1998 Scientific Session 4 Thursday October 8, 1998
Click Picture Stephen L. Winbery, Kari E. Blaho, Lynda J. Park, Brian Schietinger

Department of Emergency Medicine, UT Medical Group, Memphis, TN, USA

Cocaine has been shown to produce myocardial ischemia through various mechanisms. However, the true incidence of myocardial ischemia and its characteristics is poorly characterized. Clinical findings in 157 patients presenting to an emergency department after acute cocaine use with and without chest pain were compared.

Recent cocaine use was determined by patient history ( n = 14), a urine drug screen (n = 35) or by quantification of blood cocaine concentrations (n = 108). Blood cocaine concentrations were measured by an alkylation extraction/GC/MS procedure.

Most patients, regardless of the presence of chest pain had EKG changes that mimicked chronic hypertension including left ventricular hypertrophy, left atrial enlargement and aberrant conduction abnormalities. Rarely did those patients who were chronic abusers have normal EKG findings. The mean age of patients with cocaine related chest pain (n = 60) was 37.5 ±7.5 yr. Three patients ingested crack, 23 smoked crack and 3 patients insuflated cocaine.

The mean blood cocaine concentration (mg/L) in patients with cocaine related chest pain was 0.2 ± 0.5 and for those without chest pain, was 0.25 ± 0.4. Mean presenting vial signs in patients with chest pain were as follows: blood pressure 127.6 ± 19.0/81.9 ± 13.3 mmHg, heart rate 86.8 ± 17.1 bpm, respiratory rate 18.3 ± 6/minute and temperature 98.3 ± 1.15°F. In patients with chest pain, 2 had slight elevations of cardiac isoenzymes. Eight patients were admitted to the hospital for noncardiac reasons such as pneumonia. No patient had a myocardial infarction or demonstrable ischemia. Contrary to popular opinion, cardiac ischemia from acute cocaine use seems to be an uncommon event in the drug abusing population

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