Cardiovascular disease remains the leading cause of morbidity and mortality worldwide, especially in regions like Eastern Europe, South Asia, and Latin America. A significant portion of these cases (80%) is linked to atherosclerosis, which can lead to severe conditions like ischemic heart disease and stroke, with atherosclerosis (ATS) responsible for the majority of cases. This review explores the multifaceted relationship between insulin resistance (IR) and ATS, highlighting their roles as both independent and interrelated contributors to cardiovascular risk. ATS is characterized by lipid accumulation and chronic inflammation within arterial walls, driven by factors such as hypertension, dyslipidemia, and genetic predisposition, with endothelial dysfunction as a key early event. The early detection of subclinical ATS is critical and can be achieved through a combination of non-invasive imaging techniques—such as coronary artery calcium scoring and carotid ultrasound—and comprehensive risk profiling. IR, marked by impaired glucose uptake in liver, muscle, and adipose tissue, often precedes early diabetes and is associated with metabolic disturbances, including dyslipidemia and chronic inflammation. The diagnosis of IR relies on surrogate indices such as HOMA-IR, the QUICKI, and the TyG index, which facilitate screening in clinical practice. Compelling evidence indicates that IR independently predicts the progression of atherosclerotic plaques, even in non-diabetic individuals, and operates through both traditional risk factors and direct vascular effects. Understanding and targeting the IR–ATS axis is essential for the effective prevention and management of cardiovascular disease.

Inflammation plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS), contributing to plaque instability, thrombosis, and myocardial injury. This review aims to comprehensively examine the inflammatory mechanisms underlying ACS and evaluate current and emerging anti-inflammatory therapeutic strategies. We conducted a comprehensive literature review examining the role of inflammatory pathways in ACS pathophysiology, including innate and adaptive immune responses, key inflammatory mediators, and cellular mechanisms. We analyzed current evidence for anti-inflammatory therapies and their clinical outcomes in ACS management. Inflammatory processes in ACS involve complex interactions between innate immune cells (neutrophils, macrophages, monocytes) and adaptive immune cells (T lymphocytes, B cells). Key mechanisms include neutrophil extracellular trap (NET) formation, macrophage polarization, T cell subset imbalances (Th1/Th17 predominance with regulatory T cell dysfunction), and complement activation. Inflammatory biomarkers such as C-reactive protein, interleukin-6, and NET-specific markers demonstrate prognostic value. Anti-inflammatory therapies including colchicine, canakinumab (IL-1β inhibition), and methotrexate have shown cardiovascular benefits in clinical trials. Emerging targets include NET inhibition, T cell modulation, and precision inflammatory profiling approaches. Inflammation represents a critical therapeutic target in ACS beyond traditional risk factor modification. While colchicine and IL-1β inhibition have demonstrated clinical efficacy, future strategies should focus on precision medicine approaches targeting specific inflammatory pathways based on individual patient profiles. Integration of anti-inflammatory therapy with lipid management and antithrombotic strategies offers promise for improving ACS outcomes through comprehensive targeting of the multifactorial pathophysiology underlying coronary artery disease.

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia worldwide and is now increasingly regarded as a disease of chronic inflammation and progressive atrial fibrosis. Understanding of molecular mechanisms that mediate the linkage between systemic metabolic dysregulation, inflammation, and structural atrial changes is crucial for informing risk stratification and targeting of prevention strategies. This review provides evidence from 105 studies focusing on the contributions of transforming growth factor-β1 (TGF-β1), tumor necrosis factor-a (TNF-α), interleukin-6 (IL-6), galectin-3, and galectin-1 to cardiac fibrogenesis, atrial fibrosis, and AF pathogenesis. We also link metabolic syndrome to these biomarkers and to atrial remodeling, as well as echocardiographic correlates of fibrosis. TGF-β1 is established as the central profibrotic cytokine and promotes Smad-based fibroblast activation, collagen accumulation, and structural atrial remodeling. Its role is highly potentiated by thrombospondin-1 by turning latent TGF-β1 into its potent form. TNF-α and IL-6 also play an integral role in the inflammatory fibrotic continuum by activating NF-κB and STAT3 signaling, promoting fibroblast proliferation, electrical uncoupling, and extracellular matrix accumulation. Galectin-3 is a potent profibrotic mediator that promotes TGF-β signaling and is a risk factor for negative outcomes, whereas Gal-1 seems to regulate inflammation resolution and may exert context-dependent protective or maladaptive roles. Metabolic syndrome is strongly associated with excessive levels of these biomarkers, chronic low-grade inflammation, oxidative stress, and ventricular and atrial fibrosis. Chronic clinical findings show that metabolic syndrome (MetS) increases AF risk, exacerbates atrial dilatation, and is associated with worse postoperative outcomes. Echocardiographic data are connected to circulating biomarkers and are non-invasive for evaluating atrial remodeling. The evidence to date supports that atrial fibrosis should be considered an end point of systemic inflammation, metabolic dysfunction, and activation of profibrotic molecular pathways. Metabolic syndrome, due to its chronic low-grade inflammatory environment and prolonged levels of metabolic stress, manifests as an important upstream factor of fibrotic remodeling, which continuously promotes the release of cytokines, oxidative stress, and fibroblast activation. Circulating fibrotic biomarkers, in comparison with metabolic syndrome, serve separate yet interdependent pathways that help orchestrate atrial structural remodeling through the simultaneous process but can also provide a long-term indirect measure of ongoing profibrotic activity. The integration of these biomarkers with superior atrial imaging enables a broader understanding of the fibrotic substrate of atrial fibrillation. This combined molecular imaging approach can facilitate risk stratification, refine therapeutic decisions, and facilitate early identification of higher-risk metabolic phenotypes, thus potentially facilitating directed antifibrotic and anti-inflammatory therapy in atrial fibrillation.

