Cocaine abuse is widespread in North America. It is estimated that almost one in every four Americans has used cocaine at least once in his/her lifetime. In the past two decades, cocaine related cardiovascular complications have mushroomed because cocaine has become cheaper and more readily available. The fundamental effects of cocaine on cardiovascular system are similar to those observed following an intense, sympathetic stimulation. Cocaine intake results in marked increase in blood pressure, myocardial oxygen demand and heart rate. Coronary blood flow, which increases in response to exercise (endogenous sympathetic stimulation) however, is decreased by cocaine intake. Increased demand of oxygen by the myocardium in the face of decreased supply in subjects with cocaine use, leads to myocardial ischemia, which in turn forms a substrate for most of the cardiovascular complications, namely, myocardial infarction, cardiac arrhythmias and acute pulmonary edema. Hypertension related complications, dissection and rupture of aortic aneurysm, hemorrhagic stroke, in addition to infective endocarditis, myocarditis, cardiomyopathy all occur more frequently in cocaine addicts. In this review, pertinent clinical pharmacology and cardiovascular risks associated with cocaine abuse are presented.