Sleep deprivation is a significant risk factor for cardiovascular diseases and has a systemic effect on the body through a complex set of pathogenetic mechanisms. It is known that both acute and chronic sleep deprivation disrupts the autonomic nervous system, increasing sympathetic activity and raising blood pressure and heart rate. Endothelial dysfunction plays a significant role by reducing the bioavailability of nitric oxide and activating adhesion molecules thereby contributing to the development of atherosclerosis and hypercoagulation. We analyzed research papers published in the PubMed, Semantic Scholar, and Cochrane Library databases between 2014 and 2025 using the keywords «sleep deprivation», «endothelium», «vessels», and «cardiovascular disorders». This article highlights modern views on the mechanisms of the negative effect of sleep deprivation on the cardiovascular system. It also presents the results of experimental and clinical studies on the effect of various types of sleep restriction on the functional, biochemical, and morphological parameters of the cardiovascular system, including the endothelium.

   The need for coronary artery recanalization in the first 12 hours after myocardial infarction (MI) is undisputed, but treatment strategies later have not been defined. There are radically different opinions, ranging from a complete rejection of the need for myocardial revascularization (the impossibility of restoring nonviable myocardium) to the need for coronary artery recanalization when technically feasible (three arteries are better than two). Most specialists allow recanalization to be performed if there is sufficient volume of viable myocardium remaining in the coronary occlusion basin and the ability to re-engage the hibernated myocardium. Existing methods for preoperative differential diagnosis of myocardial hypometabolic status from irreversible changes (angiographic criteria, stress tests, ultrasound diagnostics, single-photon emission computed tomography (SPECT), positron emission tomography (PET) with fluorodeoxyglucose (FDG), magnetic resonance imaging (MRI)) have good sensitivity, but, in some cases, they have low specificity. In our opinion, this is due to the fact that most of these methods are based on residual collateral blood flow, the timing and extent of which are poorly understood. Given the low sensitivity and specificity of the angiographic criterion of myocardial non-viability in the first 6 months after coronary occlusion, it is advisable to use it at later stages.

   Introduction. The role of endothelial dysfunction (ED) in the pathogenesis of spinal cord infarction (SCInf, vascular myelopathy), unlike cerebral stroke, has been insufficiently studied. There is a lack of data on the comprehensive profile of endothelial biomarkers in this pathology.

   Objective. To study laboratory parameters reflecting various aspects of endothelial activity in patients with vascular myelopathy, including those at different periods of the disease and with different functional outcomes.

   Materials and Methods. The study included 177 patients: 77 with verified SCInf (main group) and 100 with non-ischemic myelopathies (comparison group). Serum concentrations of endothelin-1 (ET-1), tissue plasminogen activator (tPA), soluble vascular cell adhesion molecule-1 (sVCAM-1), basic fibroblast growth factor (bFGF), transforming growth factor β1 (TGF-β1), vascular endothelial growth factor A (VEGF-A), and tissue inhibitor of metalloproteinases-1 (TIMP-1) were determined using enzyme-linked immunosorbent assay. The disease outcome was assessed using the modified Rankin Scale.

   Results. Levels of ET-1, tPA, sVCAM-1, bFGF, VEGF-A, and TIMP-1 were significantly higher in patients with SCInf than in the comparison group (p < 0.0001). The level of TGF-β1 did not differ significantly between groups (p = 0.352). The tPA level peaked in the subacute period of vascular myelopathy (p = 0.012), while the other markers remained stably elevated at all-time points of the disease. The concentrations of the studied biomarkers did not differ between patients with favorable and unfavorable functional outcomes of SCInf (p > 0.05 for all comparisons).

   Conclusion. SCInf is associated with complex and persistent ED, which has a distinct pathogenetic profile. The identified ED markers are not independent predictors of neurological recovery.

   Introduction. Inflammation is one of the leading components in the pathogenesis of acute lower limb ischemia (ALLI). Interleukin-18 (IL-18), a pleiotropic proinflammatory cytokine that regulates innate and adaptive immune responses, plays a significant role in the development of chronic inflammation in atherosclerosis, creating the prerequisites for the development of ALLI. Increased IL-18 production causes autoinflammation, destabilization of atherosclerotic plaques, development of thrombosis and ALLI.

