Objectives: This study aimed to investigate the associations between serum lipid biomarkers and pulse wave analysis (PWA) variables in patients at high and very high cardiovascular risk, with particular emphasis on age-related differences. Methods: Seventy-six patients at high or very high cardiovascular risk were enrolled and stratified into middle-aged (Group 1) and elderly (Group 2). All participants underwent PWA, and multiple serum lipid biomarkers were measured, including composite lipid indices. Results: In both age groups, PWA parameters showed significant correlations with serum lipid biomarkers. Systolic blood pressure (SBP) was an independent determinant of the lipid balance index (LBI), while pulse wave velocity (PWV) and SBP were independent determinants of the triglyceride-glucose (TyG) index. PWV correlated with age in both groups and was higher in Group 2 for comparable blood pressure values. In middle-aged patients, diastolic blood pressure (DBP) showed significant, independent associations with triglycerides and TyG, indicating a close link between peripheral vascular resistance and metabolic dysfunction in earlier stages of cardiovascular risk. In elderly patients, SBP and pulse pressure were predominantly associated with lipid-derived indices, reflecting the increasing contribution of large-artery stiffness and lipid-driven vascular remodeling with advancing age. Systematic Coronary Risk Estimation 2 (SCORE2) correlated significantly with PWV, the lipid index (LI), and the LBI. Conclusions: Serum lipid biomarkers and PWA-derived hemodynamic variables exhibit a significant, age-dependent interplay in patients with high and very high cardiovascular risk. These findings underscore the importance of age-specific evaluation of lipid-hemodynamic interactions to improve early identification and targeted management of high-risk individuals.

Cardiovascular diseases, particularly ischemic heart disease and angina pectoris, remain a major health problem worldwide. Combining conventional cardiovascular drugs with antioxidant compounds may offer complementary benefits, but biosafety must be carefully evaluated. This study aimed to assess the in vitro and in ovo biosafety of labetalol (LB; 20-500 nM) and silibinin (SIL; 5-200 & micro;M), administered individually and in combination, using H9c2(2-1) cells and the chorioallantoic membrane model. After 24 h, cell viability, morphology, lysosomal and membrane integrity, and mitochondrial and nuclear morphology were evaluated using MTT, Neutral Red uptake, fluorescence staining, and AO/PI assays. In addition, irritation potential was assessed using the HET-CAM assay. The results showed that cell viability remained comparable to control following all treatments. Mitochondrial and nuclear analyses indicated that organelle structure and morphology were preserved. Furthermore, AO/PI staining revealed no significant induction of apoptosis or necrosis. The HET-CAM assay confirmed the absence of vascular irritation for the tested combination. Overall, the combined administration of LB and SIL did not cause additional cytotoxicity or irritation compared with the individual treatments, supporting the biosafety of this combination.

Background/Objectives: Sodium-glucose cotransporter 2 (SGLT2) inhibitors provide well-established cardiovascular and renal benefits in heart failure (HF), type 2 diabetes (T2DM), and chronic kidney disease (CKD). Although emerging trials suggest potential value after acute myocardial infarction (AMI), SGLT2 inhibitors currently have no formal indication for AMI, and real-world prescribing patterns in this setting remain uncharacterized. This study aimed to evaluate in-hospital and post-discharge prescribing patterns and clinical predictors of SGLT2 inhibitor initiation among AMI patients eligible for therapy based on guideline-supported indications. Methods: We conducted a retrospective cohort study including 244 consecutive AMI patients hospitalized between January 2023 and July 2024. A total of 180 (73.7%) met guideline-based eligibility criteria for SGLT2 inhibitors. Four multivariable logistic regression models were developed to identify independent predictors of SGLT2 inhibitor prescription. Results: A total of 117 patients (65%) received SGLT2 inhibitors and 63 (35%) remained untreated. Receivers were more frequently male (81% vs. 65%) and exhibited lower left ventricular ejection fraction (LVEF) (38.2 ± 6.7% vs. 42.4 ± 8.3%), larger ventricular volumes, and higher Killip class at presentation. HF patients with preserved ejection fraction (HFpEF) were markedly undertreated (25.9%) compared with mid-range (HFmrEF) (69.8%) or reduced (HFrEF) (73.7%). Across all models, HFpEF was a strong negative predictor of prescribing (OR 0.071-0.081, p < 0.001), while male sex and markers of clinical severity were associated with higher likelihood of initiation. Many untreated patients had T2DM or CKD despite guideline-based eligibility. No serious adverse events attributable to SGLT2 inhibitors were reported. Conclusions: In this real-world AMI cohort, SGLT2 inhibitors were prescribed primarily in relation to established indications for HF, T2DM, and CKD, yet their use remained highly variable in the absence of a dedicated recommendation for AMI. Significant therapeutic gaps were observed in HFpEF and high-risk cardiometabolic profiles, underscoring the need for clearer guidance and standardized pathways to support consistent initiation in eligible patients after MI.

