👤 Alla Kuznetsova

Visceral obesity plays a pivotal role in initiating and sustaining chronic systemic inflammation through complex interactions involving adipose tissue dysfunction, insulin resistance, immune system activation, and gut microbiome composition. Visceral obesity is also hypothesized to contribute to the development and progression of extraintestinal manifestations and complications in inflammatory bowel disease (IBD). The aim was to evaluate the interrelationships between ultrasound-measured visceral and subcutaneous adipose tissue thickness with carotid artery atherosclerosis indicators in IBD patients. The study included 90 patients with IBD aged 40-64 years. All patients underwent duplex ultrasound scanning of the carotid arteries with measurement of carotid plaque burden indicators. Ultrasound measurements of subcutaneous and visceral adipose tissue thickness (ATT) were performed: minimal subcutaneous adipose tissue thickness (mSATT), maximal preperitoneal adipose tissue thickness (mPATT), periumbilical subcutaneous adipose tissue thickness (PSATT), visceral abdominal adipose tissue thickness, peri- and pararenal adipose tissue thickness. Ultrasound-derived indicators of visceral obesity (mPATT and abdominal ATT), but not BMI or WC, were associated with an increased odds ratio for the presence of carotid plaque after adjustment for sex and age. Both mPATT and abdominal ATT demonstrated positive correlations with apoB concentration, LDL-C, sdLDL, eLDL-TG, and inverse correlations with adiponectin concentration. In patients with IBD aged 40-64 years, visceral adipose tissue thickness measured by ultrasound and WC were associated with the carotid plaque burdens. Ultrasound-measured mPATT and abdominal ATT, but not BMI and WC, were independently associated with carotid atherosclerosis in patients with IBD. Show less

Ageing endurance athletes have a higher prevalence of coronary artery disease (CAD) on coronary CT angiography (CCTA) than healthy controls, despite similarly low conventional cardiovascular risk. The predictive value of lipoprotein(a) [Lp(a)] for CAD in these low-risk individuals remains unclear. The Master@Heart study included 558 men (aged 45-70 years) without known cardiovascular risk factors: 191 lifelong athletes, 191 late-onset athletes, and 176 healthy controls. CCTA assessed coronary artery calcification (CAC) and plaques. The association between Lp(a) and subclinical CAD was assessed using logistic regression analysis to estimate odds ratios (ORs), adjusted for cardiovascular risk factors. Lp(a) was analysed dichotomously (<125 vs. >125 nmol/L) and continuously (per 10 nmol/L increase). 76 participants (13.6%) had elevated Lp(a) levels (>125 nmol/L). Elevated Lp(a) was significantly associated with age-specific CAC percentile≥75 (OR 1.80, p=0.049) and ≥1 mixed plaque (OR 1.76, p=0.046). Other CAD measures all tended to be more prevalent in those with elevated Lp(a). In the continuous analysis, Lp(a) was significantly associated with CAC>100 (OR 1.03, p=0.045), CAC percentile≥75 (OR 1.04, p=0.014), and ≥1 mixed or non-calcified plaque (OR 1.03, p=0.029).Lp(a) and prevalence of elevated Lp(a) were similar across lifelong athletes, late-onset athletes, and controls (p=0.586 and p=0.724, respectively). No significant interaction was found between Lp(a) and the exercise groups in predicting CAD. Lp(a) is independently associated with subclinical CAD in ageing endurance athletes and healthy controls, despite similarly low conventional cardiovascular risk. Lp(a) does not explain the higher CAD prevalence in lifelong athletes compared to controls, but may enhance risk stratification in this low-risk population. Show less

The adaptive antiviral immune response requires interaction between CD8+ T cells, dendritic cells, and Th1 cells for controlling SARS-CoV-2 infection, but the data regarding the role of CD8+ T cells in the acute phase of COVID-19 and post-COVID-19 syndrome are still limited. . Peripheral blood samples collected from patients with acute COVID-19 ( Patients with acute COVID-19 vs. HC and COVID-19 convalescents showed decreased absolute numbers of CD8+ T cells, whereas the frequency of CM and TEMRA CD8+ T cells in acute COVID-19 vs. HC was elevated. COVID-19 convalescents vs. HC had increased naïve and CM cells, whereas TEMRA cells were decreased compared to HC. Cell-surface CD57 was highly expressed by the majority of CD8+ T cells subsets during acute COVID-19, but convalescents had increased CD57 on 'naïve', CM, EM4, and pE1 2-3 months post-symptom onset. CXCR5 expression was altered in acute and convalescent COVID-19 subjects, whereas the frequencies of CXCR3+ and CCR4+ cells were decreased in both patient groups vs. HC. COVID-19 convalescents had increased CCR6-expressing CD8+ T cells. Moreover, CXCR3+CCR6- Tc1 cells were decreased in patients with acute COVID-19 and COVID-19 convalescents, whereas Tc2 and Tc17 levels were increased compared to HC. Finally, IL-27 negatively correlated with the CCR6+ cells in acute COVID-19 patients. We described an abnormal CD8+ T cell profile in COVID-19 convalescents, which resulted in lower frequencies of effector subsets (TEMRA and Tc1), higher senescent state (upregulated CD57 on 'naïve' and memory cells), and higher frequencies of CD8+ T cell subsets expressing lung tissue and mucosal tissue homing molecules (Tc2, Tc17, and Tc17.1). Thus, our data indicate that COVID-19 can impact the long-term CD8+ T cell immune response. Show less

To access the effect of lisinopril (diroton) on cerebral circulation and blood rheology in patients with arterial hypertension stage II. The trial included 37 patients (16 males, 21 females) with a mean arterial hypertension (AH) history 15.9 +/- 5.6 years. Diroton was given in a dose 10-40 mg/day for 6 months. Cerebral circulation (total cerebral circulation and venous outflow--TCC and VOF) was accessed by means of doppler ultrasonography. Blood and plasm rheology was determined using a rotational viscozymeter ACP-2. Instrumental tests were performed at baseline and at the end of the study. Rheology tests showed that diroton-treated patients achieved a significant decrease in blood viscosity in high, moderate and low shear stress and plasma viscosity, a decrease in platelet aggregation index and an increase in the index of erythrocytic deformability. All these changes were accompanied with a significant fall in fibrinogen and hematocrit. Doppler ultrasound revealed an insignificant increase in TCC and VOF. Diroton significantly improved impaired blood rheology and viscosity in AH patients as well as cerebral hemodynamics in patients with subnormal cerebral circulation and venous outflow at baseline. Show less