Background:The palmaris longus muscle is one of the most variable muscles in the human body and there have been numerous variations reported. The different palmaris longus variations are interesting not only from an anatomical point of view, but they could also have definite clinical significance.Aim:The aim of this study was to examine the different types of variations of palmaris longus muscle in the Bulgarian population.Materials and methods:Over a period of 15 years, 56 formol–carbol fixed human cadavers were studied to investigate the different variations of palmaris longus muscle (PLM).Results:Various anatomical variations of PLM have been reported: absence (2.68%); reversed palmaris longus coexisting with an additional abductor digiti minimi muscle (0.89%); digastric (0.89%); palmaris longus with intermediate muscle belly (1.79%) and duplication (1.79%).Conclusions:To reveal the wide variety of the types of palmaris longus muscle and their importance for clinical practice, we make a brief literature review concerning the different types of variations, their role in the median and ulnar neuropathy in the wrist or as structures simulating a soft tissue tumour and the application of palmaris longus tendon in plastic and reconstructive surgery as grafting material. We also present new systematic anatomical and clinical classifications of palmaris longus variations by dividing them into two simple groups.

Hypertension-induced cardiac remodeling is a complex process driven by interconnected molecular and cellular mechanisms that culminate in hypertensive myocardium, characterized by ventricular hypertrophy, fibrosis, impaired angiogenesis, and myocardial dysfunction. This review discusses the histomorphometric changes in capillary density, fibrosis, and mast cells in the hypertensive myocardium and delves into the roles of key regulatory systems, including the apelinergic system, vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) pathways, and nitric oxide (NO)/nitric oxide synthase (NOS) signaling in the pathogenesis of hypertensive heart disease (HHD). Capillary rarefaction, a hallmark of HHD, contributes to myocardial ischemia and fibrosis, underscoring the importance of maintaining vascular integrity. Targeting capillary density (CD) through antihypertensive therapy or angiogenic interventions could significantly improve cardiac outcomes. Myocardial fibrosis, mediated by excessive collagen deposition and influenced by fibroblast growth factor-2 (FGF-2) and transforming growth factor-beta (TGF-β), plays a pivotal role in the structural remodeling of hypertensive myocardium. While renin–angiotensin–aldosterone system (RAAS) inhibitors show anti-fibrotic effects, more targeted therapies are needed to address fibrosis directly. Mast cells, though less studied in humans, emerge as critical regulators of cardiac remodeling through their release of pro-fibrotic mediators such as histamine, tryptase, and FGF-2. The apelinergic system emerges as a promising therapeutic target due to its vasodilatory, anti-fibrotic, and cardioprotective properties. The system counteracts the deleterious effects of the RAAS and has demonstrated efficacy in preclinical models of hypertension-induced cardiac damage. Despite its potential, human studies on apelin analogs remain limited, warranting further exploration to evaluate their clinical utility. VEGF signaling plays a dual role, facilitating angiogenesis and compensatory remodeling during the early stages of arterial hypertension (AH) but contributing to maladaptive changes when dysregulated. Modulating VEGF signaling through exercise or pharmacological interventions has shown promise in improving CD and mitigating hypertensive cardiac damage. However, VEGF inhibitors, commonly used in oncology, can exacerbate AH and endothelial dysfunction, highlighting the need for therapeutic caution. The NO/NOS pathway is essential for vascular homeostasis and the prevention of oxidative stress. Dysregulation of this pathway, particularly endothelial NOS (eNOS) uncoupling and inducible NOS (iNOS) overexpression, leads to endothelial dysfunction and nitrosative stress in hypertensive myocardium. Strategies to restore NO bioavailability, such as tetrahydrobiopterin (BH₄) supplementation and antioxidants, hold potential for therapeutic application but require further validation. Future studies should adopt a multidisciplinary approach to integrate molecular insights with clinical applications, paving the way for more personalized and effective treatments for HHD. Addressing these challenges will not only enhance the understanding of hypertensive myocardium but also improve patient outcomes and quality of life.