   Objective. To study the contribution of interleukin-18 during ALLI, its relationship with markers of inflammation, lipid metabolism, tissue destruction and endothelial dysfunction.

   Materials and Methods. 71 patients with ALLI and basic therapy aged 70 (60; 83) years and 15 patients aged 75 (77; 88) years with vasaprostan therapy were examined in the Department of Vascular Surgery of the I. I. Dzhanelidze Research Institute of Emergency Care. The comparison group consisted of volunteers of the same age. On admission to the department before surgery, on days 1 and 10 after reconstructive surgery the following blood levels were examined: cytokines IL-6, IL-10, IL-18, C-reactive protein; tissue damage factors (creatine kinase, myoglobin) and endothelial dysfunction factor (homocysteine), glucose, total protein, and blood lipids.

   Results. After surgery, an increase in C-reactive protein and inflammatory cytokines, as well as signs of energy deficiency (hyperglycemia, hypopoproteinemia, and hypolipidemia) was observed. An increase in creatine kinase activity, myoglobin and homocysteine levels was more pronounced in deceased patients. The use of vasaprostan reduces inflammatory markers
compared to baseline therapy.

   Conclusion. IL-18 plays a significant role in the development of inflammation in ALLI. Vasaprostan therapy reduces C-reactive protein levels, inflammatory cytokines, and systemic inflammation and can be recommended for the treatment of ALLI.

   Introduction. The coexistence of infrarenal abdominal aortic aneurysm with occlusive–stenotic disease of the iliac–femoral segment significantly complicates the choice of optimal surgical strategy. Despite advances in endovascular techniques, open surgical repair remains the treatment of choice in a substantial proportion of patients. However, the impact of concomitant iliac–femoral arterial disease on early and long-term outcomes of such interventions remains controversial.

   Aim. To analyze and compare early and long-term (up to 15 years) outcomes of open surgical treatment in patients with infrarenal abdominal aortic aneurysms with and without hemodynamically significant iliac–femoral arterial disease.

   Materials and Methods. This retrospective study included 272 patients who underwent elective resection of an infrarenal abdominal aortic aneurysm with aorto-bifemoral bypass grafting at Saint Petersburg City Multidisciplinary Hospital No. 2 between 1997 and 2022. Depending on the condition of the iliac–femoral segment, patients were divided into two groups: Group 1 patients with occlusive–stenotic disease of the iliac–femoral segment (n = 107), and Group 2 patients without such disease (n = 165). We analyzed hospital mortality, early postoperative complications, rate of re-interventions, primary patency of the reconstructed segment, amputations, and overall survival. Long-term outcomes were available for 112 patients.

   Results. Overall hospital mortality was 4 % and did not differ significantly between the groups (p > 0.05). In the early postoperative period, patients with iliac–femoral arterial disease more frequently developed graft limb and lower-extremity arterial thrombosis, acute renal failure, and required repeat surgical interventions (p < 0.05). In the long-term follow-up, Group 1 demonstrated lower primary patency rates, higher rates of re-interventions, and a greater incidence of amputations (p<0.05). Cumulative overall survival did not differ significantly between the groups (p > 0.05).

   Conclusions. The presence of occlusive-stenotic disease of the iliac-femoral segment in patients with infrarenal abdominal aortic aneurysm significantly worsens both early and long-term outcomes of open surgical repair, increasing the incidence of early postoperative complications, re-interventions, and amputations. At the same time, overall survival remains comparable between groups, supporting the role of open reconstruction as a justified treatment option in this patient population. The findings emphasize the need for an individualized surgical approach and lifelong follow-up with active secondary prevention of atherosclerosis.

   Introduction. Early detection of left ventricle systolic dysfunction in patients with arterial hypertension allows timely initiation of measures to achieve reverse heart remodeling and heart failure prevention.

