Possibilities of hyperuricemia correction in acute decompensation of heart failure

Acute decompensation of heart failure (ADHF) is a period of the course of chronic heart failure (CHF), which is characterised by rapid aggravation/appearance of heart failure (HF) symptoms, requiring emergency hospitalisation of the patient and intensive care. ADHF is an urgent problem for modern healthcare and is associated with unfavourable prognosis and high mortality in this group of patients.

Aim. To evaluate the safety of allopurinol prescription in patients with ADHF, hyperuricaemia and reduced level of glomerular filtration rate irrespective of left ventricular ejection fraction.

Materials and methods. The results of standard therapy of HF with diuretic therapy in combination with xanthine oxidase inhibitor – allopurinol in the starting dose of 50 mg in 36 patients with ADHF of functional class II–IV, hyperuricemia, reduced renal filtration function calculated by the CKD-EPI formula are presented. Patients were hospitalised from February 2023 to January 2024 in the department of myocardial diseases and heart failure of FGBU ‘E.I. Chazov NMICC’ of the Ministry of Health of Russia. The study included 36 patients, the mean age was 71.6±9.8 years. Of them 72% of patients were male. The indices at the moment of inclusion in the study and at achievement of HF compensation were analysed.

Results. The median number of days spent in hospital was 14.7±5.7. On the background of optimal drug therapy of CHF in combination with allopurinol by the time of discharge the level of uric acid statistically significantly decreased – median before treatment 509 [460; 563], after 384 [330; 418] μmol/l, р<0.0001; decreased concentrations of N-terminal precursor of brain natriuretic peptide: pre-treatment median 3972 [2322; 9272], post 2132 [983; 3867] pg/ml, p=0.0001; decreased Creatine Kinase median pre-treatment 73 [55; 108], post 63 [47; 83] U/L, p=0.0011; decreased urea concentration pre-treatment 8.4 [7; 11], after 8.3 [7; 10] mmol/L, p=0.01; decreased total bilirubin median pre-therapy 23.2 [15.5; 28.8], after 18.5 [15; 25.6] µmol/L, p=0.025; C-Reactive Protein – median before treatment 4.3 [2; 14.2] mg/l, after 2.8 [1.1; 11.2] mg/l, p=0.036; there was a significant increase in distance test – six minute walk (T6X) – median before treatment 158 [149; 185], after 301 [283; 321], р<0.0001. No acute kidney injury and progression of Chronic Kidney Disease were observed during the period of hospitalisation. No dyspeptic phenomena and allergic reactions were noted on the background of allopurinol administration. Statistically significant reductions in echocardiographic parameters were observed in NPV measurement – median before therapy 2.3 [2; 2.5] cm, after 2 [1.9; 2.4] cm, p=0.0002; decrease in Systolic Pulmonary Artery Pressure before therapy 50±14.8 mmHg, after 44±13.2 mmHg, p=0.0001; statistically significant increase in LVEF-median pre-therapy 30 [25; 53], after 34 [27;55]%, p=0.0002.

Conclusion. The use of allopurinol reduces uric acid concentration, which is accompanied by improvement of renal function as HF signs are compensated, and also has a favourable safety profile when used in patients with ADHF, hyperuricemia and Chronic Kidney Disease.