Background/Objectives: Red cell distribution width, platelet distribution width, and mean platelet volume are hematological indices derived from complete blood counts that have been increasingly investigated as potential cardiovascular biomarkers. This study aimed to assess the association between these indices and the extent of coronary artery disease, quantified by the Gensini score. Methods: We conducted a retrospective observational study of 240 patients hospitalized with typical angina who underwent elective coronary angiography at the Institute of Cardiovascular Diseases in Timișoara (January 2023–April 2024). Patients with hematological disorders, prior revascularization, or severe comorbidities were excluded. CAD severity was assessed by the Gensini score, with patients stratified into a low-score group (<50) and a high-score group (≥50). Laboratory and echocardiographic data were collected. Correlation analyses, ROC curve analysis, and multivariate regression were performed to evaluate predictors of CAD complexity. Results: Among 240 patients (81% male), 161 (67%) were in the high-score group. Compared with the low-score group, these patients had higher RDW (12.43 ± 0.68 vs. 12.70 ± 1.01, 95%CI: −0.52 to −0.02, p = 0.03), MPV (9.20 ± 0.88 vs. 9.45 ± 0.84, 95%CI: −0.48 to −0.02, p = 0.03), serum creatinine (p = 0.01), and potassium (p = 0.02), and lower ejection fraction (p < 0.001). RDW correlated positively with the Gensini score (rho = 0.28, 95%CI: 0.16–0.39, p = 0.001). Multivariate analysis identified RDW, MPV, and diastolic dysfunction as independent predictors. RDW showed weak discrimination for high Gensini burden (AUC = 0.57, 95% CI: 0.49–0.65, p > 0.05), consistent with a borderline, non-significant result. Conclusions: Elevated RDW and MPV are independently associated with greater coronary lesion burden. These routinely available indices may serve as novel, cost-effective markers for CAD risk stratification, warranting validation in prospective studies.

Oxidative stress contributes to heart failure (HF) progression by mechanisms that go beyond hemodynamic overload, including mitochondrial dysfunction, endothelial injury, inflammation, and fibrotic remodeling. This review evaluates the relationship between redox imbalance, Galectin-3 (Gal-3), fibrosis, and imaging findings in HF. Reactive oxygen species (ROS) generated by mitochondria, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and xanthine oxidase may disturb calcium handling, impair mitochondrial function, activate fibroblasts, and promote ferroptosis. Biomarkers of oxidative injury and antioxidant reserve, including malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and circulating thiols, provide information complementary to natriuretic peptides. Experimental evidence supports a context-dependent role of Gal-3 in fibro-inflammatory remodeling, whereas circulating Gal-3 should be regarded as a complementary biomarker rather than as a direct measure of myocardial fibrosis. Echocardiography assesses functional remodeling through diastolic indices, myocardial deformation, and right ventricular–pulmonary arterial (RV–PA) coupling, while cardiac magnetic resonance characterizes focal scar and diffuse interstitial remodeling using late gadolinium enhancement, native T1 mapping, and extracellular volume fraction. Therapeutic strategies are increasingly shifting from nonspecific antioxidant supplementation toward targeting ROS sources and downstream pathways, with SGLT2 inhibitors emerging as clinically relevant agents with indirect redox-modulating effects. Integrated redox, fibro-inflammatory, hemodynamic, and imaging phenotyping may refine risk stratification, although prospective validation is required before routine implementation.

Background and Methods: This prospective observational study investigated the prognostic value of the hemoglobin-to-red cell distribution width ratio (HRR) in 278 patients hospitalized with decompensated heart failure (HF). The primary endpoint was a composite of all-cause mortality or HF rehospitalization at 12 months. Multivariable Cox regression was employed to adjust for risk factors including age, sex, NT-proBNP, LVEF, and eGFR. Results: The median HRR was 0.89. During follow-up, the primary endpoint occurred in 167 (60.1%) patients. Unadjusted analysis showed a lower HRR was significantly associated with reduced event-free survival (log-rank p = 0.027). However, after multivariable adjustment, this association was no longer statistically significant (p = 0.240). Older age and male sex remained independent predictors. Conclusions: In patients with decompensated HF, a lower baseline HRR correlates with increased risk but does not maintain independent prognostic value after adjusting for powerful confounders. HRR may serve as a simple, initial marker of risk rather than an independent predictor.