Background: Contribution of global and regional longitudinal strain (GLS) for clinical assessment of patients with heart failure with preserved ejection fraction (HFpEF) is not well established. We sought to evaluate subclinical left ventricular dysfunction secondary to coronary artery disease (CAD) in HFpEF patients compared with hypertensive patients and age-matched healthy subjects. Material and methods: This was a retrospective study that included 148 patients (group 1 = 62 patients with HFpEF, group 2 = 46 hypertensive patients, and group 3 = 40 age-matched control subjects). Peak systolic segmental, regional (basal, mid, and apical), and global longitudinal strain were assessed for each study group using two-dimensional speckle-tracking echocardiography (2D-STE). Results: GLS values presented statistically significant differences between the three groups (p < 0.001); markedly increased values (more negative) were observed in the control group (−20.2 ± 1.4%) compared with HTN group values (−18.4 ± 3.0%, p = 0.031) and with HFpEF group values (−17.6 ± 2.3%, p < 0.001). The correlation between GLS values and HTN stages was significant, direct, and average (Spearman coefficient rho = 0.423, p < 0.001). GLS had the greatest ability to detect patients with HFpEF when HFpEF + CAD + HTN diastolic dysfunction (n = 30) + CON diastolic dysfunction (n = 2) from HFpEF + CAD + HTN + CON was analyzed. (optimal GLS limit of −19.35%, area under curve = 0.833, p < 0.001). Conclusions: Global longitudinal strain can be used for clinical assessment in differentiating coronary and hypertensive patients at higher risk for development of systolic dysfunction.

Background and Objectives: This cross-sectional study conducted at the Timișoara Institute of Cardiovascular Diseases, Romania, and the Centre for Translational Research and Systems Medicine from “Victor Babeș” University of Medicine and Pharmacy of Timișoara, Romania, investigated the relationship between indexed epicardial adipose tissue thickness (EATTi) and oxidative stress in epicardial adipose tissue (EAT) adipocytes in the context of coronary artery disease (CAD) among open-heart surgery patients. The objective was to elucidate the contribution of EATTi as an additional marker for complexity prediction in patients with CAD, potentially influencing clinical decision-making in surgical settings. Materials and Methods: The study included 25 patients undergoing cardiac surgery, with a mean age of 65.16 years and a body mass index of 27.61 kg/m². Oxidative stress in EAT was assessed using the ferrous iron xylenol orange oxidation spectrophotometric assay. The patients were divided into three groups: those with valvular heart disease without CAD, patients with CAD without diabetes mellitus (DM), and patients with both CAD and DM. The CAD complexity was evaluated using the SYNTAX score. Results: The EATTi showed statistically significant elevations in the patients with both CAD and DM (mean 5.27 ± 0.67 mm/m²) compared to the CAD without DM group (mean 3.78 ± 1.05 mm/m², p = 0.024) and the valvular disease without CAD group (mean 2.67 ± 0.83 mm/m², p = 0.001). Patients with SYNTAX scores over 32 had significantly higher EATTi (5.27 ± 0.66 mm/m²) compared to those with lower scores. An EATTi greater than 4.15 mm/m² predicted more complex CAD (SYNTAX score >22) with 80% sensitivity and 86% specificity. The intra- and interobserver reproducibility for the EATTi measurement were excellent (intra-class correlation coefficient 0.911, inter-class correlation coefficient 0.895). Conclusions: EATTi is significantly associated with CAD complexity in patients undergoing open-heart surgery. It serves as a reliable indicator of more intricate CAD forms, as reflected by higher SYNTAX scores. These findings highlight the clinical relevance of EATTi in pre-operative assessment, suggesting its potential utility as a prognostic marker in cardiac surgical patients.

It has been shown that the E/(e’×s’) index, which associates a marker of diastolic function (E/e’, early transmitral/diastolic mitral annulus velocity ratio) and a parameter that explores LV systolic performance (s’, systolic mitral annulus velocity), is a good predictor of outcome in acute anterior myocardial infarction. There are no studies that have investigated the prognostic value of E/(e’×s’) in a non-ST-segment elevated acute coronary syndrome (NSTE-ACS) population. Echocardiography was performed in 307 consecutive hospitalized patients with NSTE-ACS and succesful percutaneous coronary intervention, before discharge and six weeks after. The primary endpoint consisted of cardiac death or readmission due to re-infarction or heart failure. During the follow-up period (25.4 ± 3 months), cardiac events occurred in 106 patients (34.5%). Receiver operating characteristic (ROC) analysis identified E/(e’×s’) at discharge as the best independent predictor of composite outcome. The optimal cut-off value was 1.63 (74% sensitivity, 67% specificity). By multivariate Cox regression analysis, E/(e’×s’) was the only independent predictor of cardiac events. Kaplan–Meier analysis identified that patients with an initial E/(e’×s’) > 1.63 that worsened after six weeks presented the worst prognosis regarding composite outcome, readmission, and cardiac death (all p < 0.001). In conclusion, in NSTE-ACS, E/(e’×s’) is a powerful predictor of clinical outcome, particularly if it is accompanied by worsening after 6-weeks.