As the leading cause of global mortality, cardiovascular diseases demand improved and innovative strategies for early detection and risk assessment to enhance prevention and timely treatment. This comprehensive review examines the potential of combining high-sensitivity cardiac troponins (hs-cTns) and homocysteine (Hcy) as complementary biomarkers for enhanced cardiovascular risk prediction. hs-cTn assays have revolutionized cardiovascular diagnostics by enabling the detection of minimal myocardial injury, improving early diagnosis of acute coronary syndrome, and providing robust prognostic information in both symptomatic and asymptomatic populations. Hcy, while established as a marker of vascular dysfunction, presents an interpretative challenge due to multiple confounding factors and inconsistent therapeutic responses. Emerging evidence demonstrates significant correlations between elevated Hcy and troponins across various clinical conditions, suggesting that their combined assessment—reflecting both myocardial injury and vascular dysfunction—may improve cardiovascular risk stratification. While initial findings are promising, additional studies are required to validate the clinical value of the combined marker approach. Future development of personalized interpretation algorithms, and multi-marker panels incorporating these biomarkers, may significantly advance cardiovascular medicine and enable more effective population-specific risk management strategies.

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.

Background and Objectives: Factor VIII (FVIII) and the von Willebrand factor (vWF) are key components of hemostatic balance. Disruption of the vWF-ADAMTS13 axis, characterized by elevated vWF and reduced ADAMTS13 activity has been implicated in thrombotic disorders, including COVID-19-asscoiated coagulopathy, where this imbalance correlates with disease severity and mortality. This study evaluated the relationship between plasma FVIII and vWF levels and the severity of coronary artery disease (CAD), as assessed by the SYNTAX score. Methods: We enrolled 82 patients with chronic coronary syndrome (CCS) and a positive treadmill test who underwent elective coronary angiography. Based on the SYNTAX score, patients were divided into three groups: Group I (≤22), Group II (23–32), and Group III (≥33). Results: FVIII levels varied significantly (Group I: 2.25 ± 0.75; Group III: 2.97 ± 0.95; p = 0.007), with an OR of 3.632 (95% CI: 1.116–11.826; p = 0.03). vWF levels differed significantly across SYNTAX groups (Group I: 1.16 ± 0.59; Group II: 1.52 ± 0.62; Group III: 1.49 ± 0.80; p = 0.040). vWF > 1.75 was more frequent in Groups II and III, with an odds ratio (OR) of 4.909 (95% CI: 1.429–16.864; p = 0.01) for Group III vs. Group I. Fibrinogen and C-reactive protein (CRP) were elevated in patients with SYNTAX scores ≥33. In multinomial logistic regression analysis, FVIII emerged as the sole independent predictor of CAD complexity (p = 0.004), while the vWF showed significance in pairwise comparison (Group II vs. Group I; OR = 3.433, p = 0.049). Conclusions: This study demonstrated significant differences in hemostatic and inflammatory biomarkers across SYNTAX score categories reflecting CAD severity in CCS patients. FVIII emerged as an independent predictor of CAD complexity, while the vWF demonstrated significant associations in specific subgroup comparisons. The observed vWF-ADAMTS13 axis dysregulation supports the rationale for investigating vWF-targeted therapeutics, including agents such as caplacizumab, in cardiovascular disease management. These findings require validation in larger studies.