Lipoprotein(a) [Lp(a)] is a highly heritable apoB-containing lipoprotein and a causal contributor to atherosclerotic cardiovascular disease that may contribute to residual cardiovascular risk after myocardial infarction (MI), while the clinical benefit of selective pharmacological Lp(a) lowering remains unresolved. This narrative review examines Lp(a) as a determinant of residual and recurrent cardiovascular risk after MI, integrating molecular biology, human genetics, coronary imaging, post-MI observational studies, measurement considerations, current management, and emerging therapies. Elevated Lp(a) has been associated with coronary plaque progression, high-risk plaque features, oxidized-phospholipid-related inflammatory pathways, recurrent ischemic events, and repeat revascularization, although prognostic associations vary across populations and endpoints. Because concentrations measured during acute MI may underestimate the stable Lp(a) phenotype in some patients, selective repeat measurement after clinical stabilization may be appropriate when classification could influence management or trial eligibility. Contemporary treatment remains centered on intensive control of LDL-C and other modifiable risk factors, while antisense oligonucleotides, small interfering RNAs, and oral particle-assembly inhibitors can produce profound Lp(a) reductions. According to sponsor-reported topline data released in September 2026, pelacarsen lowered Lp(a) but did not significantly reduce the prespecified primary cardiovascular endpoint in the overall Lp(a)HORIZON population; complete peer-reviewed results are not yet available. The sponsor-reported neutral HORIZON topline result raises unresolved questions regarding baseline Lp(a) and absolute reduction, timing of intervention and disease stage, and endpoint composition. Full peer-reviewed HORIZON data and ongoing cardiovascular outcome trials will be required to determine whether and under what conditions selective Lp(a) lowering translates into cardiovascular benefit.

Background/Objectives: Oxidative stress and galectin-3-related fibro-inflammatory processes contribute to heart failure pathophysiology, but their concurrent relationships with natriuretic peptides and structural/cardiorenal parameters remain incompletely characterized. We evaluated baseline associations of serum peroxide burden and galectin-3 with N-terminal pro-B-type natriuretic peptide (NT-proBNP) and related phenotypic parameters in chronic heart failure. Methods: This cross-sectional analysis included 57 patients from a prospective single-center cohort. Serum peroxides were quantified using the ferrous oxidation–xylenol orange assay and expressed as nmol H₂O₂ equivalents/mL. Associations were assessed using Spearman correlation and linear regression with ln-transformed NT-proBNP. Benjamini–Hochberg correction was applied to eight secondary/exploratory correlations. Results: Serum peroxide burden correlated with NT-proBNP (ρ = 0.387, p = 0.0095; n = 44) and remained significantly associated after adjustment for age, sex, and left ventricular ejection fraction (B = 0.1756, p = 0.0420; n = 43). After additional estimated glomerular filtration rate (eGFR) adjustment, the effect estimate remained similar, although statistical significance was not reached (B = 0.1646, p = 0.0525; n = 39). Galectin-3 correlated with NT-proBNP, left ventricular end-diastolic volume index (LVEDVi), and serum uric acid; all associations remained significant after false-discovery-rate correction. Serum peroxide burden and galectin-3 were not significantly correlated. In an exploratory joint model (n = 29), both biomarkers remained significantly associated with ln(NT-proBNP) (adjusted R² = 0.4294). Conclusions: Serum peroxide burden and galectin-3 showed different cross-sectional association patterns with NT-proBNP and selected structural/cardiorenal parameters. Given the limited sample size, missing data, and exploratory nature of the joint model, these findings should be considered hypothesis-generating and do not establish biological independence or incremental clinical value.

Background/Objectives: Atrial fibrillation (AF) is associated with cognitive decline even without clinically apparent stroke, but the relative contributions of demographic, vascular, inflammatory and therapeutic factors remain unclear. We aimed to explore clinical determinants of cognitive and functional performance in hospitalized patients with AF. Methods: In this exploratory cross-sectional study, 62 consecutive patients with documented AF admitted to an internal medicine department underwent assessment with the Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE) and Activities of Daily Living (ADL) scale. Associations were examined with multivariable linear regression, with false-discovery-rate correction and sensitivity analyses. Results: Mean age was 75.3 ± 8.1 years; 17 patients (27.4%) had a previous ischemic stroke. Fifty-nine patients (95.2%) scored below the MoCA threshold of 26 and 35 (56.5%) below the MMSE threshold of 24. Patients with previous stroke scored lower on all three instruments (MoCA mean difference 4.13, 95% CI 0.75–7.51; MMSE 4.84, 1.67–8.01; ADL 1.69, 0.25–3.12). After correction for multiple testing, age remained associated with all three outcomes and previous stroke with MMSE score; no association was detected for sex, education, diabetes, C-reactive protein, LDL-cholesterol or anticoagulant type. Higher CHA₂DS₂-VAScscores were associated with poorer performance, though not independently of their own components. Conclusions: In this exploratory study, cognitive impairment was common among hospitalized patients with AF and was associated with age and previous stroke. These hypothesis-generating findings require confirmation in larger prospective studies.