Vol 17, No 2 (2025)

Myocardial bridges represent segments of coronary arteries partially covered by myocardial muscle fibers. Although myocardial bridges were previously thought to be rare, recent studies indicate an increase in their prevalence, which has been associated with acute coronary syndromes, arrhythmias, myocardial infarction, and even sudden cardiac death. Some authors suggest that myocardial bridges may contribute to the formation of atherosclerotic plaques in the proximal part of the coronary arteries. Autopsy findings also demonstrate increased atherosclerotic plaque formation at sites of arterial obliteration, suggesting a shared pathogenic mechanism in the intima-media layer.

This review summarizes current knowledge regarding the role of myocardial bridges in vascular remodeling and atherosclerosis progression, while identifying gaps requiring further investigation.

The authors conducted a search of publications in the electronic databases PubMed, Google Scholar, and eLibrary using the following keywords: “atherosclerosis and myocardial bridges”, “myocardial bridges and cardiovascular diseases”, “pathophysiology of myocardial bridges”, “visualization of the cardiovascular system”, “myocardial bridges”. All works published between 1951 and 2024 were included.

The obstructive mechanism involves compression of the intramural segment of the coronary artery by myocardial tissue during systole. Hemodynamic conditions created by myocardial bridges typically feature elevated wall shear stress due to the narrowing of the arterial lumen during systole, thereby minimizing plaque formation within the bridge itself. However, proximal to the myocardial bridges, wall shear stress decreases, creating favorable conditions for atherosclerotic plaque development.

Myocardial bridges influence the thickness of the intima and the area of the arterial lumen, as well as the segments located proximally and distally. The location, thickness, and length of myocardial bridges directly affect the degree of obstruction and intimal hypertrophy. Vascular remodeling under mechanical forces plays a crucial role in maintaining vessel function, and its disruption can lead to cardiovascular disease.

Patients with rheumatic diseases exhibit a markedly increased risk of developing and accelerating cardiovascular pathology, which is largely attributed to the significant role of chronic inflammation as one of the etiological factors in both atherogenesis and heart failure. Achieving sustained clinical and laboratory remission of the Immune-mediated inflammatory disease has been shown to reduce the risk of cardiovascular complications. Given the direct association between persistent inflammation and a wide range of comorbid conditions, this factor must be carefully considered when planning and implementing rational pharmacotherapy in multimorbid patients.

It is well established that pharmacological agents used in rheumatology exert diverse effects on the cardiovascular system. Over the past decade, growing research interest has been directed toward the potential application of anti-inflammatory agents with different mechanisms of action for both the prevention and treatment of atherosclerosis and ischemic heart disease. Particular attention has been paid to the modulation of the “NLRP3 inflammasome – interleukin-1 – interleukin-6 – C-reactive protein” signaling pathway. According to several studies, inhibition of this cascade may contribute to reduced likelihood of cardiovascular events.

This review summarizes current data on the effects of various classes of antirheumatic drugs on the cardiovascular system, including both their beneficial and adverse effects.

BACKGROUND: Cerebral venous thrombosis is a multifactorial and difficult-to-diagnose disease, complicated by venous stroke, intracerebral hemorrhage, progressive cerebral edema, dislocation syndrome, and even death. The broad variability of clinical symptoms and lack of pathognomonic manifestations complicate timely diagnosis of cerebral venous thrombosis.

AIM: To identify significant risk factors for cerebral venous thrombosis and to evaluate the dynamics of neuroimaging findings at 1, 3, and 6 months after cerebral venous thrombosis onset in young and middle-aged patients with a history of COVID-19, comparing outcomes between those treated with direct oral anticoagulants (DOACs) and vitamin K antagonists (VKAs).

METHODS: Young and middle-aged patients with a history of novel coronavirus infection (COVID-19) were examined and divided into two groups depending on the presence or absence of cerebral venous thrombosis. The main risk factors, structural features of the major arteries and cerebral venous sinuses, as well as the course of cerebral venous and sinus thrombosis during anticoagulant therapy (with direct oral anticoagulants and vitamin K antagonists) at 1, 3, and 6 months after the development of cerebral venous thrombosis were analyzed.

