Hyperuricemia, A new cardiovascular risk

Background and aims

Hyperuricemia is strongly linked to increased cardiovascular risk, including hypertension, coronary artery disease, arrythmia, and heart failure. Uric acid, as the end-product of purine metabolism, plays a critical role in cellular processes, but elevated levels can drive inflammation and oxidative stress. This review aims to emphasize the robust association between hyperuricemia and cardiovascular diseases, exploring whether uric acid-lowering therapies can mitigate cardiovascular events and improve patient outcomes.

Methods and results

A comprehensive review of PubMed sources was conducted, underscoring the significant link between high uric acid levels and cardiovascular events, particularly in patients with gout. Gender differences were observed, where premenopausal women have lower uric acid levels, likely due to hormonal effects, suggesting the potential need for gender-specific definitions in assessing cardiovascular risk. Epidemiological studies demonstrate a consistent correlation between hyperuricemia and adverse cardiovascular outcomes. However, interventional trials using xanthine oxidase inhibitors, such as allopurinol and febuxostat, have shown mixed results regarding their impact on reducing cardiovascular events. Additionally, emerging evidence suggests a "xanthine oxidase withdrawal syndrome" upon discontinuation of these therapies, highlighting the need for cautious management.

Conclusion

The strong association between elevated uric acid levels and cardiovascular diseases is well-documented. While lowering uric acid shows potential for reducing cardiovascular risk, current evidence from interventional trials remains inconclusive. Future research should focus on patient-specific therapeutic strategies, particularly for those at high cardiovascular risk with hyperuricemia and/or gout, to better define the benefits of targeted treatments.