Search Results (411)

Atherosclerosis (AS) is a lipid-driven chronic inflammatory disease and the principal pathological basis of coronary artery disease, ischemic stroke, and peripheral artery disease. Despite advances in lipid-lowering, antiplatelet, anti-inflammatory, and revascularization strategies, current treatments do not selectively modulate the heterogeneous cellular and inflammatory microenvironments within individual plaques. Cell membrane-coated nanoparticles (CMNs) have therefore emerged as biomimetic delivery platforms that combine the functional versatility of synthetic nanocores with selected biological properties of donor-cell membranes. This review summarizes the fabrication of CMNs and critically compares platelet-, macrophage-, neutrophil-, monocyte-, erythrocyte-, and hybrid membrane-coated nanoplatforms, together with emerging T-cell-targeted nanotherapeutic strategies. Particular attention is given to membrane-source selection, receptor–ligand interactions, immune evasion, lesion-directed accumulation, stimulus-responsive cargo release, and the modulation of inflammation, oxidative stress, lipid metabolism, and defective efferocytosis. We further discuss major translational barriers, including donor- and activation-state-dependent membrane heterogeneity, incomplete or unstable coating, manufacturing reproducibility, scalability, thrombogenicity, immunogenicity, and the limited predictive value of short-term small-animal models. A pathology-matched and minimum-sufficient-complexity framework is proposed to guide the rational development of safer, more reproducible, and clinically relevant biomimetic nanotherapies for AS. Full article

Patients with chronic liver disease are systematically excluded from acute myocardial infarction (AMI) trials, and prior real-world data rely on administrative coding alone. Whether ICD-coded liver disease and laboratory-defined liver fibrosis identify the same patients, and whether they predict the same outcomes, is unknown. We conducted a single-center retrospective cohort study of 1037 consecutive adults admitted with AMI (ICD-10 I21.x) to a tertiary New York center between November 2022 and December 2024. The primary exposure was ICD-defined advanced liver disease (cirrhosis, hepatic failure, or portal hypertension/decompensation; n = 102). The secondary, lab-based exposure was the Fibrosis-4 (FIB-4) index calculated from earliest admission AST, ALT, and platelet count (computable in 1031 patients, 99.4%), stratified as low (<1.45), indeterminate (1.45–3.25), or advanced (>3.25). Co-primary outcomes were invasive management (diagnostic angiography, percutaneous coronary intervention, or coronary artery bypass grafting) and in-hospital mortality. Multivariable logistic regression adjusted for age, sex, diabetes, chronic kidney disease, heart failure, and ST-elevation; the trend across FIB-4 tiers was assessed with the Cochran–Armitage test. Denominators throughout (including the 168/909 occult-fibrosis estimate) use the full exposure group as denominator under a missing-as-not-exposed convention; the four no-LD and two advanced-LD patients with missing FIB-4 are counted as non-advanced fibrosis for this calculation. Patients with ICD-defined advanced liver disease received invasive management less often (12.7% vs. 50.4%; adjusted odds ratio [aOR] 0.17, 95% CI 0.09–0.32) and died in hospital more often (43.1% vs. 7.9%; aOR 8.22, 95% CI 5.02–13.46) than patients without coded liver disease. Outcomes worsened monotonically across FIB-4 tiers (mortality 4.4% → 9.2% → 27.5%; invasive management 55.2% → 45.6% → 33.5%; both p < 0.001 by Cochran–Armitage trend test). Critically, 168 of 909 patients with no coded liver disease (18.5%) had FIB-4 > 3.25, representing a substantial population of unrecognized advanced fibrosis missed by clinical coding. Coded liver disease identifies a small, severely affected subgroup with markedly lower rates of invasive management and 6- to 8-fold higher mortality after AMI. Routine FIB-4 calculation, a free, three-variable lab score, identifies a much larger population with occult advanced fibrosis and graded excess risk that ICD codes miss entirely. Pending prospective validation, FIB-4 may serve as a low-cost adjunct to bedside risk stratification in AMI care. Full article