The aim of this study was to assess the epiligament theory by determining the normal epiligament morphology of the proximal and distal parts of the anterior cruciate ligament in humans and analyzing the differences between them and the midportion of the ligament in terms of cell numbers and expression of CD34 and α-SMA. Samples were obtained from the anterior cruciate ligaments of 12 fresh knee joints. Monoclonal antibodies against CD34 and α-SMA were used for immunohistochemistry. Photomicrographs were analyzed using ImageJ software, version 1.53f. The cell density was higher in the epiligament than in the ligament connective tissue. Cell counts were higher in the proximal and distal thirds than in the midsubstance of the epiligament. CD34 was expressed similarly in the proximal and distal thirds, although it seemed slightly more pronounced in the distal third. α-SMA expression was more robust in the proximal than the distal part. The results revealed that CD34 and α-SMA are expressed in the human epiligament. The differences between the numbers of cells in the proximal and distal parts of the epiligament and the expression of CD34 and α-SMA enhance epiligament theory. Future investigations into improving the quality of ligament healing should not overlook the epiligament theory.

Background: Cardiovascular diseases (CVDs) are the leading cause of global mortality and disability. Acute myocardial infarction (AMI) in young individuals is a rare condition but can cause devastating socioeconomic and psychological consequences for both the patient and their family and an economic burden for the government. There is a paucity of data concerning the specific profile of these young patients in Bulgaria, a country with a high burden of cardiovascular morbidity and mortality. Therefore, the aim of the present study was to assess the baseline characteristics, demographic and risk factor profile, clinical features, angiographic findings and in-hospital outcomes of young patients with AMI. Additionally, these data were compared to those of the older age group. Methods: Retrospective data on 172 patients treated for AMI in “Prof. Alexandar Tschirkov”, Bulgaria, from January 2018 to December 2021 were collected for the purpose of this study. Baseline characteristics, risk factor profile and clinical and angiographic features were compared in young (≤45 years) and older patients (>45 years). Results: Males were significantly predominant in the two age groups (p < 0.01), with an obviously increasing proportion of females in the older age group. Young patients were more likely to be smokers (55.7% vs. 28.8%; p=0.001); in contrast, hypertension (70.5% vs. 91.9%; p <0.001) and obesity (16.4% vs. 31.5%; p=0.031) were more prevalent in older patients. Anterior localization of myocardial infarction (MI) was most common in the two age groups (47.5% vs. 41.4%), respectively. Regarding the time delay from symptom onset to first medical contact, we found that young patients tended to present earlier than their older counterparts. Young patients had a higher incidence of single vessel disease (SVD) (49.2%) and nonobstructive coronary disease (NOCD) (11.5%) than older patients. Young patients with AMI had a lower in-hospital morbidity rate than older patients, but the in-hospital mortality, although lower, was not significantly different. A high prevalence of modifiable cardiovascular risk factors (RFs), such as smoking, dyslipidemia and arterial hypertension (AH), among the young group, less evolved CAD and similar high procedural success between age groups were established. Approximately 30% of young patients tend to present late in the hospital. The in-hospital mortality in the young population was lower than that in the older population but was still relatively higher than that previously reported. Conclusion: The reported high prevalence of modifiable RFs and late presentation of young patients with AMI highlight the need for early recognition of these RFs, better prevention, deployment of educational programs, easy access to health care and high awareness of clinicians to reduce disability and mortality from CVD.

The azygos lobe is a rare anatomical variant, most often encountered in the right lung. Its etiology is related to a defect of the migration of the azygos vein during the embryonic development. Here, we describe a rare case of an azygos lobe of the right lung, diagnosed incidentally on a computed tomography (CT) scan in a 40-year-old male patient who presented with chest pain, shortness of breath, and fever. The initial differential diagnosis included acute myocardial infarction, aortic dissection, and myocarditis. Chest CT with contrast matter demonstrated a peculiar finding in the right lung which was recognized as an azygos vein passing through the upper lobe and separating an azygos lobe with its mesoazygos. The azygos lobe may be rarely associated with neoplastic processes or spontaneous pneumothorax and its differential diagnosis on imaging studies includes various conditions. Knowledge of this variation is important to avoid misdiagnosis or complications during thoracic surgery.

Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate the role of the apelin receptor (APLNR), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF) in hypertension-induced renal damage. We used two groups of spontaneously hypertensive rats aged 6 and 12 months, representing different stages of AH, and compared them to age-matched normotensive controls. The kidney tissue samples were prepared through a well-established protocol. All data analysis was conducted with a dedicated software program. APLNR was localized in tubular epithelial cells and the endothelial cells of the glomeruli, with higher expression in older SHRs. The localization of nNOS and VEGF was similar. The expression of APLNR and nNOS increased with AH progression, while VEGF levels decreased. CD was lower in young SHRs compared to controls and decreased significantly in older SHRs in comparison to age-matched controls. Our statistical analysis revealed significant differences in molecule expression between age groups and varying correlations between the expression of the three molecules and CD.