Gout and hyperuricemia in cardiovascular disease

Abstract

In humans, uric acid (UA) is the final product of purine metabolism, and its increased level in the serum is known to cause gout, a common inflammatory arthropathy incited by intra-articular monosodium urate crystal deposition. In addition to its role in the development of crystalline arthritis, elevated UA levels have been further associated with a significantly increased risk for cardiovascular disease, including hypertension, atrial fibrillation, coronary artery disease, myocardial infarction, and valvular disease. In this review, the authors summarize the current understanding of the biomolecular mechanism and clinical association of hyperuricemia in gout and cardiovascular disease. They further discuss the possible use of current urate-lowering therapies to manage and/or prevent cardiovascular disease. As an increasing number of clinical studies have suggested that elevated UA levels may be an independent risk factor for adverse cardiovascular disease, there is impetus to better understand and develop novel therapies to improve cardiovascular outcomes.