LEFT-VENTRICULAR FUNCTION IMMEDIATELY AFTER INTRAVENOUS COCAINE - A QUANTITATIVE 2-DIMENSIONAL ECHOCARDIOGRAPHIC STUDY

Objectives. We tested the hypothesis that intravenous cocaine, in dose s commonly self administered in nonmedical settings, causes acute myoc ardial ischemia and left ventricular dysfunction. Background. Cocaine induced cardiac complications are responsible for a growing number of deaths in young people, but the mechanism by which cocaine induces the se complications is unclear. Methods. We performed 12-lead electrocard iography and quantitative two dimensional echocardiography in 20 subje cts before and after single intravenous doses of high dose cocaine (1. 2 mg/kg body weight), low dose cocaine (0.6 mg/kg) and placebo. Result s. At 2 to 7 min after cocaine administration, the rate pressure produ ct was increased significantly from baseline (high dose 73%, low dose 63%, placebo 8%, p < 0.001 for either dose vs. placebo). During this t ime, electrocardiography demonstrated dose related nonspecific changes (high dose in 14 of 20 subjects, low dose in 9 of 20 subjects, placeb o in 2 of 20 subjects, p < 0.002 for either dose vs. placebo). In cont rast, echocardiography showed that the frequency of hyperdynamic left ventricular wall segments doubled after high dose cocaine compared wit h placebo (34% [108 of 318] vs. 16% [51 of 319], respectively, p = 0.0 001) but that there was no change in either left ventricular ejection fraction (high dose 66 +/- 9%, placebo 67 +/- 6%, p = NS) or wall moti on score index (high dose 0.67 +/- 0.44, placebo 0.85 +/- 0.30, p = NS ). Conclusions. We conclude that intravenous cocaine, in doses commonl y self-administered in nonmedical settings, does not cause acute myoca rdial ischemia or left ventricular dysfunction. We speculate that coca ine induced cardiac complications are caused by idiosyncratic coronary artery vasospasm, by exceptionally high dosages or by cocaine-induced coronary artery thrombosis.