Several physiological and pathophysiological stimuli or drugs modulate endothelial progenitor cell (EPC) mobilization. Moreover, levels of circulating EPCs predict cardiovascular risk and left ventricular remodelling after myocardial infarction. Nevertheless, our understanding in this field is complicated by lack of an unequivocal definition of EPCs, thus limiting their clinical applications. This review summarizes current knowledge and uncertainties on EPC characterization and mobilization in the attempt to define their role in the management of cardiovascular diseases.

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Cocaine is associated with important cardiac complications such as sudden death, acute myocarditis, dilated cardiomyopathy, life-threatening arrhythmias, and myocardial ischemia as well as infarction. It is well known that cocaine may induce vasospasm through adrenergic stimulation of the coronary arteries. Moreover, cocaine may promote intracoronary thrombosis, triggered by alterations in the plasma constituents, and platelet aggregation, leading to subsequent myocardial infarction. The long-term use of cocaine may stimulate atherosclerosis, probably through endothelial cell dysfunction. Significant and severe coronary atherosclerosis is common in young chronic cocaine users and there is probably a relationship between the duration and frequency of cocaine use and the extent of coronary disease.