Abstract (USA): Cardiovascular disease remains the leading cause of death in the United States. There is evidence that hyperuricemia is directly related to increased cardiovascular events, and this underlies our study of the role of uric acid-lowering drugs in the treatment of cardiovascular disease. Allopurinol, the traditional cornerstone of gout treatment, competitively blocks xanthine oxidase, a key enzyme required for uric acid production, and has recently been evaluated in clinical studies for its role as a cardiovascular drug. Epidemiological and biochemical studies of uric acid production have shown that not only can uric acid itself lead to increased and worsened cardiovascular events, but also free radicals and superoxide generated by the action of xanthine oxidase can lead to increased cardiovascular events. Uric acid salts and free radicals ultimately lead to impaired coronary endothelial function and decreased myocardial oxidative stress. Allopurinol reduces uric acid formation while also scavenging anionic superoxide and free radicals released during uric acid formation. Clinical studies have shown that allopurinol can improve impaired endothelial function and consequently improve exercise tolerance in patients with angina pectoris. Allopurinol may reduce the incidence of congestive heart failure and mortality by improving mechanical uncoupling, enhancing myocardial contractility, improving left ventricular ejection fraction, and reducing oxidative stress. This article reviews the pharmacological effects of allopurinol on the cardiovascular system and suggests allopurinol as a potential drug for the treatment of two cardiovascular diseases – ischemic heart disease and congestive heart failure.