   Aim. To identify patterns of changes in left ventricular global longitudinal strain (GLS) at rest and during exercise in individuals with arterial hypertension (AH).

   Materials and Methods. The study involved 105 men with AH, divided into two groups based on the presence or absence of left ventricular hypertrophy (LVH) according to transthoracic echocardiography. The control group consisted of 52 apparently healthy individuals. All patients underwent stress echocardiography using a standard protocol, assessing left ventricular lon-gitudinal strain both at baseline and during exercise.

   Results. Left ventricular G LS values in the control group and in patients with hypertension before exercise did not differ significantly. During exercise, healthy individuals experienced significant increases in longitudinal strain in all segments, resulting in a statistically significant increase in GLS. In the hypertensive groups, longitudinal strain values increased exclusively in the apical segments during exercise. In hypertensive patients without LVH, this resulted in an increase in left ventricular GLS, while in hypertensive patients with LVH, this phenomenon did not lead to an increase in GLS.

   Conclusion. Healthy LV myocardium responds to physical exertion with a significant increase in deformation of all its segments, along with an increase in GLS. Patients with hypertension exhibit subclinical impairment of left ventricular pumping function, manifested during physical exertion by increased deformation only in the apical segments, with no significant changes in the remaining segments. In patients with hypertension without LVH, this response leads to an increase in GLS, while in patients with hypertension and LVH, increased deformation of the apical segments does not result in a significant increase in GLS, indicating a decrease in myocardial contractile reserve.

   Introduction. Reconstructive surgery of small-diameter vessels remains an urgent task due to the limitations of autovenous grafts and problems with nonresorbable synthetic prostheses, especially in pediatric surgery, where the need for repeated operations is high. Polylactide prostheses represent a promising bioresorbable alternative with thromboresistance and stimulation of tissue regeneration.

   Objective. To evaluate the efficacy and safety of poly(L-lactide) tissue-engineered vascular prostheses of small diameter in an experiment on rats, including mechanical properties, biocompatibility and risks of complications.

   Materials and Methods. This study used 50 male Wistar rats with polylactide prostheses implanted in the infrarenal aorta. The surgical technique included median laparotomy and end-to-end anastomoses. The condition of the prostheses was monitored by ultrasound angioscanning, multispiral computed tomography angiography, histological and immunohistochemical analysis at 4, 12, 24 and 48 weeks.

   Results. During the 48-week follow-up, the animals showed no signs of impaired blood flow and trophic changes. The diameter of the prostheses remained stable, and the histological examination data showed the formation of a neointima. Vascular patency with polylactide prostheses was 83 %, while thrombosis occurred in 17 % of cases. However, 53 % of the animals had prosthetic aneurysms in the anastomosis areas.

   Conclusion. Poly(L)-lactide prostheses have bioresorbability, thromboresistance and optimal mechanical properties, which makes them promising for vascular reconstructive surgery. At the same time, the high risk of aneurysms in the area of anastomoses requires further research and improvement of implantation materials and techniques.

   Introduction. Vitamin D deficiency is associated with many chronic diseases, especially cardiovascular diseases. It has been associated with the severity of coronary atherosclerosis and the risk of myocardial infarction (MI). There is no consensus on the role of hypervitaminosis D in the development and progression of coronary heart disease and heart failure. In this regard, it is important to study echocardiographic and morphological changes in the myocardium in rats with hypervitaminosis D, who underwent MI.

   Aim. To study echocardiographic and morphological parameters of postinfarction myocardial remodeling in rats with hypervitaminosis D.

   Materials and methods. The animals were divided into 3 groups: Group 1 (comparison group), Group 2 (those who received 300 IU of cholecalciferol per os), and Group 3 (those who received 1,500 IU of cholecalciferol for 21 days after MI modeling). Echocardiography was performed using a MyLabTouchSL 3116 ultrasound machine. Histological examination determined the scar size and the severity of myocardial remodeling.