Background/Objectives: Alcohol septal ablation (ASA) is an established interventional therapy for patients with obstructive hypertrophic cardiomyopathy (OHCM) who remain symptomatic despite optimal medical treatment. Nevertheless, 10-20% of patients fail to achieve a satisfactory hemodynamic or clinical response, highlighting the need for improved patient selection. Given that mitral valve (MV) morphology plays a central role in left ventricular outflow tract (LVOT) obstruction, we aimed to evaluate the impact of MV anatomical parameters on ASA outcomes. Methods: We retrospectively analyzed 38 OHCM patients who underwent ASA and had complete echocardiographic data before and at 6-month follow-up. Patients were stratified into responders (n = 32, defined as >50% reduction in LVOT pressure gradient and/or residual LVOT gradient < 50 mmHg) and non-responders (n = 6, <50% reduction or persistent gradient ≥ 50 mmHg), consistent with criteria used in previous ASA outcome studies. MV parameters-including redundant anterior mitral leaflet (AML) length, posterior mitral leaflet (PML) projection, and anterior displacement of the coaptation point (AML/PML projection ratio)-were compared between groups. Results: Non-responders demonstrated significantly greater AML redundancy (13.16 ± 1.72 vs. 9.96 ± 1.99 mm, p < 0.001), larger PML projection (18.5 ± 3.78 vs. 13.65 ± 3.8 mm, p = 0.006), and lower AML/PML projection ratio (0.80 ± 0.15 vs. 1.34 ± 0.45, p = 0.007). These parameters were associated with reduced post-procedural LVOT gradient reduction in univariate logistic regression (p = 0.01, p = 0.027, p = 0.015, respectively). Multivariate modeling was not pursued due to collinearity among MV parameters and the limited number of non-responder events, which precluded robust adjustment. Conclusions: Mitral valve morphological features-particularly redundant AML, greater PML projection, and anterior displacement of the coaptation point-were associated with suboptimal ASA outcomes in univariate analysis. These data emphasize the need for comprehensive MV imaging in pre-procedural assessment. Integrating MV morphology into current selection algorithms may refine ASA patient selection and improve long-term success rates.

Background: Sleep quality (SQ) and physical activity (PA) are among the strongest behavioral determinants of healthy aging, while dietary behavior and psychological factors act as complementary modulators of these relationships. Although each domain has been studied extensively, their combined influence on subjective life expectancy (SLE)-an individual's perceived likelihood of living to an advanced age-remains largely unexplored. Methods: This narrative review synthesizes evidence from sleep science, exercise physiology, behavioral medicine, and psychological aging. Literature published between January 2015 and 15 December 2025 was examined across PubMed, Scopus, and Web of Science using integrative keyword strategies. Studies addressing SQ, PA, circadian rhythms, psychological health, SLE, or aging-related outcomes were included. Results: The review identifies several converging pathways linking sleep and PA to aging trajectories. Sleep architecture, circadian stability, metabolic regulation, inflammatory balance, and autonomic function represent key biological mechanisms. PA contributes through improvements in mitochondrial efficiency, VO2max, muscle metabolism, and anti-inflammatory signaling (IL-6 as a myokine). Across studies, both sleep and PA strongly influence psychological health, health perception, and future-oriented expectations, within a broader lifestyle context supported by nutritional status and dietary quality. SLE emerges as a central psychological mediator that shapes motivation, adherence to health behaviors, and long-term health outcomes. Contextual moderators-including age, gender, socioeconomic status, cultural norms, and wearable technology engagement-further influence these relationships. Conclusions: SQ and PA form the core behavioral components of a dynamic system that is further shaped by dietary behavior and psychological well-being and centered on SLE. Our proposed integrative model positions SLE as a key psychological link between lifestyle behaviors and longevity. This framework is hypothesis-generating and requires empirical validation through future longitudinal and interventional studies, underscoring the need for multidomain research integrating behavioral, biological, nutritional and psychological indicators of aging.

