Vascular age is determined by functional and structural changes in the arterial wall. When measured by its proxy, pulse wave velocity, it has been shown to predict cardiovascular and total mortality. Disconcordance between chronological and vascular age might represent better or worse vascular health. Cell senescence is caused by oxidative stress and sustained cell replication. Senescent cells acquire senescence-associated secretory phenotype. Oxidative stress, endothelial dysfunction, dysregulation of coagulation and leucocyte infiltration are observed in the aging endothelium. All of these mechanisms lead to increased vascular calcification and stiffness. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can involve the vascular endothelium. It enters cells using angiotensin-converting enzyme 2 (ACE-2) receptors, which are abundant in endothelial cells. The damage this virus does to the endothelium can be direct or indirect. Indirect damage is caused by hyperinflammation. Direct damage results from effects on ACE-2 receptors. The reduction of ACE-2 levels seen during coronavirus disease 2019 (COVID-19) infection might cause vasoconstriction and oxidative stress. COVID-19 and vascular aging share some pathways. Due to the novelty of the virus, there is an urgent need for studies that investigate its long-term effects on vascular health.

Background and Objectives: Kidney transplant recipients represent a unique population with metabolic abnormalities, altered nutritional and immune status, as well as an imbalanced regulation of adipocytokine metabolism. Leptin is a hormonally active protein mainly produced by fat tissue that modulates appetite, satiety, and influences growth, energy, and bone metabolism. There has been great interest in the role of this hormone in chronic kidney disease-related protein energy wasting; thus, a positive leptin correlation with body mass index and fat mass was confirmed. This study was designed to determine the association of pre and post-kidney transplant leptin concentration with nutritional status and body composition. Materials and Methods: We studied 65 kidney transplant recipients. Nutritional status was evaluated before kidney transplantation and 6 months later using three different malnutrition screening tools (Subjective Global Assessment Scale (SGA), Malnutrition Inflammation Score (MIS), and Geriatric Nutritional Risk Index (GNRI)), anthropometric measurements, and body composition (bioelectrical impedance analysis (BIA)). Demographic profile, serum leptin levels, and other biochemical nutritional markers were collected. Statistical analysis was performed with R software. Results: Median age of the studied patients was 45 years, 42% were females, and 12% had diabetes. Leptin change was associated with body weight (p < 0.001), waist circumference (p < 0.001), fat mass (p < 0.001) and body fat percentage (p < 0.001), decrease in parathyroid hormone (PTH) (p < 0.001) transferrin (p < 0.001), diabetes mellitus (p = 0.010), and residual renal function (p = 0.039), but not dependent on dialysis vintage, estimated glomerular filtration rate (eGFR), or delayed graft function at any time during the study. After adjustment for age and sex, body mass index (BMI) (p < 0.001), fat mass (p < 0.001), and body fat percentage (p < 0.001) were independent variables significantly associated with post-transplant leptin change. Lower leptin values were found both before and after kidney transplantation in the SGA B group. GNRI as a nutritional status tool was strongly positively related to changes in leptin within the 6-month follow-up period. Conclusions: Kidney transplant recipients experience change in leptin concentration mainly due to an increase in fat mass and loss of muscle mass. GNRI score as compared to SGA or MIS score identifies patients in whom leptin concentration is increasing alongside an accumulation of fat and decreasing muscle mass. Leptin concentration evaluation in combination with BIA, handgrip strength measurement, and GNRI assessment are tools of importance in defining nutrition status in the early post-kidney transplant period.

Background and objectives: early reports showed a decrease in admission rates and an increase in mortality of patients with acute myocardial infarction (AMI) during the first wave of COVID-19 pandemic. We sought to investigate whether the COVID-19 pandemic and associated lockdown had an impact on the ischemia time and prognosis of patients suffering from AMI in the settings of low COVID-19 burden. Materials and Methods: we conducted a retrospective data analysis from a tertiary center in Lithuania of 818 patients with AMI. Data were collected from 1 March to 30 June in 2020 during the peri-lockdown period (2020 group; n = 278) and compared to the same period last year (2019 group; n = 326). The primary study endpoint was all-cause mortality during 3 months of follow-up. Secondary endpoints were heart failure severity (Killip class) on admission and ischemia time in patients with acute ST segment elevation myocardial infarction (STEMI). Results: there was a reduction of 14.7% in admission rate for acute myocardial infarction (AMI) during the peri-lockdown period. The 3-month mortality rate did not differ significantly (6.9% in 2020 vs. 10.5% in 2019, p = 0.341 for STEMI patients; 5.3% in 2020 vs. 2.6% in 2019, p = 0.374 for patients with acute myocardial infarction without ST segment elevation (NSTEMI)). More STEMI patients presented with Killip IV class in 2019 (13.5% vs. 5.5%, p = 0.043, respectively). There was an increase of door-to-PCI time (54.0 [42.0–86.0] in 2019; 63.5 [48.3–97.5] in 2020, p = 0.018) and first medical contact (FMC)-to-PCI time (101.0 [82.5–120.8] in 2019; 115 [97.0–154.5] in 2020, p = 0.01) during the pandemic period. Conclusions: There was a 14.7% reduction of admissions for AMI during the first wave of COVID-19. FMC-to-PCI time increased during the peri-lockdown period, however, it did not translate into worse survival during follow-up.

