| Abstract: | The liver plays an important role in the development of atherogenic dyslipidemia, since changes in lipid metabolism begin at the hepatocyte level. Given the prevalence of dyslipidemias and their proven effect on the development of thrombotic cardiovascular complications in patients with non-alcoholic fatty liver disease (NAFLD), it is important to understand the role of platelets and hemostatic blood activity. Objective - to determine the state of platelet-plasma hemostasis in patients with essential hypertension, with concomitant non-alcoholic fatty liver disease. 152 patients were examined: 72 men and 80 women. Three groups were identified: I - 46 patients with hypertension stage II, II - 54 patients with NAFLD without hypertension, Group III - 52 patients with hypertension stage II with concomitant NAFLD. The total amount of spontaneous and induced platelet aggregation ability, coagulation activity, anticoagulant and fibrinolytic potential of blood was studied. The degree of spontaneous aggregation was significantly higher in patients with hypercholesterolemia - by 32.4% (p<0.05). that the level of fibrinogen was higher by 13.5% (p<0.05) precisely in hypercholesterolemia. In a cohort with a comorbid course of hypertension and NAFLD, patients on statin therapy had a 16.5% (p<0.05) lower degree of spontaneous aggregation than patients who did not receive this treatment. In patients with NAFLD without statin treatment, prothrombin time (PTT) was shortened by 19.2% (p<0.01) and international normalization ratio (INR) by 15.3% (p<0.01) than in patients who received lipid-lowering therapy. A decrease in thrombin time (TT) by 12.2% (p<0.05) was observed in the subgroup receiving statins among NAFLD patients. The use of statins in the general cohort increased the activity of antithrombin (AT) III by 10.7% (p<0.01), and in the NAFLD group by 14.3% (p<0.001). In patients with essential hypertension (HT) and NAFLD with a high level of cholesterolemia, spontaneous aggregation was 17.1% (p<0.05) less than in patients who did not receive statins and had high cholesterol levels, and the degree of collagen-induced aggregation decreased by 33.7% (p<0.05). In the subgroup with hypercholesterolemia, statins contributed to an increase in PTT by 32.5% (p<0.05), INR by 25.4% (p<0.05), and thrombin time - by 23.2% (p<0.05) and increased the activity of the anticoagulant link of hemostasis - the level of AT III increased by 3.1% (p<0.05) Hypercholesterolemia is associated with a higher functional activity of platelets, hyperfibrinogenemia. Statin therapy in patients with HT stage. and NAFLD is accompanied by a decrease in the activity of spontaneous aggregation, the coagulation link and increases the anticoagulant potential of the blood. |
