Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated not only with respiratory illness but also with profound vascular and coagulation disturbances. Long COVID (LC) is characterized by persistent symptoms such as fatigue, dyspnea, cognitive impairment, and palpitations. Mechanistically, SARS-CoV-2 induces direct endothelial injury, promotes a pro-inflammatory cytokine milieu, and activates platelets, leading to immunothrombosis and impaired fibrinolysis. Consequently, patients exhibit microthrombosis, elevated plasma D-dimer, fibrinogen dysregulation, and persistent hypercoagulability. Clinically, this translates into an increased risk of venous thromboembolism, including deep vein thrombosis and pulmonary embolism, as well as arterial thrombotic events such as myocardial infarction and stroke, which may persist months after acute infection. Understanding the interplay between endothelial injury, inflammation, and coagulation is crucial for risk stratification and the development of preventive and therapeutic strategies. We conducted a systematic narrative review of the literature, including human clinical and mechanistic studies identified through PubMed, Scopus and Web of Science up to 30 September 2025. This review synthesizes current evidence on vascular complications in LC, highlighting endothelial dysfunction as a central pathophysiological nexus linking the acute phase of SARS-CoV-2 infection with chronic LC manifestations.

Endothelial dysfunction (characterized by reduced vasodilation or vasoconstriction, oxidative stress, inflammation, and pro-thrombotic condition) is a critical factor in the pathophysiology of various cardiovascular conditions, and the application of anesthetics can affect this dysfunction. Patients undergoing major surgery, especially cardiovascular surgery, are at increased risk of endothelial dysfunction. The impact of anesthetics on endothelial function can vary depending on the specific agent, dosage, duration of exposure, comorbidities, etc. Certain anesthetics, especially at higher doses, may increase the production of reactive oxygen species (ROS), leading to oxidative stress and endothelial dysfunction through reduced nitric oxid (NO) availability. Some anesthetics can modulate inflammatory responses, either by suppressing or exacerbating inflammation, or may affect the permeability of the endothelium, potentially leading to pulmonary edema and disruption of the blood-brain barrier. Anesthetics can influence endothelial glycocalyx. Understanding anesthetics effects is crucial for optimizing anesthetic management, particularly in patients with pre-existing cardiovascular issues. Therefore, the aim of this review is to critically evaluate the effects of different classes of anesthetics on endothelial function and oxidative stress. Specifically, we address how anesthetics influence NO bioavailability, endothelial glycocalyx integrity, inflammatory and oxidative pathways, and clinical outcomes in surgical patients. By summarizing current evidence, we aim to highlight mechanistic insights and identify potential perioperative strategies to minimize endothelial dysfunction.

Intraabdominal hypertension (IAH) occurs frequently in patients with acute pancreatitis and adds to their morbidity and mortality. The main aim of the study was to identify the determination of the predictive factors connected to IAH that influence the evolution of acute pancreatitis. The prospective cohort study was conducted on 100 patients who had acute pancreatitis. According to obtained intraabdominal pressure (IAP) values, the patients were divided into two groups: one group (n = 40) with normal IAP values and the other (IAH group, n = 60) with increased IAP values. Deceased patients were specially analyzed within the IAH group in order to determine mortality predictors. Statistical significance of IAP (P = 0.048), lactates (P = 0.048), peak pressure (P = 0.043), abdominal perfusion pressure (P = 0.05), and mean arterial pressure (P = 0.041) was greater for deceased than for surviving patients in the IAH group. High mortality appears for patients younger than 65 years old, with lactate level higher than 3.22 mmol/L and filtration gradient (GF) lower than 67 mmHg. Age, lactates, GF, and APACHE II score are determined as mortality predictors for patients suffering from acute pancreatitis who developed IAH. The mortality rate is higher when the level of GF is decreasing and the level of lactate increasing.