Neseniai buvo iškelta idėja, kad COVID-19 gali būti laikoma endotelio liga. SARS-CoV- 2 patenka į ląste­les, naudodamas S baltymą, kuris atpažįsta angiotenziną konvertuojantį fermentą- 2 (angl. angiotensine-conver­ting enzyme, ACE2). ACE2 randami epitelyje, plonosios žarnos enterocituose, arterijų miocituose ir kardiovasku­linės sistemos endotelyje. COVID-19 sukeltos endotelio­patijos lygis koreliuoja su ligos sunkumu. ACE ir ACE2 receptoriai veikia antagonistiškai. ACE2 skatina vazodilataciją, mažina uždegimą ir oksidacinį stresą. ACE veikia vazokonstrik­tiškai, skatina uždegimą ir oksidacinį stresą. COVID-19 metu mažėja ACE2 kiekis, sutrinka pusiausvyra tarp ACE ir ACE2 poveikio, labiau pasireiškia ACE efektai. CO­VID-19 metu endotelio pažaidą sukelia tiesioginiai ir netiesioginiai veiksniai. Tiesioginiai veiksniai – dėl viruso sumažėjęs ACE2 kiekis bei imuninių ląstelių po­veikis infekuotoms endotelio ląstelėms. Netiesioginiai veiksniai žaloja endotelį dėl hiperaktyvaus uždegiminio atsako ir padidėjusios cito­kinų koncentracijos. Įrodymų dėl ilgalaikio COVID-19 poveikio kraujagyslėms nėra, bet aprašyti galimi pažai­dos mechanizmai, skatinantys endotelio remodeliaciją ir fibrozę.

Objective The current study aimed to check whether early vascular aging, measured as carotid-femoral pulse wave velocity (cfPWV), is related to kidney function, measured as creatinine-based estimated glomerular filtration (eGFR) and urinary albumin-to-creatinine ratio (UACR), in middle-aged subjects with metabolic syndrome. Methods Participants were recruited from Lithuanian high-risk cohort (LitHiR). The cohort consists of middle-aged individuals with high cardiovascular risk but without overt cardiovascular disease. Participants underwent baseline and second visit hemodynamics measurement, including aortic mean arterial pressure (MAP), cfPWV, crPWV, carotid-intima media thickness measurement (CIMT) and biochemical analysis and all fulfilled NCEP/ATPIII criteria for metabolic syndrome diagnosis. First of all, we had determined correlations among hemodynamic measurement and eGFR together with albuminuria, expressed as UACR. Then we compared subjects who experienced significant eGFR decline with the remaining population and determining factors influencing this. Results A total of 689 subject data were eligible for analysis. We observed relationship between cfPWV and MAP, crPWV, glucose, BMI, C-reactive protein, waist circumference except kidney function measured as eGFR at the baseline and at the second visit. eGFR was not associated with MAP or albuminuria. Baseline but not second visit UACR significantly positively correlated with cfPWV (r-spearman = 0.146, P = 0.003) and MAP (r-spearman = 0.142, P = 0.005). eGFR decline was mainly observed in subjects with higher baseline eGFR and was independently influenced by increase in cfPWV. Conclusion In middle-aged subjects with prevalent metabolic syndrome eGFR decline is related to aortic and not peripheral arterial stiffening. Better baseline kidney function could be possibly an effect of glomerular hyperfiltration, and it allows us to conclude that this phenomenon indicates early vascular damage and it should be addressed seriously in metabolic syndrome patients with normal kidney function.