Hyperuricemia and gout in patients with heart failure
Voronkov L.G. , Tkach N.A., Mitchenko O.I., Lyashenko A.V.
Summary. Hyperuricemia in heart failure (HF) associated with all-cause cardiovascular mortality and the risk of hospitalization for HF. Uric acid is the product of purine metabolism. The xanthine oxyreductase is the enzyme, which plays main role in this metabolism. This enzyme exists in two interconvertible forms: reduced (xanthine dehydrogenase) and oxidized (xanthine oxidase). The xanthine dehydrogenase dominates in tissues. The level of xanthine oxidase in plasma is low and this form is’nt detected in the myocardium. During in hypoxia, inflammation, and oxidative stress, xanthine dehydrogenase converts to xanthine oxidase which increases in plasma and myocardium. High levels of xanthine oxidase are characteristic of pathological conditions with systemic inflammation and oxidative stress — obesity, diabetes, and HF. According to a meta-analysis of 10 clinical trials published in 2024, which included 17,328 patients with HF, the use of xanthine oxyreductase inhibitors was accompanied by a statistically significant increase in overall mortality. It is known that loop and thiazide diuretics increase the concentration of uric acid in plasma by increasing the reabsorption of urates. Spironolactone reduces the excretion of uric acid in patients with chronic kidney disease. ACE inhibitors and some sartans have a moderate uric acid-lowering effect due to their mild uricosuric effects. Sacubitril/valsartan lowers plasma uric acid by uricosuric effects and inhibition of uric acid synthesis. The effect of beta-blockers on uric acid levels is uncertain, but carvedilol can lower uric acid levels. Use of empagliflozin (EMPEROR — Reduced study) was associated with a 32% reduction in gout point (acute gout, onset of gouty arthritis, or initiation of xanthine oxidase inhibitors or colchicine) compared with placebo. In the analysis of two large clinical trials of another SGLT2 inhibitor, dapagliflozin (DAPA-HF and DELIVER), the drug was equally effective in reducing the risk of reaching the primary endpoint (cardiovascular death or worsening of HF) in patients without gout and with gout. SGLT2 inhibitors are the most promising of the modern HF pharmacotherapy agents, which improve the clinical prognosis of patients, reduce the risk of gout manifestations and the need for antigout therapy.
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