Background/Objectives: Carotid intima–media thickness (CIMT) is widely recognized as an established biomarker of systemic atherosclerosis and coronary artery disease (CAD). Nevertheless, the connection between circulating miR-29 family members, CIMT and CAD severity has not yet been determined. The aim of this study was to investigate the association of plasma miR-29a and miR-29c with CIMT and CAD severity. Methods: A total of 628 patients scheduled for elective coronary angiography were included in the study. CAD severity was estimated using the Gensini scoring system and was classified into mild, moderate, and severe categories. Additionally, CIMT was evaluated using high-resolution B-mode ultrasonography, while plasma miR-29a and miR-29c levels were detected using qRT-PCR. Results: CIMT increased significantly with CAD severity (0.76 ± 0.15, 0.94 ± 0.18, and 1.12 ± 0.22 mm for mild, moderate, and severe CAD, respectively; p < 0.001). MiR-29a expression progressively increased, whereas miR-29c expression decreased with advancing CAD (both p < 0.001). MiR-29a correlated positively with CIMT (r = 0.612) and Gensini score (r = 0.658), while miR-29c showed negative correlations (r = −0.527 and −0.584, respectively; all p < 0.001). CIMT, miR-29a, and miR-29c were found to be independently associated with CAD severity. Their combined model demonstrated a powerful association with severe CAD (AUC = 0.927; sensitivity 88.6%; specificity 84.1%). Conclusions: Plasma miR-29a and miR-29c are independent biomarkers of CIMT and CAD severity. Their combination with CIMT can improve diagnosis of severe CAD and may enhance cardiovascular risk stratification. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) is a global epidemic strongly associated with an increased risk of heart failure, independent of coronary artery disease or hypertension. This condition, historically termed diabetic cardiomyopathy (DCM) and recently redefined as “diabetic myocardial disorder,” remains frequently underdiagnosed in its subclinical stages. The objective of this non-systematic review is to synthesize current evidence on the pathophysiological mechanisms, diagnostic advancements, and evolving therapeutic strategies for diabetic myocardial involvement. Methods: A comprehensive review of contemporary literature was conducted, focusing on recent consensus statements from the ESC and AHA, large-scale epidemiological data (IDF/WHO), and pivotal clinical trials (EMPA-REG, DAPA-HF, and LEADER). We analyzed the role of multimodal imaging—specifically speckle-tracking echocardiography (STE) and multiparametric cardiac magnetic resonance (CMR)—and circulating biomarkers in early phenotyping. Results: Pathophysiological drivers include lipotoxicity, oxidative stress, and AGE-mediated fibrosis. Advanced imaging techniques, such as global longitudinal strain (GLS) and CMR T1-mapping/ECV quantification, demonstrate superior sensitivity over LVEF in detecting early subendocardial dysfunction and diffuse fibrosis. Furthermore, NT-proBNP serves as a robust prognostic marker for the HFpEF-like trajectory typical of diabetes. Clinically, the therapeutic landscape has shifted with SGLT2 inhibitors and GLP-1 receptor agonists, which provide significant cardioprotection and reduction in heart failure hospitalizations through mechanisms beyond glycemic control. Conclusions: Diabetic myocardial disorder represents a complex continuum within the cardiometabolic spectrum. Early detection through multimodal imaging and biomarkers is essential for risk stratification. Integrating novel glucose-lowering therapies with proven cardiovascular benefits is now mandatory to alter the natural history of the disease and prevent progression to overt heart failure. Full article

