Background: Fetuin-A, a hepatokine implicated in metabolic regulation, has been associated with both metabolic syndrome and cardiovascular disease. However, its specific role in type 2 diabetes mellitus (T2DM) remains incompletely understood. Objective: This study aimed to investigate the relationship between fetuin-A levels and key components of metabolic syndrome (abdominal obesity, arterial hypertension, hyperglycemia, hypertriglyceridemia and low high-density lipoprotein cholesterol) as well as other cardiovascular risk markers, including metabolic dysfunction-associated fatty liver disease (MAFLD), carotid intima-media thickness (CIMT), and the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR). Methods: A total of 51 patients with T2DM not receiving insulin therapy were enrolled. Participants underwent clinical, biochemical, and imaging evaluations. Hepatic steatosis was assessed via abdominal ultrasonography, and subclinical atherosclerosis was evaluated using CIMT measured with Doppler ultrasonography. Serum fetuin-A was quantified by ELISA. Results: Hepatic steatosis was significantly associated with metabolic syndrome, increased CIMT, and dyslipidemia (elevated total cholesterol, triglycerides, and reduced HDL cholesterol). Although no direct correlation was found between fetuin-A levels and hepatic steatosis, multivariate analysis revealed that fetuin-A concentrations were significantly influenced by total cholesterol and LDL cholesterol levels. Conclusions: Fetuin-A appears to be linked to lipid abnormalities in T2DM and may contribute to cardiovascular risk in this population. These findings support the potential utility of fetuin-A as a biomarker and possible therapeutic target for dyslipidemia management in diabetic patients.

Background and Objectives: Atherosclerosis continues to be a major determinant of the global health burden, with ischemic heart disease representing one of the leading causes of morbidity and mortality worldwide. Although cardiovascular (CV) prevention strategies focus on pro-atherogenic lipoproteins, such as LDL-C, non-HDL-C, and apoB, the balance between atherogenic and anti-atherogenic lipoproteins may better reflect the overall atherogenic burden. Apolipoprotein B (apoB) reflects the total number of circulating atherogenic particles, whereas apolipoprotein A-I (apoA) is the main protein component of HDL, the major anti-atherogenic lipoprotein. Integrating these two parameters into the apoB/apoA ratio results in a composite biomarker that reflects this balance. In this study, we aimed to evaluate whether the apoB/apoA ratio can predict the presence and the severity of coronary artery disease (CAD) in a cohort from an Eastern European hospital, under moderate-intensity statin treatment. Additionally, we assessed whether lipoprotein(a) [Lp(a)] provides any additional diagnostic value. Materials and Methods: We consecutively enrolled 121 statin-treated patients, who presented for elective invasive coronary angiography. Patients with history of coronary revascularization or acute coronary syndrome were excluded. The study cohort was further divided into two groups, according to the severity of coronary stenosis: 69 patients with non-significant CAD (N-CAD) and 52 patients with hemodynamically significant CAD (S-CAD). Apolipoprotein B, apolipoprotein A-I, and lipoprotein(a) were measured using a standardized immunoturbidimetric assay, at the moment of enrollment. The severity of coronary stenosis was measured using Quantitative Coronary Analysis (QCA) software and the total coronary atherosclerotic burden of each patient was quantified using the Gensini score. Results: The apoB/apoA ratio was significantly higher in the S-CAD groups, compared with N-CAD patients (0.53 ± 0.16 vs. 0.73 ± 0.18). Furthermore, in the apoB/apoA-based analysis, the Gensini score increased progressively across the three tertiles (8.55 ± 19.60 vs. 14.57 ± 21.65 vs. 29.8 ± 27.78, p = 0.000) and so did the percentage of patients with three-vessel disease (5% vs. 19.5% vs. 32.5%, p = 0.000) and left main disease (5% vs. 7.3% vs. 20%, p = 0.031). The apoB/apoA ratio showed a significant correlation with the severity of CAD, as expressed by the Gensini score (r = 0.513, p < 0.001, 95% CI: 0.357–0.641). The association between apoB/apoA ratio and the presence and severity of CAD expanded beyond group comparison. In the logistic regression, this biomarker proved to be a valuable predictor for S-CAD (per SD increase: OR 2.509, 95% CI: 1.441–4.369, p = 0.001), three-vessel disease (per SD increase: OR 2.339, 95% CI: 1.427–3.892, p = 0.001), and left main disease (per SD increase: OR 2.771, 95% CI: 1.489–5.156, p = 0.001). The apoB/apoA ratio remained significant after adjusting for other CV risk factors and independent to LDL-C, as shown by the analysis that we performed among the lowest LDL-C tertile patients. Participants with S-CAD showed higher concentrations of Lp(a). However, adding this lipoprotein to the multivariate analysis, resulted only in a marginal improvement in the predictive power. Conclusions: The ApoB/apoA ratio emerged as an independent predictor for hemodynamically significant coronary stenosis and for CAD severity. Additionally, higher apoB/apoA values were associated with anatomical high-risk features, such as three-vessel disease or left main disease. In contrast, Lp(a) did not provide a substantial increase in the predictive power of multivariate models in this stable CAD cohort.