   Results. Serum 25(OH)D concentration in rats from group 1 (n = 5) was 57.05 ± 1.37 nmol/l, in group 2 (n = 5) – 150.96 ± 4.93 nmol/l, in group 3 (n = 5) exceeded the laboratory limits (> 300 nmol/l) (p = 0.001 for all groups). Cholecalciferol therapy at a dosage of 300 IU was accompanied by a decrease in heart rate (HR) in group 2 compared to group 1 (p = 0.02). HR in group 3 was higher compared to groups 1 and 2 (p < 0.05). The end-diastolic size (EDS) and end-systolic size (ESS) were larger, while the shortening fraction (SF) and the left ventricular ejection fraction (LVEF) were less in animals from group 3 than in groups 1 and 2 (p < 0.05). Rats from groups 1 and 3 had higher ESD and ESS and lower SF and LVEF compared to group 2 (p < 0.05). The largest scar area and length was in group 3 than in the other groups (p < 0.05). The hypertrophy index and dilation indices were higher, and the scar wall thickness was lower in group 3 than in group 2 (p < 0.05).

   Conclusions. Post-infarction administration of vitamin D at a dosage of 1,500 IU for 21 days worsened echocardiographic and morphometric parameters, whereas the dosage of 300 IU improved them.

   Introduction. Chronic inflammation (CI) leads to encephalopathies, destabilization of cognitive abilities and psychoemotional state. The functioning of neurons depends on cerebral blood flow, which is regulated by changes in arterial diameter. Arterial reactivity is largely determined by the functioning of K_ATP channels, which can worsen in CI under the influence of
pro-inflammatory cytokines and free radicals.

   Aim. To study the contribution of K_ATP channels to the dilation of rat cerebral arteries during the development of chronic inflammation.

   Materials and Methods. In pial arteries of Wistar rats 3 months after cecal ligation and puncture (a model of CI), the following were performed: investigation of the dilatory response of arteries of different diameters to acetylcholine (ACh) and sodium nitroprusside (NP) before and after blockade of K_ATP channels with glibenclamide (GB); assessment of the contribution of K_ATP channels to the formation of vascular tone based on the number of arteries that constricted in response to the blocker GB and dilating in response to the activator pinacidil (PI).

   Results. In CI, the number of dilations in response to ACh decreased by 1.4–3.4 times in arteries with a diameter less than 40 µm and by 1.7–1.9 times in larger vessels compared to the control. Under the influence of NP, CI rats showed 1.6–1.7 times fewer dilations in large and 1.5 times fewer in small pial arteries compared to the control. In the control group, the number of dilations to ACh when co-applied with GB decreased by 2.2–3.4 times compared to the response to ACh alone, and for NP by 2.5–3 times. In the CI group, blockade of KATP channels did not significantly reduce the number of dilated arteries either in response to ACh or to NP. The contribution of KATP channels in large cerebral arteries to the formation of tone in large pial arteries during CI did not change compared to the control, while in small arteries it slightly decreased.

   Conclusion. In rats, the development of chronic inflammation led to a significant impairment of pial artery dilation. Unlike in controls, KATP channels of smooth muscle cells of animals with CI do not participate in the formation of the dilatory response of these vessels, although the contribution of K_ATP channels to maintaining vascular tone was preserved in large arteries and slightly reduced in small ones.

   Introduction. CD68 is a glycoprotein from the family of lysosome-associated membrane proteins. The study of CD68-immunopositive structures in the rat brain’s pineal gland is of particular interest because data on the role of CD68-immunopositive cells and their presence in this neuroendocrine organ, which regulates the body’s circadian rhythm, are contradictory, and the interpretation of their functional role is ambiguous.

   The aim of this study was to identify the most convenient method for immunocytochemical visualization of CD68-immunopositive objects in the rat pineal gland and to determine the localization of the identified structures.

   Materials and Methods. The brain of mature male Wistar rats (n=8) was used for the study. Three primary antibody variants were used: monoclonal antibodies ED1 and KP1 and polyclonal antibodies to CD68.