Background: Advancing age is incorporated as a strong risk variable in EuroSCORE II and is consistently associated with adverse outcomes after conventional coronary artery bypass grafting (CABG). Whether minimally invasive direct coronary artery bypass (MIDCAB)—which avoids both sternotomy and cardiopulmonary bypass—modifies this age-related risk in patients with single-vessel or LAD-predominant coronary artery disease remains insufficiently characterised. Methods: We retrospectively analysed 350 consecutive patients who underwent MIDCAB at Hannover Medical School between July 1999 and April 2025 (follow-up to April 2025). Elderly patients (age ≥70 years; n = 117) were compared with younger patients (age <70 years; n = 233) before and after 1:1 propensity score matching using greedy nearest-neighbour matching with a caliper of 0.2 × SD of the logit propensity score; age was excluded from the propensity model as it represented the exposure variable. A pre-specified sensitivity propensity model that additionally excluded EuroSCORE II (because EuroSCORE II contains an age component) was also evaluated. The primary endpoint was all-cause long-term mortality; secondary endpoints included perioperative complications and in-hospital outcomes. Long-term survival was assessed by Kaplan–Meier analysis and multivariable Cox proportional hazards regression, with a pre-specified parsimonious Cox model (age, LVEF, renal impairment) and cluster-robust standard errors on matched-pair identifiers. Results: Matching produced 109 pairs with excellent covariate balance (all standardized mean differences < 0.20). MIDCAB was completed without intraoperative conversion in all patients. No 30-day mortality, perioperative stroke, or new postoperative dialysis was observed in either age stratum (Clopper–Pearson 95% CI 0.00–3.33% for each zero-event outcome). Perioperative complications—including new-onset atrial fibrillation, re-exploration for bleeding, and intensive care unit and hospital length of stay—did not differ significantly between elderly and younger patients in the matched cohort (Newcombe 95% CI for risk differences all crossing zero; McNemar’s exact tests non-significant for all matched-pair binary endpoints; Hodges–Lehmann median difference for hospital length of stay +1.0 day, bootstrap 95% CI 0.0–1.0 days). At a median follow-up of 19.0 years (IQR 11.5–24.3; reverse Kaplan–Meier potential median 19.7 years), all-cause mortality was higher in the elderly (20.2% vs. 5.5%, p = 0.002; log-rank p = 0.001; exact McNemar’s p = 0.0025 for the matched-pair mortality endpoint). After multivariable adjustment, elderly age (≥70 years) was independently associated with long-term mortality (adjusted hazard ratio 4.48, 95% CI 1.79–11.20, p = 0.001), as was EuroSCORE II (HR 2.40 per unit, p = 0.034); a pre-specified parsimonious model (age, LVEF, renal impairment) with pair-cluster robust standard errors yielded an essentially identical adjusted HR for elderly age of 4.08 (95% CI 1.65–10.04, p = 0.002), and a sensitivity propensity model without EuroSCORE II yielded HR 3.95 (95% CI 1.68–9.29, p = 0.002). Conclusions: In this propensity-matched analysis with a median follow-up of ~19 years, MIDCAB was associated with excellent observed perioperative outcomes in appropriately selected elderly patients (no 30-day mortality, stroke, or new dialysis observed; upper 95% CI 3.3%) and no evidence of an excess of major in-hospital complications compared with younger patients within the statistical resolution of the cohort. The long-term mortality excess in the elderly is consistent with age-related life-expectancy curves in the source population; cause-specific mortality was not available in this cohort. External benchmarks from large MIDCAB cohorts in which long-term survival approximates that of the age-matched general population support this interpretation indirectly. These findings support MIDCAB as a feasible revascularization strategy associated with favourable observed early outcomes and long-term survival consistent with published MIDCAB literature, in appropriately selected elderly patients with single-vessel or LAD-predominant coronary artery disease treated at experienced centres. Full article

