INFLUENCE OF COCAINE, ETHANOL, OR THEIR COMBINATION ON EPICARDIAL CORONARY ARTERIAL DIMENSIONS IN HUMANS

Citation
Mj. Pirwitz et al., INFLUENCE OF COCAINE, ETHANOL, OR THEIR COMBINATION ON EPICARDIAL CORONARY ARTERIAL DIMENSIONS IN HUMANS, Archives of internal medicine, 155(11), 1995, pp. 1186-1191
Citations number
52
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00039926
Volume
155
Issue
11
Year of publication
1995
Pages
1186 - 1191
Database
ISI
SICI code
0003-9926(1995)155:11<1186:IOCEOT>2.0.ZU;2-I
Abstract
Background: Cocaine and ethanol are often abused concomitantly, and th is combination may be more lethal than either substance alone. Althoug h previous studies showed that cocaine causes coronary arterial vasoco nstriction, the combined effect of cocaine and ethanol on the coronary vasculature in humans is unknown. Thus, we assessed the effects of in tranasal cocaine, intravenous ethanol, or a cocaine-ethanol combinatio n on heart rate, systemic arterial pressure, and coronary arterial dim ensions in humans. Methods: Thirty-four subjects with chest pain (27 m en and seven women, aged 34 to 67 years) who were referred for cathete rization received one of the following pharmacologic interventions: (1 ) intranasal (2 mL) and intravenous (5 mL/kg) saline (n=8 [group A]); (2) intranasal cocaine (2 mg/kg) and intravenous saline (5 mL/kg) (n=9 [group B]); (3) intranasal saline (2 mL) and intravenous 10% ethanol (5 mL/kg) (n=9 [group C]); or (4) intranasal cocaine (2 mg/kg) and int ravenous 10% ethanol (5 mL/kg) (n=8 [group D]). Heart rate, systemic a rterial pressure, left coronary arterial dimensions (by computer-assis ted quantitative angiography), as well as blood cocaine, ethanol, and cocaine metabolite concentrations were measured before and 30, 60, and 90 minutes after initiation of the intravenous infusions. Results: No hemodynamic or angiographic changes were observed in the group A (sal ine) subjects. In the group B (cocaine) subjects, the heart rate-systo lic arterial pressure product increased by 5% and 10% at 30 and 90 min utes, respectively, and coronary arterial diameter decreased by 14% at these times. In the group C (ethanol) subjects, no hemodynamic change s were noted, but coronary arterial diameters increased by 12%, 11%, a nd 12% at 30, 60, and 90 minutes, respectively. In the group D (cocain e-ethanol) patients, rate-pressure product increased by 17%, 10%, and 16%, and coronary arterial diameters increased by 7%, 12%, and 13%, at 30, 60, and 90 minutes, respectively Conclusion: The combination of i ntranasal cocaine and intravenous ethanol causes an increase in the de terminants of myocardial oxygen demand. However, it also causes a conc omitant increase in epicardial coronary arterial diameter.