Abstract
Coronary arterial disease (CAD) is the leading cause of mortality in the world. Hyperuricemia has recently emerged as a novel independent risk factor of CAD, in addition to the traditional risk factors such as hyperlipidemia, smoking, and obesity. Several clinical studies have shown that hyperuricemia is strongly associated with the risk, progression and poor prognosis of CAD, as well as verifying an association with traditional CAD risk factors. Uric acid or enzymes in the uric acid production pathway are associated with inflammation, oxidative stress, regulation of multiple signaling pathways and the renin-angiotensin-aldosterone system (RAAS), and these pathophysiological alterations are currently the main mechanisms of coronary atherosclerosis formation. The risk of death from CAD can be effectively reduced by the uric acid-lowering therapy, but the interventional treatment of uric acid levels in patients with CAD remains controversial due to the diversity of co-morbidities and the complexity of causative factors. In this review, we analyze the association between hyperuricemia and CAD, elucidate the possible mechanisms by which uric acid induces or exacerbates CAD, and discuss the benefits and drawbacks of uric acid-lowering therapy. This review could provide theoretical references for the prevention and management of hyperuricemia-associated CAD.