Transcatheter aortic valve implantation (TAVI) has redefined the management of severe aortic stenosis, particularly in surgical high-risk patients. As the number of TAVI procedures increases, there is a growing need for effective post-procedural care. Cardiac rehabilitation (CR) has emerged as a critical component of treatment in these patients. The most recent update of the European recommendations highlights the importance of including post-TAVI patients in CR programs. However, the benefits of CR in this particular patient group still need to be fully understood. The objective of this narrative review is to summarize the safety and benefits of post-TAVI CR by evaluating its impact on functional capacity, frailty, muscular strength, mental health, quality of life, and long-term survival. While emerging evidence supports its safety and effectiveness in the aforementioned outcomes, gaps remain regarding the optimal rehabilitation protocols, including the timing, duration, and intensity of CR as well as its long-term cardiovascular benefits. Further research is needed to develop personalized approaches for different patient groups. This article highlights the current knowledge, identifies critical gaps, and underlines the need for tailored rehabilitation strategies to improve post-TAVI recovery and patient outcomes.

Carpal Tunnel Syndrome (CTS) is the most common entrapment neuropathy, yet its etiology remains multifactorial and incompletely understood. While often considered idiopathic, recent evidence points to a complex interplay of genetic predisposition, immunological factors, and environmental exposures. Objective: This narrative review aims to synthesize current evidence on the genetic, immunological, and environmental underpinnings of CTS to provide a holistic understanding of its pathogenesis. Furthermore, it seeks to highlight the novel integration of these three domains, discuss the practical applications for clinical practice, and acknowledge the limitations of the current evidence base. Methods: A narrative review of the literature was conducted, analyzing studies concerning genetic polymorphisms, immune system alterations, occupational risks, and histopathological changes in CTS. Results: Genetic studies highlight polymorphisms in genes encoding collagen types (COL1A1, COL5A1, COL11A1), matrix metalloproteinases (MMPs), and glutathione S-transferases (GSTs) as contributors to connective tissue susceptibility and oxidative stress response. Immunological findings indicate a role for adaptive immunity, with elevated levels of T-cells (particularly CD4+ and memory T-cells) and chemokines like CCL5 and VEGF in the synovial tissue and serum, suggesting a low-grade inflammatory or immune-mediated process. Environmental factors, particularly repetitive biomechanical stress, high job strain, and low social support, are significant modifiable risk factors. The core pathophysiology involves increased intracarpal pressure leading to ischemic and mechanical damage to the median nerve, exacerbated by individual susceptibility. Conclusion: CTS arises from a convergence of genetic susceptibility, dysregulated immune responses, and environmental triggers. A better understanding of these interactions is crucial for developing targeted prevention strategies, personalized risk assessment, and novel therapeutic interventions beyond mechanical decompression.

Background: Anemia is frequently observed in patients undergoing transcatheter aortic valve implantation (TAVI) and may reflect persistent biological vulnerability in the post-procedural period. The relationship between systemic immune–inflammatory burden and anemia at entry into structured cardiac rehabilitation (CR) after TAVI remains insufficiently explored. Methods: This retrospective observational study included 80 consecutive patients referred to CR after successful TAVI. Anemia was defined by World Health Organization (WHO) criteria (hemoglobin <13 g/dL in men; <12 g/dL in women). Systemic inflammatory burden was assessed using C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), and the systemic immune–inflammation index (SII = platelet × neutrophil/lymphocyte). Multivariable logistic regression, adjusted for age, sex, body mass index (BMI), type 2 diabetes mellitus, and estimated glomerular filtration rate (eGFR), was used to evaluate independent associations with anemia. Results: Anemia was present in 67.5% of patients at CR entry. Compared with non-anemic patients, anemic patients exhibited significantly higher CRP (4.25 vs. 2.58 mg/L; p = 0.014), NLR (2.86 vs. 2.34; p = 0.004), PLR (132.33 vs. 102.13; p = 0.003), and SII (566.01 vs. 448.30; p = 0.011). In multivariable models, NLR (OR 4.09; 95% CI 1.50–11.19; p = 0.006), PLR (OR 4.89; 95% CI 1.41–17.02; p = 0.013), SII (OR 4.96; 95% CI 1.35–18.14; p = 0.016), and CRP (OR 2.17; 95% CI 1.07–4.39; p = 0.032) were independently associated with anemia. Area under the ROC curve (AUC) was 0.70 for NLR and PLR, 0.68 for SII, and 0.67 for CRP. Conclusions: Systemic inflammatory burden is independently associated with anemia at the time of entry into CR facility after TAVI. These findings support an integrated approach to patient evaluation and provide a basis for future mechanistic and interventional studies.

(1) Background: Peripheral arterial disease (PAD) is associated with substantial cardiovascular morbidity and functional impairment. This study evaluated the feasibility and adherence of a 6-month home-based telerehabilitation (TR) program and longitudinal changes in functional capacity, health-related quality of life (HRQoL), and selected cardiometabolic parameters. (2) Methods: This prospective, single-arm study enrolled 42 patients with PAD. Daily ambulation was monitored using a Xiaomi Smart Band 8, and participants received weekly telephone counseling. Assessments were performed at baseline, 3 months, and 6 months. (3) Results: Median daily step count increased from 5868 to 6905 steps/day (p < 0.001), whereas attainment of progressively increasing weekly targets decreased from 58.33% to 16.66% (p < 0.001). Median 6 min walk test (6MWT) distance increased from 390 m to 445 m at 6 months, a 55 m increase (p = 0.001). HRQoL, systolic blood pressure, body mass index, and total cholesterol showed significant longitudinal changes, while resting ankle–brachial index and selected cardiopulmonary exercise testing parameters remained relatively stable (p > 0.05). (4) Conclusions: The TR program was feasible and accompanied by increased activity and improved walking capacity. The divergence between absolute activity and target attainment supports multidimensional adherence assessment. Causal effects cannot be established given the single-arm design.