RESULTS: We examined 120 young and middle-aged patients with COVID-19 divided into 2 groups: Group I – 70 patients who developed cerebral venous thrombosis during COVID-19 – 21 (30%) men and 49 (70%) women; Group II – 50 patients who had COVID-19 without cerebral venous thrombosis development – 27 (54%) men and 23 (46%) women. The main risk factor for developing cerebral venous thrombosis among women in the first group (with cerebral venous thrombosis during COVID-19) compared to the second group (patients who had COVID-19 without developing cerebral venous thrombosis) was the use of combined oral contraceptives: 22.9% and 4.0%, respectively (р = 0.001). Among group I patients, 32 (45.7%) cases of cerebral venous thrombosis were accompanied by the development of venous stroke: ischemic in 13 (18.6%) patients, hemorrhagic in 7 (10%), mixed (ischemic stroke with hemorrhagic infiltration) in 12 (17.1%) patients. In a comparative analysis of the variants of the structure of the cerebral arteries (absence of the posterior communicating arteries, pathological tortuosity of the internal carotid artery [ICA], trifurcation of the ICA, open arterial circle of Willis) and venous sinuses (presence of hypo-/aplasia), no statistically significant difference was detected. The analysis of the course of cerebral venous thrombosis during treatment with vitamin K antagonists (warfarin) and direct oral anticoagulants in 53 patients with cerebral venous thrombosis (age 41 ± 12 years) at 1,3, and 6 months after the development of cerebral venous thrombosis onset showed that with anticoagulants, recanalization was observed in 44 (83%) patients: complete – in 21 patients (47.7%), partial – in 23 (52.3%). Recanalization was absent in 9 (17.0%) cases. No recurrent cerebral venous thrombosis cases were observed among the study patients.

CONCLUSION: Verification of cerebral venous thrombosis in the context of COVID-19 necessitates a detailed examination of risk factors, patient history, assessment of clinical manifestations, and comprehensive implementation of laboratory and instrumental, as well as neuroimaging diagnostic methods. Timely verification and immediate initiation of anticoagulant therapy ensure a relatively favorable prognosis for the disease course.

BACKGROUND: The selection of surgical strategies for large adrenal tumors remains clinically critical. For determining eligibility for endoscopic video-assisted surgery, the absence of malignancy features is essential. Steroid metabolome analysis by gas chromatography-mass spectrometry (GC-MS) provides the highest diagnostic yield for detecting early signs of malignancy during preoperative evaluation and, according to multiple studies, exceeds the accuracy of radiologic imaging techniques.

AIM: To evaluate the clinical utility of urine steroid profiling by GC-MS for preoperative diagnosis and surgical decision-making in large malignant adrenocortical neoplasms.

METHODS: Patients with adrenal tumors larger than 50 mm and without clinical or laboratory signs of hypercortisolism were examined. Based on histological analysis, the following diagnoses were established: adrenocortical carcinoma, adrenocortical adenoma (with malignancy grade assessed using the L.M. Weiss scoring system), and rare adrenal diseases (schwannoma, ganglioneuroma, myelolipoma, etc.). Patients with adrenocortical adenomas smaller than 50 mm served as the control group. Urinary steroid profiles were analyzed by gas chromatography-mass spectrometry in all patients before surgical treatment. The Mann-Whitney U test was used for comparison of urinary steroid excretion.

RESULTS: According to gas chromatography-mass spectrometry (GC-MS), 23 patients (33.8%) with adrenal tumors >50 mm exhibited biochemical features of adrenocortical carcinoma (ACC) prior to surgery, which was later confirmed histologically. In patients with adrenocortical adenoma and a malignancy score of 2 on the L.M. Weiss scale (n = 16, 23.5%), urinary excretion of tetrahydro-11-deoxycortisol, androgens, progestogens, and mineralocorticoids was significantly higher than in patients with adrenocortical adenoma lacking malignant features (n = 14) and the control group (n = 30). No statistically significant differences were observed in the urinary excretion of 9 ACC biomarkers compared to patients with confirmed ACC. Open adrenalectomy was recommended for patients with large adrenal tumors and GC-MS evidence of malignancy.

CONCLUSION: Preoperative GC-MS detection of early malignant features in large adrenal tumors is critical for determining the optimal surgical approach. Minimally invasive adrenalectomy is not recommended for large adrenal lesions with GC-MS signs of malignancy.

BACKGROUND: Advanced ankylosing spondylitis can be characterized by the formation of disabling spinal deformities. However, the effect of cervicothoracic kyphosis on the cardiovascular system is poorly understood. In routine rheumatology practice, the occiput-to-wall distance is used as a reliable method to confirm the presence of kyphosis in patients.

AIM: To assess the association between kyphosis (measured by occiput-to-wall distance, the occiput-to-wall distance) and the development of comorbidities in patients with late-stage ankylosing spondylitis.

METHODS: The study included men with advanced-stage ankylosing spondylitis. As part of the standard assessment of the primary disease, clinical and laboratory examinations were performed, including additional measurement of myostatin levels. Cardiovascular status was also evaluated using echocardiography and ultrasound examination of the brachiocephalic arteries.