Panvascular diseases, characterized by systemic vascular dysfunction across multiple organ systems, represent a complex interplay of genetic susceptibility and environmental triggers. Ring Finger Protein 213 (RNF213), initially identified as the principal susceptibility gene for moyamoya disease (MMD), has emerged as a central regulator of panvascular pathophysiology. This review synthesizes current evidence elucidating RNF213′s multifaceted roles in vascular homeostasis, spanning its functions as an E3 ubiquitin ligase, mechanosensor, and immune modulator. The “second-hit” hypothesis posits that RNF213 mutations establish a genetic predisposition, while secondary insults—such as infection, hypoxia, or hemodynamic stress—precipitate pathological manifestations. Mechanistically, RNF213 orchestrates critical processes including endothelial integrity, angiogenesis, and inflammatory responses through pathways such as HIF-1α/VEGF, NF-κB, and Wnt signaling. Its dysfunction disrupts vascular remodeling, promotes aberrant smooth muscle proliferation, and exacerbates hypoxia-inflammation cycles, contributing to diverse pathologies ranging from intracranial aneurysms and arterial dissections to pulmonary hypertension and coronary artery disease. Emerging insights into RNF213′s interactions with gut microbiota, lipid metabolism, and epigenetic regulators further underscore its systemic influence. Despite advancements, unresolved questions persist regarding the context-dependent duality of RNF213 variants and organ-specific regulatory mechanisms. This review highlights the imperative for integrated approaches combining genetic, molecular, and environmental perspectives to unravel RNF213′s panvascular roles. We also outline unresolved questions regarding context-dependent effects of RNF213 variants and organ-specific regulatory mechanisms, and discuss potential avenues for future research integrating genetic, molecular, and environmental perspectives to advance understanding of RNF213′s panvascular roles. Full article

Cardiovascular disease (CVD) remains the leading global cause of morbidity and mortality. While low-dose aspirin is well established for secondary prevention, its role in primary prevention is controversial because modest benefits in cardiovascular benefits must be balanced against increased bleeding risk, as highlighted by recent large trials. Current guidelines recommend restricting aspirin use to individuals at higher cardiovascular risk without elevated bleeding risk, yet significant heterogeneity persists in defining these thresholds. Evidence from randomized trials, guidelines, cohort and modeling analyses, and post hoc or observational subgroup studies suggests that selected patients with advanced subclinical atherosclerosis or specific high-risk markers may have a more favorable risk–benefit profile, although the certainty and directness of evidence vary across subgroups. This narrative review and pragmatic clinical guide presents an illustrative tiered framework based on clinical, imaging, and biomarker markers—such as coronary artery calcium score, carotid plaque score, and lipoprotein(a)—to support individualized discussion of preventive aspirin therapy. The framework is not a validated risk calculator or standalone treatment algorithm, and decisions should balance absolute cardiovascular risk, major bleeding risk, evidence certainty, and patient preferences. Full article

Background: Older adults commonly experience a progressive decline in functional capacity and exercise tolerance, particularly among residents of residential care homes. Advanced age is associated with a higher prevalence of coronary heart disease (CHD) and arterial hypertension, both of which further reduce physical activity levels. Evidence indicates that regular, structured physical activity can improve physical functioning and cardiovascular parameters. This study aimed to assess functional capacity and exercise tolerance in residential care home residents with treated arterial hypertension and CHD compared with individuals without cardiovascular disease. Methods: The study included 74 men aged 65–80 years residing in residential care homes. Participants were divided into two groups: Group I consisted of 44 men without diagnosed cardiovascular disease, and Group II included 30 men with diagnosed CHD and arterial hypertension. Functional capacity was assessed using the Short Physical Performance Battery (SPPB), and exercise tolerance was evaluated using the 6-Minute Walk Test (6MWT). Results: The mean SPPB score was 8.7 ± 2.1 points in Group I and 5.2 ± 2.5 points in Group II (p < 0.001). In the 6 MWT, participants in Group I covered a mean distance of 312.7 ± 89.4 m, whereas those in Group II covered 168.4 ± 84.4 m (p < 0.001). Multivariable regression analysis confirmed that group allocation remained an independent predictor of both SPPB and 6MWT outcomes after adjusting for age and somatic parameters (p < 0.001). Conclusions: Residential care home residents with CHD and arterial hypertension demonstrate significantly lower functional capacity and exercise tolerance compared with individuals without cardiovascular disease. Both groups achieved results markedly below national reference values for the Polish older adult population. These findings highlight the need for targeted physical activity programs in residential care homes, with particular emphasis on individuals with cardiovascular disease. Full article

