Uric acid (UA), the metabolic mediator of gout and urate renal stones, is associated with increased cardiovascular risk burden. Hyperuricemia is a common metabolic disorder, and interaction among UA and cardiovascular diseases has been clearly described. Several illnesses, including hypertension, myocardial infarction, metabolic syndrome, and heart failure, are related to increases in UA levels. In this article, we discuss the pathophysiology of hyperuricemia and describe the biologic plausibility of this metabolite's participation in the pathogenesis of cardiovascular illness. We conclude by discussing the implications of lowering plasma UA concentrations to reduce the risk of cardiovascular events, including myocardial infarction, stroke, heart failure, and cardiovascular death.