Background/Objectives: Healthcare-associated infections (HAIs) remain an important cause of morbidity in coronary care units (CCUs). Although left ventricular ejection fraction (LVEF) is central to cardiovascular risk stratification, its relationship with infection susceptibility in CCU patients is poorly defined. We explored the association between LVEF and HAI incidence in a real-world CCU population. Methods: We performed a retrospective cohort study including 870 consecutive adult patients admitted to a tertiary CCU. Patients were stratified by LVEF into reduced (<40%) and preserved or mildly reduced (≥40%) groups. HAIs were defined using Centers for Disease Control and Prevention/National Healthcare Safety Network (CDC/NHSN) criteria and required microbiological confirmation. Demographic data, comorbidities, exposure to invasive devices, colonization status and clinical outcomes were collected. Associations with HAIs were assessed using univariate and exploratory multivariable logistic regression. Results: Of the 870 patients, 235 (27.0%) had LVEF < 40%. The overall HAI incidence was 1.8% (16/870) and was significantly higher in patients with reduced LVEF compared with those with LVEF ≥ 40% (3.82% vs. 1.10%, p = 0.018). Patients with LVEF < 40% had greater exposure to invasive devices (OR 2.06, 95% CI 1.52-2.79, p < 0.001). The excess HAI burden was mainly driven by urinary tract infections (1.70% vs. 0.15%, p = 0.021). Colonization rates at admission were similar between groups. In univariate analysis, reduced LVEF was associated with higher HAI occurrence, but it did not remain independently associated after adjustment. Admission infection, malignancy, CPAP use, and CCU length of stay ≥5 days emerged as independent factors in the exploratory multivariable model (Nagelkerke R2 = 0.247). Conclusions: Reduced LVEF is associated with higher HAI incidence in CCU patients, reflecting greater clinical severity, longer hospitalization, and increased exposure to invasive devices. Although not an independent predictor, LVEF appears to function as a clinically useful marker of vulnerability that may support early risk stratification and targeted infection-prevention strategies in CCU settings.

Introduction: Artificial intelligence (AI) and robot-assisted platforms are increasingly influencing cardiothoracic surgery. AI enhances risk prediction, imaging interpretation, and early complication detection, while robotics improves visualization, dexterity, and minimally invasive access. This systematic review evaluates the current evidence supporting these technologies and their implications for clinical practice. Methods: A systematic literature search was conducted across PubMed, Embase, Scopus, Web of Science, and Google Scholar (January 2000–May 2025) following PRISMA 2020 guidelines. After screening and eligibility assessment, 67 studies met predefined inclusion criteria and were incorporated into the qualitative synthesis. Additional high-impact reviews and consensus documents were consulted for contextual interpretation. Results: Machine learning models demonstrated modest but consistent improvements in predictive performance compared with EuroSCORE II and STS scores, particularly in high-risk cohorts. Robot-assisted mitral and coronary procedures showed reduced postoperative pain, blood loss, ICU stay, and recovery time in experienced centers, though early learning phases were associated with longer operative, cross-clamp, and bypass times. AI-enabled intraoperative tools, such as video analysis, workflow recognition, and real-time anatomical segmentation, emerged as promising adjuncts for surgical precision. Structured robotic training programs, especially simulation-based and dual-console pathways, accelerated proficiency acquisition. Conclusions: AI and robotic systems act as augmentative technologies that enhance rather than replace the surgeon’s role. Their safe and effective adoption requires standardized training, transparent AI decision pathways, and clear ethical and medico-legal governance.