Coronary artery bypass grafting (CABG) remains one of the most effective treatments for advanced coronary artery disease; however, substantial variability persists in both perioperative and long-term outcomes despite advances in surgical technique, myocardial protection, and risk stratification. Oxidative stress is a central mediator of tissue injury during cardiac surgery, contributing to ischemia–reperfusion injury, endothelial dysfunction, systemic inflammation, and postoperative organ complications. At the same time, chronic exposure to ambient air pollution has emerged as an important environmental determinant of cardiovascular disease through mechanisms that converge on many of the same redox-sensitive pathways. We propose the concept of environmental oxidative priming, whereby long-term exposure to particulate matter, nitrogen oxides, ozone, and other pollutants establishes a persistent state of endothelial dysfunction, mitochondrial impairment, chronic inflammation, nitric oxide depletion, and reduced antioxidant reserve before surgery. Within this framework, CABG represents a second oxidative challenge superimposed on a pre-existing environmentally conditioned phenotype. We discuss the mechanistic overlap between air pollution-induced cardiovascular injury and cardiac surgical stress and examine how this interaction may contribute to postoperative complications, graft adaptation, major adverse cardiovascular events, and long-term survival. Recognition of air pollution as a modifier of biological resilience provides a novel framework for understanding outcome heterogeneity after CABG and may support future precision-based risk stratification and preventive strategies. Full article

Background/Objectives: Atrial fibrillation (AF) and chronic kidney disease (CKD) frequently coexist and are associated with a high risk of cardiovascular complications. Previous studies have primarily focused on differences in clinical profiles by anticoagulant therapy or arrhythmia. Only a limited number of studies have evaluated the impact of CKD severity on patients’ clinical characteristics. Methods: This retrospective observational study aimed to characterize the clinical profile of contemporary patients with AF and CKD with an estimated glomerular filtration rate (eGFR) of 15–49 mL/min/1.73 m². The analysis included patients with AF from the CRAFT registry (NCT02987062). Patients were divided into two groups according to eGFR: 15–49 mL/min/1.73 m² and ≥50 mL/min/1.73 m². The groups were compared with respect to demographic characteristics, comorbidities, and treatment patterns. Statistical analyses included the Mann–Whitney U test, the chi-square test and multivariable logistic regression analysis. Results: A total of 3203 patients with AF were included, of whom 1153 had eGFR < 50 mL/min/1.73 m². Compared with patients with eGFR ≥ 50 mL/min/1.73 m², those with lower eGFR were significantly older, more often female, and had a higher burden of comorbidities, including arterial hypertension, heart failure, coronary artery disease, and diabetes mellitus. Direct oral anticoagulants were the predominant anticoagulant therapy, irrespective of renal function. Conclusions: Patients with AF and moderate-to-severe CKD present a distinct clinical profile characterized by advanced age and a higher burden of comorbidities. These findings improve the understanding of the clinical profile of patients with AF and moderate-to-severe CKD and may support risk assessment and clinical decision-making. Full article

Cardiovascular and vascular diseases remain major causes of morbidity and mortality worldwide, despite substantial advances in prevention, diagnosis, and treatment. In recent years, cardiovascular imaging has moved beyond the traditional assessment of anatomy and morphology toward a multidimensional evaluation of function, tissue composition, haemodynamics, inflammation, and individualized risk. This evolution has been driven by technological progress in echocardiography, cardiovascular magnetic resonance, computed tomography, nuclear imaging, intravascular imaging, and point-of-care ultrasound, together with the rapid development of artificial intelligence, radiomics, and predictive analytics. Advanced echocardiographic techniques, including contrast stress echocardiography and emerging methods for myocardial scar detection, may improve functional and prognostic assessment in patients with suspected or established coronary artery disease. Cardiac magnetic resonance, through tissue mapping, late gadolinium enhancement, and 4D flow imaging, provides unique information on myocardial fibrosis, perfusion, ventricular remodelling, and vascular haemodynamics. Computed tomography, particularly with the introduction of photon-counting technology, is expanding the non-invasive characterization of coronary plaques, vascular calcification, and thromboembolic disease. Hybrid imaging with PET/CT and PET/MR offers additional insight into vascular inflammation, myocardial metabolism, and active disease processes. At the same time, intravascular ultrasound, optical coherence tomography, and augmented-reality-supported imaging are refining interventional guidance, while point-of-care ultrasound is broadening access to rapid bedside cardiovascular and vascular assessment. The integration of imaging findings with circulating biomarkers, clinical scores, lipid profiles, coagulation parameters, and machine-learning models represents a promising strategy for personalized risk stratification, particularly in complex conditions such as coronary artery disease, venous thromboembolism, pulmonary embolism, and bleeding risk during antithrombotic therapy. This review summarizes current advances in cardiovascular imaging, discusses their translational implications, and highlights future directions for integrating imaging, artificial intelligence, and precision medicine into daily clinical practice. Full article

