HYPERCOAGULATION OF BLOOD AND THROMBOCYTOPENIA AFTER SARS-COV-2 – PNEUMONIA AS PREDICTORS OF AN UNFAVORABLE PROGNOSIS IN PATIENTS WITH ARTERIAL HYPERTENSION

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Objective: To evaluate the dynamics of hypercoagulation parameters of blood plasma and platelets in patients with arterial hypertension (AH) in the early and late post-covid period. Design and method: The prospective study included 340 AH patients aged 41 to 89 years (mean 69; m/f 175/165) infected with SARS-CoV-2 diagnosed by PCR. Of these, 177 people (group 1) were diagnosed with acute pneumonia with the lung damage volume according to CT ranging from 15% to 85%; 163 patients (group 2) had an acute respiratory viral disease. The groups were comparable in age, gender, and concomitant comorbid pathology. Coronary heart disease (CHD) was detected in 85.6% of patients; diabetes mellitus (DM) in 31.5%. The patients were examined three times: on the 30th day from the onset of the disease, at the end of the 3rd month and after 9 months. C-reactive protein (CRP) (0-5 mg/l), ferritin (20-250 mg/l), D-dimer (0-230 ng/ml), fibrinogen (2-4 g/l), lymphocytes, and blood platelets were analyzed. Results: On day 30, group 1 patients showed signs of inflammation: ferritin 258±61.2; CRP 12.3±5.1; lymphocytes 27±8.3%; platelets 160±70.4∗10^9/l; ESR 17±13.7 mm/h. The tendency to hypercoagulation was detected by the indicators of D-dimer (715±241.3) and fibrinogen (3.7±0.9). By the end of the 3rd month, the levels of D-dimer (585±159.4; p=0.015); ferritin (177±59.1; p=0.0002) and CRP (7±5.6; p=0.001) remained elevated. Only after 9 months, D-dimer (100±9.1; p=0.0001) and CRP (2.6±0.2; p=0.0001) were normalized; lymphocyte (32±5.1%; p=0.00001) and platelets (305±69.2∗10^9/l; p=0.00001) increased with a persistent elevated ferritin level (213±124.8; p=0.047). In group 2, the indicators of hypercoagulation and inflammation were moderately elevated. Only after 9 months CRP and D-dimer levels were normalized and the number of platelets increased. Conclusions: In the early and late post-covid period, AH patients with comorbid pathology retain an inflammatory reaction and a procoagulant state, which, in combination with endothelial dysfunction, is a trigger for venous and arterial thrombosis.