Background/Objectives: Cardiovascular diseases are a major cause of morbidity and mortality worldwide. Acute chest pain is a frequent reason for emergency department presentation and requires structured evaluation to identify life-threatening conditions. This study evaluated clinical characteristics, cardiovascular risk profile, risk stratification patterns, and hospitalization status in adults with acute chest pain. Methods: We conducted a retrospective study using registry data from Arad County Clinical Emergency Hospital between January 2021 and December 2024. Adult patients with documented acute chest pain were included according to predefined criteria. Demographics, comorbidities, clinical presentation, troponin values, hospitalization status, and HEART, and EDACS categories were extracted when available. The Marburg Heart Score was also assessed as an exploratory complementary score. Statistical analysis used descriptive statistics, contingency tables, and chi-square testing, with available-case analysis. Results: Overall, 2070 patients were included. Most patients were aged 35-54 or 55-69 years. Hypertension and diabetes mellitus were the most common comorbidities, and pressure-like chest pain predominated. In unadjusted analyses, HEART and EDACS categories were significantly associated with hospitalization status across all study years. Score categories were significantly associated with hospitalization status across all study years. Age was consistently associated with cardiovascular comorbidity burden and higher-risk score categories. Conclusions: Structured risk stratification scores were associated with hospitalization status, while age was associated with cardiovascular risk burden.

Background/Objectives: Heart failure (HF) in patients with conventional right ventricular pacing with significant pacing percentages is still a subject of concern, and management of HF in this population has historically been difficult; however, novel HF pillar medications, such as SGLT2 inhibitors (SGLT2i) and angiotensin receptor/neprilysin inhibitors (ARNi), have fundamentally transformed contemporary pharmacological HF management. The aim of this study was to assess left ventricular (LV) function after current guideline-directed medical therapy (GDMT) in patients with chronic right ventricular (RV) pacing and HF. Methods: Patients with a lifetime ventricular pacing percentage > 20% (Vp > 20%) and HF diagnosed according to ESC guideline criteria were included. Device interrogation and transthoracic echocardiography (TTE), including assessment of left ventricular ejection fraction (LVEF) and mitral annular plane systolic excursion (MAPSE), were performed at GDMT initiation and during subsequent follow-up. Changes in LVEF and MAPSE were assessed overall and according to baseline HF phenotype. Multivariable linear regression analyses were performed to identify independent predictors of changes in LVEF and MAPSE. Results: Among 550 conventionally paced patients screened for HF, 127 (23.1%) met the inclusion criteria and underwent GDMT initiation. Mean age was 68.2 ± 12.1 years, and mean follow-up duration was 10.2 ± 6.3 months. Baseline LVEF and MAPSE were 48.7 ± 6.3% and 12.0 ± 2.4 mm, respectively. All patients received SGLT2i therapy, while 24 (18.9%) received ARNi. Overall, LVEF increased by 1.94 ± 2.47% and MAPSE by 0.84 ± 0.96 mm (both p < 0.001). Patients with HFrEF (n = 25) showed an increase in LVEF of 5.84 ± 2.53% and MAPSE of 1.72 ± 1.21 mm. In patients with HFmrEF, LVEF increased by 2.50 ± 1.54% and MAPSE by 0.83 ± 0.92 mm, whereas in HFpEF, LVEF increased by 0.67 ± 0.78% and MAPSE by 0.58 ± 0.71 mm. NYHA functional class improved by at least one class in 100 patients (78.7%). In multivariable analysis, ARNi use was independently associated with greater improvement in LVEF and MAPSE, while lower baseline LV function was associated with greater subsequent improvement. Conclusions: In patients with HF and chronic RV pacing, GDMT was associated with modest but statistically significant improvements in LV systolic function, assessed by LVEF and MAPSE, across the HF spectrum. The greatest improvements were observed in patients with HFrEF. However, given the observational design, absence of a control group, and universal use of SGLT2i, these findings do not establish a causal treatment effect or demonstrate superiority of any specific GDMT combination. Prospective controlled studies are warranted to determine the clinical significance of these changes and the independent contribution of individual therapies.

