Abstract
Aim of study. To reveal the most significant risk factors of chronic heart failure (CHF) decompensation against the background of rheumatoid arthritis (RA) and to carry out a regression analysis of galectin-3 level. Material and methods. Study group: 134 CHF RA patients; comparison group: 122 CHF patients without RA. The functional CHF class of the study participants was I-II according to the NYHA. The RA diagnosis was established based on X-ray examination and serological testing including determination of the rheumatoid factor, antibodies to the cyclic citrullinated peptide and C-reactive protein. The activity of the inflammatory process was evaluated using the DAS28 index and the visual analogue scale for pain. The X-ray stage of RA was I-III according to Steinbrocker classification in all patients enrolled. The medicines for CHF treatment were comparable in the groups. The disease-modifying anti-rheumatic drug was methotrexate. Patients who did not receive methotrexate due to development of adverse effect and/or individual intolerance were administered 20mg leflunomide per day. Additionally, NSAIDS were used (enteral, parenteral, local application). Haematological, biochemical and instrumental tests were used. The data processing was performed via the STATISTICA 10.0 software; the paper presents statistically reliable results. The significance level was set at p<0.05. Results. As a result, logistic regression analysis revealed statistically significant associations between galectin-3 and the level of atrial natriuretic peptide (r=0.3; beta=0.36; p=0.02), triglycerides (r=0.3; beta=0.6; p=0.04), low-density lipoproteins (r=0.3; beta=0.2; p=0.001) and the glomerular filtration rate (r=0.5; beta=0.3; p=0.01). Conclusion. The analysis has revealed data pointing to the possibility of heart failure compensation against the background of RA at the level of galectin-3 concentration of 17.6ng/ml or higher. The regression model attests to the association between the cytokine levels observed and the possible destabilisation of dyslipidaemia progression, kidney function and water-salt metabolism.
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