Background: Heart failure with supranormal ejection fraction (HFsnEF) has recently emerged as a distinct phenotype within the preserved ejection fraction spectrum. However, its clinical profile, underlying mechanisms, and prognostic significance remain incompletely understood. Methods: A systematic review was conducted according to PRISMA recommendations. PubMed, Scopus, and EMBASE were searched from inception to May 2026 for studies investigating HFsnEF. Demographic, clinical, laboratory, echocardiographic, prognostic, and therapeutic data were extracted. Weighted descriptive analyses were performed to compare HFsnEF and conventional heart failure with preserved ejection fraction (HFpEF) populations. Random-effects meta-analyses of study-specific event rates were conducted for all-cause mortality and for the composite endpoint of cardiovascular death or heart failure hospitalization. Results: Fourteen studies involving 17,158 HFpEF patients and 7493 HFsnEF patients were included. Compared with HFpEF, HFsnEF patients exhibited broadly similar clinical, laboratory, haemodynamic, and treatment profiles, with a higher prevalence of women and a lower prevalence of coronary artery disease representing the most consistent clinical differences. Conventional laboratory parameters and natriuretic peptide concentrations showed substantial overlap between groups. Echocardiographically, HFsnEF was characterized by significantly smaller left ventricular end-systolic dimensions and volumes and higher ejection fraction despite similar stroke volume and cardiac output. Mechanistic studies further demonstrated significantly higher end-systolic elastance and lower ventriculo-arterial coupling ratios despite comparable arterial elastance, supporting the presence of distinct ventricular–vascular mechanical properties. Prognostic analyses consistently identified HFsnEF as a phenotype associated with adverse clinical outcomes. Pooled event-rate analyses demonstrated significantly higher rates of both all-cause mortality and the composite endpoint of cardiovascular death or heart failure hospitalization in HFsnEF compared with HFpEF. Emerging evidence also suggests a potential benefit of sodium–glucose cotransporter-2 inhibitors in this population. Conclusions: HFsnEF appears to represent a distinct and potentially high-risk phenotype within the preserved ejection fraction spectrum. Its characteristic structural, haemodynamic, and prognostic features challenge the traditional assumption that progressively higher ejection fraction necessarily reflects better cardiovascular health. Further prospective studies incorporating advanced imaging and haemodynamic assessment are needed to refine its pathophysiological characterization and therapeutic management. Full article

Cardiovascular disease remains the leading cause of mortality among women worldwide, yet coronary syndromes in women continue to be under-recognized and insufficiently represented in clinical research. This review summarizes sex-specific pathophysiological mechanisms, risk factors, clinical presentation, and management considerations in women with coronary syndromes. Women are more likely than men to present with non-obstructive and non-atherosclerotic ischemic phenotypes, including ischemia or angina with non-obstructive coronary arteries, coronary microvascular dysfunction, myocardial infarction with non-obstructive coronary arteries, spontaneous coronary artery dissection, vasospastic angina, and Takotsubo syndrome. These entities often require diagnostic strategies beyond the detection of flow-limiting epicardial stenosis, including cardiac magnetic resonance imaging, intracoronary imaging, and coronary function testing. Traditional cardiovascular risk factors remain important, but several female-specific risk enhancers, including premature menopause, adverse pregnancy outcomes, polycystic ovary syndrome, autoimmune disease, and psychosocial stressors, further modify risk and remain incompletely integrated into routine clinical assessment. Women may also experience diagnostic delays due to symptom misclassification, lower baseline troponin concentrations, and clinical algorithms historically derived from male-predominant populations. Management should follow guideline-directed therapy when appropriate, while recognizing sex-related differences in pharmacology, bleeding risk, revascularization outcomes, and the need for phenotype-specific treatment in INOCA, MINOCA, SCAD, and Takotsubo syndrome. Finally, transgender and gender-diverse individuals remain largely absent from cardiovascular trials, highlighting the need for inclusive research frameworks that distinguish sex, gender identity, and hormone exposure. Improved recognition of sex- and gender-related differences is essential to advance equitable cardiovascular care. Full article

