Redefining Uric Acid and Cardiovascular Risk

Urate-lowering trials have not consistently demonstrated benefits in preventing coronary events, revealing an interventional gap and challenging the causal role of uric acid in cardiovascular disease. Advances in dual-energy computed tomography have revealed monosodium urate crystal deposition within vessel walls and atherosclerotic plaques, leading to the concept of vascular gout. Persistent hyperuricemia, particularly in Asian populations characterized by urate underexcretion, may facilitate crystal deposition and innate immune pathway activation. These inflammatory processes may promote vascular inflammation, plaque instability, and cardiovascular events. Xanthine oxidase inhibition effectively lowers serum uric acid levels and reduces monosodium urate crystal burden in articular tissues. However, whether urate-lowering therapy reduces monosodium urate crystal deposition and crystal-driven inflammation within the vascular wall remains unknown. Therefore, we aimed to reframe uric acid from a metabolic marker to a mediator of urate crystal-driven vascular inflammation and discuss future therapeutic strategies targeting crystal burden and inflammation in Asian populations.