Background. The comorbid course of liver cirrhosis and atrial fibrillation causes higher levels of hospitalizations, mortality, and ischemic stroke. Theoretically, rebalanced state of hemostasis in patients with liver cirrhosis may shift towards hypercoagulation on the background of atrial fibrillation and provoke adverse clinical consequences. The purpose of the study was to assess abnormalities in primary, secondary hemostasis and fibrinolytic system in patients with liver cirrhosis and atrial fibrillation using standard laboratory coagulation parameters and to investigate their changes depending on the stage of liver cirrhosis A, B, C according to Child-Pugh score. Materials and methods. A cross-sectional prospective study was conducted with the inclusion of 106 patients aged 42 to 83 years: group I (n = 70) included the patients with liver cirrhosis and atrial fibrillation, II (n = 36) consisted of subjects with liver cirrhosis, which were distributed depending on the Child-Pugh score stages of cirrhosis, and 20 healthy individuals. The levels of platelets, APTT, INR, PT, TT, fibrinogen, D-dimer were assessed on a Steellex M200 coagulometer. Statistical analysis (IBM SPSS Statistics) was performed. Results. The platelets count in group I patients was reduced by 37.4 % ((200.00 ± 8.33) vs. (274.7 ± 3.4), p < 0.001), a prolonged APTT time by 38.6 % ((44.35 ± 1.39) vs. (32.01 ± 0.63), p < 0.001), PT by 73.5 % ((19.40 ± 0.87) vs. (11.18 ± 0.53), p < 0.001), TT by 2.07 times ((25.70 ± 1.31) vs. (12.40 ± 0.66), p < 0.001), the INR increased by 24.3 % ((1.38 ± 0.04) vs. (1.11 ± 0.01), p < 0.001). The fibrinogen level was 20.9 % higher ((4.17 ± 0.17) vs. (3.45 ± 0.11), p < 0.001) than in the control group and was 83.7 % higher ((4.17 ± 0.17) vs. (2.27 ± 0.13), p < 0.001) than in group II. The D-dimer level was 83 % higher than in control ((675.0 ± 22.3) vs. (368.80 ± 21.85), p < 0.001) and 44 % higher ((675.0 ± 22.3) vs. (469.00 ± 37.18), p < 0.001) compared with group II. Conclusions. In patients with liver cirrhosis and atrial fibrillation, the abnormalities of primary hemostasis are detected due to the decrease of platelet count on the background of portal hypertension. At the secondary stage of hemostasis, the indicators of external and internal coagulation mechanisms are prolonged due to the reduced synthesis of coagulation factors by the liver. A more intensive generation of fibrinogen is determined at the stage of compensated and subcompensated cirrhosis with a gradual decrease at the stage of decompensation. The high activity of the fibrinolytic system is observed due to an increase in the D-dimer levels, which may indicate a prothrombotic state in these patients.
