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Cocaine increases myocardial oxygen demand by increasing both heart rate and blood pressure (Table 1).25,26 The influence of cocaine on heart rate and blood pressure is dose dependent and is mediated through α-adrenergic stimulation.25,26 At the same time, cocaine decreases oxygen supply via coronary vasoconstriction.25 Cocaine-induced coronary vasoconstriction occurs in normal (nondiseased) coronary artery segments but is more pronounced in atherosclerotic segments.27 Combining cocaine use with cigarette smoking has additive effects on coronary vasoconstriction while markedly increasing the rate-pressure product.28 Long-term cocaine users demonstrate coronary endothelial dysfunction.29 Because endothelial dysfunction increases the sensitivity of a vessel to the constrictor effects of catecholamines,30 it may be particularly detrimental for cocaine users. Even in the absence of epicardial coronary disease, cocaine causes microvascular disease31,32 and is associated with thrombosis.24,33,34