Does cocaine cause coronary vasospasm in chronic cocaine abusers? a study of coronary and systemic hemodynamics

The pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha-adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST- and T-wave changes were studied. Cocaine administered intravenously (maximum 32 mg) produced subjective sensation of central nervous stimulation (the 'high') in all patients. However there was no significant change in coronary artery diameter (assessed by computer- assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two- dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (thermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p < 0.007). Despite a significant elevation in heart rate (average 56%, p < 0.007), mean systemic arterial pressure (average 12%, p < 0.05) and rate-pressure product (average 69%, p < 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine. The results of this study are consistent with the hypothesis that cocaine-induced activation of platelets may have an important role to play in producing myocardial ischemia by occlusion and spasm of diseased small coronary vessels; this was proven previously on biopsy and also in the initiation of acute coronary occlusion.