Dynamics of uric acid concentration against the background of early dapagliflozin use in patients with acute decompensation of heart failure

Background. Acute decompensation of heart failure (ADHF) is an urgent problem of modern cardiology due to unfavourable prognosis and high frequency of repeated hospitalizations. The risk of acute kidney injury in patients with ADHF, which significantly worsens clinical outcomes, is high, including due to elevated uric acid levels. Aim. To evaluate the effect of sodium-glucose cotransporter type 2 inhibitor dapagliflozin in patients with ADHF with reduced left ventricular ejection fraction (LVEF) on uric acid levels. Materials and methods. The study included 122 patients with ADHF and reduced LVEF (28±6%), III FC 97 (79.5%) patients and II FC 25 (20.5%). All patients received therapy for ADHF according to available guidelines. Patients were divided into two groups: the first group standard therapy, patients in the second group were added dapagliflozin at a dose of 10 mg to standard therapy. Dapagliflozin was administered on average on the 2nd day (1–3) from admission to the hospital on condition of stable haemodynamics. The duration of follow-up was 6 months. The level of uric acid, creatinine, glomerular filtration rate, NT-proBNP, CRP and ST2 at the time of inclusion in the study and 6 months after hospital discharge were analysed. Results. In patients with ADHF and reduced LVEF, a uric acid level equal to or greater than 667.9 μmol/L during hospitalisation predicted a high risk of death during the 6-month follow-up period. Decrease of uric acid level was observed only on the background of dapagliflozin therapy 472 (366–594) μmol/L initially, 326 (275–419) μmol/L when ADHF compensation was achieved (p0.001), after 6 months the significant changes remained – 359 (263–410) μmol/L (p0.001). Against the background of dapagliflozin therapy there was a significant decrease in NT-proBNP level after 6 months from 2059 pg/ml (1456–4204.5) to 1101 pg/ml (415.8–3371.5); p0.006; decrease in ST2 concentration after 6 months from 24. 4 ng/ml (15.1–35) to 19.4 ng/ml (13.3–30.1); p0.041; decrease in SRP after six months from 2.9 mg/L (1.2–7.1) to 2.1 mg/L (0.9–2.8); p0.015; no worsening of renal function was noted. Conclusion. It can be concluded that dapagliflozin has a favourable safety and efficacy profile when used in patients with ADHF and hyperuricemia.