Structure of Cardiovascular Comorbidity in Patients with Non-Alcoholic Fatty Liver Disease

Purpose of the study – to optimise patient management, to assess the pattern of cardiovascular comorbidity in patients with non-alcoholic fatty liver disease (NAFLD). Material and methods. An open comparative study with the formation of a cohort of 126 patients with NAFLD with different stages of liver fibrosis was conducted. The sample was divided into two groups: group-1 included 97 patients with comorbid course of cardiovascular diseases and group-2 – 29 patients without it. Complaints, medical and life history, examination, general laboratory tests and hormonal status, liver elastometry to assess the severity of fibrosis were collected. Work with the study data and graphical analysis was carried out using Microsoft office 2019 software package statistical analysis using Statistica 12.0 (StatSoft Inc, USA). Results. In group-1, arterial hypertension was detected in 90 patients (92.78%), atrial fibrillation in 6 patients (6.19%), other rhythm disturbances (paroxysm, extrasystole in 27 patients (27.84%), postinfarction cardiosclerosis in 15 patients (15.46%), and stage I chronic heart failure in 14 patients (14.43%). FIB-4 fibrosis index (U = -2.62; p < 0.01), and FLI leptin/ObR (U = 3.77; p < 0.01) were statistically higher for patients with comorbid course of CHF. A positive correlation of moderate degree in trimethylamine-N-oxide and zonulin levels in faeces was recorded (rs = 0.37). In patients with comorbid course, the prevalence of steatosis (Z = -4.22, p < 0.01) and fibrosis (Z = -2.44, p < 0.01) stage was statistically significantly higher in patients with comorbid course than in patients without SWD according to the results of transient elastometry. Conclusions. The most common cardiovascular pathology in patients with NAFLD is arterial hypertension. Progressive stages of liver fibrosis in this group are associated with the phenomenon of leptin resistance. The syndrome of increased intestinal permeability is a possible mechanism influencing the formation of cardiovascular comorbidity.