Background: Patients with acute pancreatitis develop numerous complications and organ damage due to increased intra-abdominal pressure (IAP). These extrapancreatic complications determine the clinical outcome of the disease. Materials and methods: A total of 100 patients with acute pancreatitis were included in the prospective cohort study. Observed patients were divided into two groups according to their mean values of IAP (normal IAP values and elevated IAP values), which were compared with examined variables. Patients with intra-abdominal hypertension (IAH) were divided into four groups by IAP values, and those groups of patients were also compared with the examined variables. Results: Differences between body mass index (BMI) (p = 0.001), lactates (p = 0.006), and the Sequential Organ Failure Assessment (SOFA) score (p = 0.001) were statistically significant within all examined IAH groups. Differences between the mean arterial pressure (MAP) (p = 0.012) and filtration gradient (FG) (p < 0.001) were statistically significant between the first and second IAH groups in relation to the fourth. Differences in diuresis per hour (p = 0.022) showed statistical significance in relation to the first and third groups of IAH patients. Conclusions: Changes in IAP values lead to changes in basic vital parameters MAP, APP, FG, diuresis per hour, and lactate levels in patients with acute pancreatitis. Early recognition of changes in the SOFA score accompanying an increase in the IAP value is essential.

Personalized anesthesia has emerged as a key direction in modern perioperative medicine, driven by advances in molecular biology, analytical technologies, and digital monitoring. Traditional physiological parameters often fail to detect early stages of organ dysfunction, whereas molecular biomarkers provide earlier and more sensitive insight into inflammation, oxidative stress, neurotoxicity, and renal or hepatic injury. Inflammatory markers such as IL-6, CRP, and PCT indicate early immune activation, while oxidative stress biomarkers, including 8-isoprostanes and malondialdehyde, quantify metabolic imbalance and ischemia–reperfusion injury. Neurotoxicity biomarkers such as S100β, NSE, and GFAP allow early detection of subclinical cerebral injury, whereas kynurenine-pathway metabolites reflect neuroinflammation and the risk of postoperative cognitive dysfunction. Renal biomarkers such as NGAL, KIM-1, and cystatin C detect acute kidney injury significantly earlier than creatinine, and miR-122 holds strong potential as an early marker of hepatocellular injury. Genetic and epigenetic biomarkers—including polymorphisms in CYP2D6, CYP3A4/5, RYR1, OPRM1, and COMT, as well as microRNA-based signatures—enable individualized drug dosing and optimization of anesthetic strategies. Meanwhile, digital biomarkers such as EEG-derived indices, HRV, and NIRS provide continuous real-time physiological monitoring and can integrate with AI-based algorithms for predictive, adaptive anesthesia management. Although no single biomarker meets all criteria for an ideal clinical indicator, combining molecular, genetic, and digital biomarkers represents the most promising pathway toward fully personalized, safe, and outcome-optimized perioperative care.

Introduction. Diabetes mellitus patients represent vulnerable group of people who are prone to getting infected with severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). The virus has a high binding affinity to angiotensin-converting enzyme 2 receptor which allows efficient host cell entering, prolonged virus retention and possibility of insulin resistance and ketoacidosis development. Case outline. We describe a case of a 20-year-old patient with a past medical history of type-1 diabetes mellitus who presented with bilateral COVID-19 pneumonia. Initially treatment with polyvitamin therapy, corticosteroids, tocilizumab and convalescent plasma did not improve the patient condition, but might have led to the worsening of underlying disease, high blood glucose level and ketoacidosis. Patient developed a rapid progression of the disease and severe pneumonia that required intubation and mechanical ventilation. Intravenous immunoglobulin (IVIg) has been administrated in order to suppress a hyperactive immune response through its immunomodulatory effect. Forty-eight hours later respiratory gas exchange had been improved, almost complete regression of changes in the lungs have been seen, normalization of metabolic and gas exchange parameters have been detected. After 14 days in the hospital the patient was discharged home in good general condition. Conclusion. COVID-19 complicated by diabetes mellitus leads to a poor outcome of the disease, but antiviral and anti-inflammatory activity of IVIg suggests that they may be useful therapeutic agent and in the case of COVID-19. In the presented case, the application of IVIg very fast led to an improvement in the patient’s condition.