Heart failure & cardiomyopathiesSecondary analysis

Uric Acid and SGLT2 Inhibition With Empagliflozin in Heart Failure With Preserved Ejection Fraction

JACC Heart FailPublished

  • Post hoc analysis of the EMPEROR-Preserved randomised trial

Authors' conclusion

Hyperuricemia is a common complication in HFpEF and is related to advanced disease severity and adverse outcome. Empagliflozin induced a rapid and sustained reduction of SUA levels and of clinical events related to hyperuricemia.

Study context

Population
Patients with heart failure with preserved ejection fraction (HFpEF)
Comparison
Empagliflozin vs placebo; Serum uric acid (SUA) levels in relation to outcomes
Primary endpoint
Effect of empagliflozin on SUA in relation to therapeutic efficacy (trial primary outcome: CV mortality or HF hospitalization)

Primary result

As reported in the abstract

SUA change with empagliflozin and treatment benefit by baseline SUA

Difference

−0.99 mg/dL

P < 0.0001

Treatment benefit on primary endpoint not influenced by baseline SUA
HR: 0.79 [95% CI: 0.69-0.90]; P = 0.0004
Change in SUA an independent correlate of treatment benefit on primary endpoint
P = 0.07

Further findings

OutcomeHR (95% CI)P value
Elevated SUA (highest tertile, 8.8 ± 1.4 g/dL) and outcomes — Highest SUA tertile vs Placebo · primary endpoint1.23 (0.98–1.53)P = 0.07
Elevated SUA (highest tertile, 8.8 ± 1.4 g/dL) and outcomes — Highest SUA tertile vs Placebo · HF hospitalization1.42 (1.08–1.86)P = 0.01

Hyperuricemia prevalence (SUA >5.7 mg/dL women, >7.0 mg/dL men)

Prevalence of hyperuricemia
49%

Elevated SUA (highest tertile, 8.8 ± 1.4 g/dL) and outcomes

Elevated SUA associated with advanced heart failure (HF) severity

Original publication

Uric Acid and SGLT2 Inhibition With Empagliflozin in Heart Failure With Preserved Ejection Fraction. JACC Heart Fail. Published 23 October 2024. doi:10.1016/j.jchf.2024.08.020

Summarised from the published abstract; every number is checked against it