Cardiac computed tomography (CT) has evolved into a pivotal tool in precision cardiology, enabling comprehensive, non-invasive evaluation of coronary anatomy, plaque composition, vascular function, and inflammation. From calcium scoring to advanced physiological imaging, CT now integrates multiple layers of cardiovascular information within a unified diagnostic framework. Coronary artery calcium (CAC) quantification provides a robust, reproducible measure of atherosclerotic burden and refines risk estimation beyond traditional algorithms, particularly in asymptomatic individuals with an intermediate likelihood. Building upon this anatomical foundation, coronary CT angiography (CCTA) extends evaluation to the anatomical and morphological characterization of coronary artery disease (CAD), identifying both obstructive and non-obstructive plaques with high prognostic accuracy. The addition of CT-derived fractional flow reserve (FFR-CT) and stress perfusion CT (CTP) bridges anatomy and physiology, improving identification of flow-limiting stenoses and guiding revascularization decisions while reducing unnecessary invasive procedures. Beyond luminal assessment, CT-derived biomarkers such as the perivascular fat attenuation index (pFAI) have introduced a new dimension of vascular inflammation imaging, revealing residual risk even in patients without significant stenosis and suggesting novel pathways for individualized therapeutic targeting. Driven by advances in artificial intelligence and photon-counting detector technology, cardiac CT is transitioning from a purely diagnostic modality to an integrative platform for cardiovascular phenotyping. Taken as a whole, this integration of structural, functional, and biological data provides a genuinely holistic view of coronary health. In practical terms, it shifts clinical decision-making from population-based risk models toward precision-guided patient-specific strategies. Full article

Background: Lipoprotein metabolism, inflammation, and oxidative stress (OS) play interconnected roles in the pathogenesis of acute coronary syndrome (ACS). However, the relationship between oxidative stress biomarkers and coronary artery disease (CAD) complexity, particularly as assessed by the SYNTAX II score, remains incompletely understood. This study aimed to evaluate serum levels of oxidative stress–related biomarkers and to investigate their association with the SYNTAX II score in patients with newly diagnosed ACS. Methods: This was a retrospective, single-center observational study. A total of 60 patients with newly diagnosed ACS who underwent percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) were consecutively enrolled. Serum levels of superoxide dismutase (SOD), advanced oxidation protein products (AOPP), glutathione, catalase, and malondialdehyde (MDA) were measured using ELISA methods. Associations between oxidative stress markers and the SYNTAX II score were analyzed using correlation and regression analyses. Results: Median levels of SOD, AOPP, and glutathione were 261.0 (244.18–324.86) U/L, 23.81 (22.62–25.80) ng/mL, and 6.08 (5.28–11.46) ng/mL, respectively. Mean catalase and MDA levels were 339.07 ± 44.81 pg/mL and 0.66 ± 0.07 mmol/L. The SYNTAX II score was positively correlated with SOD, AOPP, glutathione, catalase, and MDA, as well as with age, female sex, and potassium levels, while it was negatively correlated with hemoglobin, creatinine clearance, and left ventricular ejection fraction (all p < 0.05). Patients with higher SYNTAX II scores demonstrated elevated levels of both oxidant and antioxidant biomarkers. Conclusions: Oxidative stress-related biomarkers were associated with the SYNTAX II score in patients with newly diagnosed ACS. Full article