12-LEAD AND CONTINUOUS ECG RECORDINGS OF SUBJECTS DURING INPATIENT ADMINISTRATION OF SMOKED COCAINE

Cocaine can cause myocardial ischemia or infarction. The incidence of these events, and the influence of specific dosing routes or regimens on their occurrence is not established. In the current study, we obtai ned frequent 12-lead electrocardiograms (ECGs) and continuous 2 or 3 c hannel ECGs from 20 subjects participating in a behavioral study of sm oked cocaine. Subjects received 10 or 11 doses of cocaine 0.4 mg/kg pe r dose, or 10 doses of 35 mg per dose at 30 min intervals (range 233-4 08 mg total dose per session). ECGs were also recorded on control days on which subjects received no cocaine. The mean peak plasma cocaine c oncentration on cocaine days was 640 +/- 262 ng/ml. There were no chan ges in digitized ST segment amplitude on 12-lead ECGs obtained during cocaine administration (P = 0.098). Of 17 subjects who had technically satisfactory continuous ECGs, four had significant ST segment depress ion (> 1 mm below the PR segment); two on cocaine days and two on cont rol days (P > 0.5). One subject had frequent premature beats on both c ocaine and control days. One subject had an asymptomatic run of 4 vent ricular beats 30 s after cocaine administration that could have been d ue to cocaine. All episodes of ST depression or premature beats were a symptomatic. No evidence of either symptomatic or subclinical cardiac ischemia related to cocaine administration was found. Thus no clinical ly important adverse events were found as a result of smoked cocaine a dministered by this dosing regimen to healthy males with a history of heavy cocaine use. Additional study with larger numbers of subjects wi ll be helpful in further assessing the safety of administering smoked cocaine to research subjects.