RESULTS: Forty men (33 to 67 years old) with advanced ankylosing spondylitis participated in the study. All patients were divided into 2 groups: 1) with the occiput-to-wall distance < 10 cm (n = 45%), 2) with the occiput-to-wall distance ≥ 10 cm (n = 55%). The analysis of cardiovascular system status showed that all patients in the occiput-to-wall distance ≥ 10 cm group had hypertension (100% vs 66.7%, p = 0.005) with predominance of grade 2 arterial hypertension (45.5% vs 27.8%, p = 0.010) in contrast to the occiput-to-wall distance ≥ 10 cm group. Echocardiography revealed statistically significant reductions in left ventricular function values in the occiput-to-wall distance ≥ 10 cm group compared to the occiput-to-wall distance < 10 cm group. Notably, the occiput-to-wall distance ≥ 10 cm group was more frequently overweight (86.23 ± 14.03 vs. 74.83 ± 14.44, p = 0.016) with a predominance of class I–II obesity (45.5% vs. 11.1%, p < 0.001). Also in our patients we found a correlation between serum myostatin level and the occiput-to-wall distance (r = 0.404, p = 0.01), ASDAS (Axial Spondyloarthritis Disease Activity Score; r = 0.405, p = 0.009) and BASFI (Bath Ankylosing Spondylitis Functional Index; r = 0.344, p = 0.03).

CONCLUSION: The occiput-to-wall distance increase should be considered as a predictor of the development of cardiovascular pathology, which is confirmed by echo-CG, and other comorbidities. Patients with progressive cervicothoracic kyphosis are characterised by lower values of left ventricular ejection fraction, which may be due to adaptation mechanisms caused by spinal axis displacement. In the future, myostatin measurements should be considered as a complementary method for assessing the function of the cardiovascular system and skeletal muscles.

BACKGROUND: Against the background of significant achievements in the treatment and prevention of various diseases, the direction of “medicine for the healthy” currently does not adequately meet the public demand for active longevity. Developing age assessment systems (epigenetic, biochemical and other “clocks”) allow us to get closer to the assessment of biological age, which is an important step towards finding technologies that can slow down aging.

AIM: To identify the relationship between clinical characteristics, phenotypic age and genetic factors in a cohort of people without clinically significant pathology who lead a healthy lifestyle.

METHODS: A single-center, cross-sectional study was conducted. A retrospective analysis of clinical, laboratory and instrumental examination results of participants in wellness programs at the “First Line” preventive medicine resort was performed. Genetic polymorphism was determined using commercially developed biochip technology. Gene polymorphisms (222 single nucleotide variants) potentially associated with cardiometabolic risks according to published scientific data were analyzed.

RESULTS: In a cohort of 29 patients aged 27 to 68 years, 14 single nucleotide variants were identified, associated with changes in systolic (rs6920220 of the TNFAIP3 gene, rs1137101 of the LEPR gene) and diastolic (rs1137101 of the LEPR gene, rs7903146 of the TCF7L2 gene, rs12255372 of the TCF7L2 gene) blood pressure, dyslipidemia (rs266729 of the ADIPOQ gene, rs1045642 of the ABCB1 gene, rs1815739 of the ACTN3 gene), increased body weight (rs4961 of the ADD1 gene), as well as with decreased phenotypic age (rs17553719 of the AQP3 gene, rs1801197 of the CALCR gene, rs2470152 of the CYP19A1 gene, rs1800955 of the DRD4 gene, rs17782313 of the MC4R gene). Most of these associations have not been previously studied or have been reported in only a few publications.

CONCLUSION: The assessment of the influence of a wide range of genetic polymorphisms seems to be a promising direction for the future choice of effective strategies for prolonging life in the absence of diseases. The success of new technologies and methods to slow down aging largely depends on the introduction of a multidisciplinary approach that combines various fields: clinical, genetic, “multi-omic” (including metabolomic), microbiomic, immune, psychological and others.

This article presents two clinical observations of successful treatment of victims with closed abdominal trauma complicated by duodenal injury, with an emphasis on key aspects of treatment and prevention of complications.

Injuries to internal organs in closed abdominal trauma pose a serious threat to the lives of victims, especially in cases of damage to the duodenum. Despite the fact that duodenum injuries constitute a relatively small proportion of all abdominal injuries, they are accompanied by a high mortality rate, reaching 30% in isolated injuries and up to 80% in combined injuries. Diagnosis of such injuries is a particular problem. The absence of pathognomonic symptoms, as well as the frequent combination with other injuries (e.g., pancreas, retroperitoneal hematomas, or pelvic fractures) complicates the timely detection of these injuries. In addition, inadequate surgical tactics can lead to severe postoperative complications, including duodenal fistula (2%–16%), intra-abdominal abscess (15%), and pancreatitis (0.5%). The high incidence of severe complications and significant mortality emphasizes the importance of studying effective diagnostic methods, surgical tactics, and postoperative management of patients with duodenal injury.

According to the literature, the incidence of duodenal injury in closed abdominal trauma ranges from 0.6 to 5% of all abdominal injuries. The most common injuries are to the retroperitoneal part of the intestine; the horizontal part is injured in 30%–40% of cases, the descending part in 20%–30%, and the upper part in 15%–22%. A significant problem is the recognition of retroperitoneal ruptures in combination with pancreatic injury and the presence of retroperitoneal hematomas caused by kidney injury or pelvic bone fracture. There are no pathognomonic symptoms of duodenal injury.