Uric Acid Level and Increased Cardiovascular Risk

Uric acid is a normal waste product created when the body breaks down purines — chemical compounds found naturally in our cells and in certain foods like red meat, organ meats, and shellfish. Under normal conditions, our kidneys filter uric acid from the blood and excrete it in urine. However, if the body produces too much uric acid or the kidneys excrete too little, levels rise. In Singapore, a serum uric acid level above 7.0 mg/dL (420 µmol/L) for men or 6.0 mg/dL (360 µmol/L) for women is clinically defined as hyperuricemia. While some individuals remain asymptomatic, others experience urate crystallisation, leading to the painful joint inflammation known as gout, a condition we frequently diagnose at our Orchard Road clinic.

For decades, epidemiological studies in Singapore and globally have highlighted a clear association between elevated serum uric acid and an increased rate of cardiovascular events. High levels of uric acid are consistently linked with hypertension, metabolic syndrome, and chronic kidney disease. Clinicians have observed that patients with high uric acid often exhibit signs of endothelial dysfunction — where the inner lining of blood vessels fails to dilate properly — as well as increased arterial stiffness and systemic inflammation. Because dissolved uric acid can promote oxidative stress inside vascular cells and activate the NLRP3 inflammasome pathway, researchers hypothesised that hyperuricemia might be a direct contributor to atherosclerosis, directly compounding a patient's overall uric acid cardiovascular risk.

To determine if lowering uric acid directly prevents heart disease, researchers conducted the landmark ALL-HEART trial published in 2022. This major clinical trial investigated whether adding allopurinol (a common urate-lowering drug) to standard therapy improved outcomes in 5,721 UK patients aged 60 and older with established ischaemic heart disease but no history of gout. The results were definitive: after an average follow-up of 4.8 years, allopurinol did not reduce the risk of non-fatal myocardial infarction, non-fatal stroke, or cardiovascular death compared to usual care. This indicates that in patients without gout, uric acid is likely a biological bystander or marker of cardiovascular risk rather than a direct causative driver, suggesting routine urate-lowering therapy is not justified for general heart protection in Singapore.

While lowering uric acid does not appear to prevent primary heart events in patients without gout, the clinical picture is different for patients who actually suffer from gout. In 2018, the CARES trial raised alarm by reporting that the urate-lowering drug febuxostat was associated with a higher risk of cardiovascular and all-cause mortality compared to allopurinol in gout patients with pre-existing heart disease. However, the subsequent 2020 FAST trial conducted in Europe provided reassurance, showing no increased cardiovascular risk or mortality associated with febuxostat compared to allopurinol. In Singapore, these safety profiles are closely analysed when tailoring gout therapies, ensuring that patients with high cardiovascular risk are prescribed the safest and most effective medication for their specific cardiac profile.

Because elevated uric acid is heavily associated with traditional cardiovascular risk factors, we believe a comprehensive evaluation is crucial. At our clinic located at Paragon Medical Centre on Orchard Road, we perform comprehensive evaluations to assess your specific uric acid cardiovascular risk. Rather than focusing solely on a single blood marker, we analyse a patient's full metabolic profile, including lipid panels, glucose levels, and blood pressure. We also utilise advanced diagnostic tools such as coronary artery calcium (CAC) scoring and CT coronary angiograms to directly measure arterial plaque burden. This comprehensive approach allows us to differentiate between benign asymptomatic hyperuricemia and high-risk patients who require intensive cardiovascular protection in the Singapore context.

Deciding when to treat high uric acid levels depends on whether a patient has clinical gout. For patients with gout, Singapore clinical guidelines recommend a strict treat-to-target strategy to lower serum uric acid below 6.0 mg/dL (360 µmol/L) to dissolve existing crystals and prevent flares. In these cases, allopurinol or febuxostat is essential, and doing so can reduce the chronic systemic inflammation that increases your uric acid cardiovascular risk. However, for asymptomatic hyperuricemia — where uric acid is high but the patient has never had gout or kidney stones — pharmacological treatment is generally not recommended solely for cardiovascular prevention, as trials like ALL-HEART showed no benefit. In our Singapore practice, we focus instead on addressing the underlying metabolic issues.

For Singapore patients looking to manage their uric acid levels naturally while reducing their overall cardiovascular risk, lifestyle modifications are highly effective. We recommend adopting a diet rich in vegetables, whole grains, and low-fat dairy while limiting high-purine foods like shellfish, red meat, and alcohol. Crucially, patients should avoid sugar-sweetened beverages containing high-fructose corn syrup, as fructose metabolism directly increases uric acid production. Maintaining a healthy weight through regular moderate exercise and staying well-hydrated also supports renal uric acid excretion. These changes not only lower urate levels but also improve blood pressure, cholesterol, and insulin sensitivity, providing multi-layered protection for your heart and blood vessels.