European journal of heart failure · 2025
Effects of empagliflozin on uric acid levels during acute heart failure recompensation: A sub-analysis of the EMPAG-HF trial (Effects of Empagliflozin on Diuresis and Renal Function in Patients with Acute Decompensated Heart Failure).
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
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Bogoviku Jurgen, Nguyen Tien Dung, Westphal Julian Georg, Haertel Franz, Aftanski Pawel, Möbius-Winkler Sven, Busch Martin, Schulze P Christian
Аннотация
BACKGROUND: Sodium-glucose cotransporter 2 inhibitors improve prognosis in chronic heart failure as part of currently recommended therapeutic strategies. Elevated levels of serum uric acid (SUA) have been associated with worsening of outcomes in cardiovascular disease and may lead to hyperuricaemia and gout as well as exacerbation of renal failure. The effects of empagliflozin on SUA in patients with acute decompensated heart failure (ADHF) remain unknown.
METHODS AND RESULTS: In the single-centre, prospective, double-blind, placebo-controlled EMPAG-HF trial, patients with ADHF were screened and randomized within 12 h following hospital admission to receive either empagliflozin or placebo in addition to standard medical treatment over 5 days. Sixty patients were enrolled and randomized irrespective of left ventricular ejection fraction or diabetes. Serum and urine uric acid were evaluated as part of the standard monitoring protocol. Baseline patient characteristics did not differ between the two groups. SUA increased in the placebo group during diuretic therapy but decreased in the empagliflozin group. At 3, 4 and 5 days, SUA was significantly lower in the empagliflozin group compared to placebo. The reduction in SUA following empagliflozin treatment was associated with an enhanced renal excretion of uric acid.
CONCLUSIONS: Addition of empagliflozin to standard diuretic therapy may prevent the rise in SUA during decongestion in patients with ADHF and thus may prevent negative effects of hyperuricaemia including the occurrence of acute gout episodes.
METHODS AND RESULTS: In the single-centre, prospective, double-blind, placebo-controlled EMPAG-HF trial, patients with ADHF were screened and randomized within 12 h following hospital admission to receive either empagliflozin or placebo in addition to standard medical treatment over 5 days. Sixty patients were enrolled and randomized irrespective of left ventricular ejection fraction or diabetes. Serum and urine uric acid were evaluated as part of the standard monitoring protocol. Baseline patient characteristics did not differ between the two groups. SUA increased in the placebo group during diuretic therapy but decreased in the empagliflozin group. At 3, 4 and 5 days, SUA was significantly lower in the empagliflozin group compared to placebo. The reduction in SUA following empagliflozin treatment was associated with an enhanced renal excretion of uric acid.
CONCLUSIONS: Addition of empagliflozin to standard diuretic therapy may prevent the rise in SUA during decongestion in patients with ADHF and thus may prevent negative effects of hyperuricaemia including the occurrence of acute gout episodes.