   Results. The use of monoclonal antibodies KP1 revealed the absence of an immunohistochemical reaction in the rat brain; however, they showed immunoreactivity with the control (human cerebral cortex). Monoclonal antibodies ED1 revealed granules of approximately 0.2 μm in size in the rat pineal gland, forming a dense network in the pineal parenchyma. Granules ranging from 0.3 μm to 2.5 μm in size are located near blood vessels. The granules are primarily located in the central part of the pineal gland; however, their mesh-like distribution limits the ability to characterize the cells themselves. The product of an immunohistochemical reaction using polyclonal antibodies to CD68 is localized discretely throughout the pineal gland as individual granules and their clusters. Granule size ranges from less than 0.2 μm to 4.5 μm, which is comparatively larger than in the case of monoclonal antibodies ED1. The granules are also predominantly located along the vessels.

   Conclusion. Thus, polyclonal antibodies to CD68 are most suitable for detecting macrophages in the rat pineal gland. Clone ED1 yields inconclusive results, and clone KP1 is unsuitable for this purpose. Perivascular localization of cells and granules was detected, indicating that they belong to perivascular macrophages. However, further studies are needed to precisely determine their cellular identity.

   Introduction. Recanalization of a previously ligated patent ductus arteriosus (PDA), followed by the development of a pulmonary trunk aneurysm and its rupture in middle-aged adulthood, represents a rare clinical observation accompanied by significant diagnostic and therapeutic challenges in the management of such cases in adults.

   The aim of this publication is to present a clinical case of recanalization of a previously ligated patent ductus arteriosus complicated by irreversible pulmonary hypertension, aneurysm, and rupture of the pulmonary trunk.

   Case report. A 41-year-old female patient, who had undergone ligation of a patent ductus arteriosus via left-sided thoracotomy at the age of 5 years, had been under follow-up since 2018 for progressive dyspnea and syncopal episodes. Diagnostic work-up confirmed a recanalized ductus arteriosus and an aneurysm of the pulmonary trunk in the setting of pre-capillary pulmonary hypertension. The patient received specific conservative (pulmonary vasodilator) therapy. In May 2023, rupture of the pulmonary trunk aneurysm occurred, resulting in cardiac tamponade and a fatal outcome.

   Conclusion. This observation demonstrates the unfavorable prognosis of a conservative management strategy in cases of recanalized patent ductus arteriosus complicated by pulmonary trunk aneurysm and supports the rationale for early surgical or endovascular correction prior to the development of irreversible changes in the pulmonary vasculature.

   Objective. To present a clinical case of successful management of severe stage III secondary lower limb lymphedema that developed after radical abdominal trachelectomy for stage IIIB cervical cancer in a patient with morbid obesity (BMI = 42,06) and recurrent episodes of erysipelas.

   Materials and Methods. An intensive 15-day course of Complete Decongestive Therapy (CDT) was administered, including manual lymphatic drainage; multilayer bandaging, and skin care education, combined with micronized purified flavonoid fraction (MPFF, 1000 mg/day). Treatment efficacy was assessed through daily circumference measurements at seven standardized points, volumetric calculation using the truncated cone method, quality of life evaluation via the LYMQOL scale, and statistical modeling of treatment dynamics (linear regression, Pearson correlation coefficient).

   Results. The volume of the left lower limb decreased from 10.84 L to 6.22 L (–42.7 %) over 15 days. The greatest reduction occurred in the thigh region (point E): from 93.0 cm to 50.5 cm (Δ = – 42.5 cm). A strong negative correlation was observed between treatment day and limb circumference (r = –0.972, p < 0.0001). Quality of life improved significantly: physical domain
scores increased from 28 to 58, and psychosocial domain scores from 35 to 62. Thirty days after completing the intensive phase, limb volumes remained stable under maintenance therapy.

   Conclusion. Even in the presence of highly unfavorable factors (such as morbid obesity, recurrent erysipelas, and delayed presentation), significant edema regression and quality-of-life restoration are achievable through individualized CDT combined with MPFF. This case underscores the importance of quantitative outcome assessment and demonstrates the potential of a comprehensive approach in managing complex forms of lymphedema.