Background/Objectives: Elevated homocysteine (Hcy) levels are associated with endothelial dysfunction, oxidative stress, and inflammation, contributing to cardiovascular disease development. The aim of this study was to examine the effects of vitamin B6 and folic acid on cardiometabolic biomarkers, cardiac oxidative stress, metabolic enzyme activities and cardiovascular histomorphometric parameters in homocysteine-loaded rats. Methods: Male Wistar albino rats were divided into four groups (n = 10, per group): C—saline 0.2 mL/day s.c. + saline 0.5 mL i.p; H: Hcy 0.45 µmol/g b.w./day s.c. + saline 0.5 mL i.p; C-B6+FA—saline 0.2 mL/day s.c. + vitamin B6 (7 mg/kg b.w. i.p./day) and folic acid (FA) (5 mg/kg b.w. i.p./day); and H-B6+FA—Hcy (0.45 µmol/g b.w./day s.c.) + vitamin B6 (7 mg/kg b.w. i.p./day) and FA (5 mg/kg b.w. i.p./day). Substances were applied s.c. for 2 weeks and i.p for 4 weeks. Results: B6+FA supplementation significantly reduced serum Hcy and LDL concentrations and attenuated Hcy-associated increases in cardiac SOD activity and right ventricular wall thickness. However, B6+FA was associated with increased cardiac MDA levels. MDH activity increased mainly in non-Hcy-loaded supplemented rats, whereas LDH activity, the cardio-somatic index, and aortic histomorphometric parameters remained unchanged. Conclusions: Combined B6+FA supplementation may improve Hcy metabolism, the LDL profile, and selected cardiac structural/oxidative alterations, but its association with increased lipid peroxidation suggests complex redox effects requiring cautious interpretation.

Translocator protein (TSPO) regulates mitochondrial function, inflammation, and oxidative stress; however, its role in acute myocardial injury (MI) remains incompletely understood. While previous studies have examined TSPO ligands in cardiac injury, the interplay between TSPO modulation and nitric oxide (NO) signaling in AMI has not been systematically investigated. The aim of this study was to investigate the effects of TSPO modulation by PK11195, alone or in combination with nitric oxide synthase (NOS) inhibition by Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME), on cardiometabolic, inflammatory, oxidative stress, and histopathological parameters in an experimental model of isoprenaline-induced MI in rats. Male Wistar albino rats were divided into four groups: control (C); isoprenaline + saline-treated (ISO); isoprenaline + PK11195-treated (IP); and isoprenaline + PK11195 + L-NAME-treated (IPLN) groups. Isoprenaline administration induced MI, evidenced by elevated cardiac biomarkers, electrocardiographic (ECG) alterations, and histopathological damage. PK11195 treatment significantly attenuated MI and reduced pro-inflammatory cytokine levels while increasing anti-inflammatory cytokine levels, indicating protective effects. Nevertheless, TSPO modulation was associated with adverse metabolic effects, notably elevated fibrinogen and plasma homocysteine levels. Co-administration of L-NAME mechanistically demonstrated that NO availability is essential for PK11195 cardioprotective effects, as NOS inhibition partially abolished cardioprotection and modified oxidative stress parameters. Overall, TSPO modulation exerts complex actions in acute MI through regulating mitochondrial function, inflammatory signaling, and NO pathways, suggesting that TSPO is a potential, multifaceted therapeutic target.

Background: The COVID-19 pandemic revealed an unexpected pattern known as the “smoker’s paradox”, with lower rates of severe disease among smokers compared to non-smokers, highlighting the need for the specific investigation of disease progression in non-smoking populations. Objective: To identify early mortality predictors in non-smoking patients with severe COVID-19 through the evaluation of clinical, laboratory, and oxygenation parameters. Methods: This retrospective observational cohort study included 59 non-smokers hospitalized with COVID-19 between November and December 2020. Clinical parameters, laboratory findings, and respiratory support requirements were analyzed on Days 1 and 7 of hospitalization. ROC curves were constructed to assess the predictive value of the parameters. Results: The overall mortality rate was 54.2%. The seventh-day SOFA score showed the strongest predictive value (AUC = 0.902, p = 0.004), followed by pCO₂ (AUC = 0.853, p = 0.012). Significant differences between survivors and non-survivors were observed in acid–base parameters, oxygenation indices, and hematological markers. Mortality rates varied significantly with ventilation type: 84.6% for IMV and 50% for NIMV, with no deaths in HFNC patients. Conclusions: Multiple parameters measured on Day 7 of hospitalization demonstrate significant predictive value for mortality in non-smoking COVID-19 patients, with the SOFA score being the strongest predictor. The type of respiratory support significantly influences outcomes, suggesting the importance of careful ventilation strategy selection.