Uric acid is the final product of purine metabolism. Classically it is recognized as the cause of gouty arthritis and kidney stones. Western civilization has increased serum levels of uric acid which is no longer considered a benign plasma solute. It has been postulated and recently demonstrated that it can penetrate cell membrane and exerts damaging intracellular actions such as oxidation and inflammation. These observations have stimulated several epidemiological researches suggesting that hyperuricemia is linked or even provokes hypertension and coronary artery disease. In this review we summarize the current evidences regarding uric acid which contribute in the pathophysiology of coronary artery disease.