Background/Objectives: Acute coronary syndromes (ACS) encompass a spectrum of clinical entities from unstable angina to non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI), all associated with significant morbidity and mortality. Inflammation plays a central role in the pathophysiology of ACS, contributing to atherosclerotic plaque destabilization, myocardial injury, and adverse clinical outcomes. Inflammatory biomarkers, together with N-terminal pro-B-type natriuretic peptide (NT-proBNP), are increasingly used for risk stratification, yet their prognostic value across different ACS presentations remains unclear. This study aimed to assess the prognostic value of inflammatory status in patients with acute coronary syndromes in a single-center cohort. Methods: This prospective observational study included 100 consecutive patients with ACS and elevated inflammatory biomarkers, enrolled in 2024-2025 at a tertiary cardiovascular center. Inflammatory status was assessed by using C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII); NT-proBNP was also measured. The primary endpoint was in-hospital MACE, defined as cardiovascular death, recurrent myocardial infarction, stroke, urgent coronary revascularization, or acute heart failure requiring escalation of therapy. Multivariable logistic regression and ROC analyses were performed. Results: Among the 100 ACS patients, half experienced in-hospital MACE. Compared with those without events, patients with MACE were older (p = 0.003) and had higher inflammatory biomarkers-CRP (p < 0.001; strongest association), NLR (p = 0.030), and SII (p = 0.042)-as well as higher NT-proBNP (p = 0.002). Patients with MACE also showed reduced renal function (p < 0.001) and lower left ventricular systolic function, reflected by reduced LVEF (p = 0.001), indicating concomitant renal impairment and ventricular dysfunction. Hypertension was more prevalent in the MACE group (p = 0.028), and new-onset atrial fibrillation was significantly more common among these patients (p < 0.001). In multivariable analysis, LVEF emerged as an independent predictor of short-term outcomes (OR 0.934 per 1% increase; p = 0.047). Conclusions: Inflammatory activation appears closely linked to the occurrence of in-hospital adverse events in patients with acute coronary syndromes. While left ventricular ejection fraction remained an independent determinant of short-term outcomes, inflammatory biomarkers may provide complementary insight into the inflammatory burden accompanying ACS.

Background: Patients with type 2 diabetes mellitus (T2DM) who present with ST-segment elevation myocardial infarction (STEMI) remain at high risk of adverse remodeling after reperfusion. This observational study examined whether pre-admission glucose-lowering therapy class was associated with six-month left ventricular (LV) reverse remodeling and myocardial work recovery. Methods: We analyzed 253 patients with STEMI, baseline LV ejection fraction ≤ 50%, successful primary PCI, and complete baseline and six-month echocardiography. The primary inferential analyses focused on 75 patients with T2DM, grouped according to pre-admission therapy with SGLT-2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors, or conventional therapy; non-diabetic patients were retained as a descriptive reference group. Clinical outcome, propensity-score, subgroup, and mediation analyses were considered exploratory because of small subgroup and event counts. Results: SGLT-2 inhibitor and GLP-1 receptor agonist exposure was associated with larger improvements in LVEF, LV volumes, and global work efficiency than DPP-4 inhibitors or conventional therapy. Crude MACE rates were highest in the conventional-therapy group, but event estimates were imprecise and confounded by baseline risk, revascularization status, and discharge therapy. Conclusions: In patients with T2DM recovering from STEMI, pre-admission exposure to SGLT-2 inhibitors and, to a lesser extent, GLP-1 receptor agonists was associated with more favorable structural and myocardial work recovery. These hypothesis-generating findings should be interpreted as associations and require confirmation in adequately powered prospective studies.

Background/Objectives: Cardiac resynchronization therapy (CRT) is a cornerstone treatment for heart failure with reduced ejection fraction (HFrEF), yet many patients remain symptomatic despite long-term electrical optimization. Although sacubitril/valsartan (ARNI) is central to guideline-directed medical therapy (GDMT), data on its late initiation in patients with chronic CRT are scarce. This study evaluated the impact of delayed ARNI initiation on clinical status, functional capacity, and cardiac remodelling in a real-world CRT population. Methods: We performed a single-centre, retrospective observational study including 76 HFrEF patients with chronic CRT who started ARNI between 2022 and late 2024. Patients underwent standardized assessment at baseline (T0) and after 12 ± 3 months (T1), including clinical evaluation, 12-item Kansas City Cardiomyopathy Questionnaire (KCCQ-12), symptom-limited bicycle exercise testing, and comprehensive echocardiography. The primary endpoint was change in quality of life (QoL). Secondary endpoints included exercise capacity, echocardiographic reverse remodelling, NYHA class, loop diuretic dose, and device-detected arrhythmias. Dose-response and multidimensional response patterns were explored. Results: KCCQ-12 increased from 52.96 ± 16.33 to 75.55 ± 18.12 (Δ +22.59 ± 13.22, p < 0.001), with 89.5% achieving a clinically meaningful improvement. Exercise duration and peak workload improved significantly. LVEF increased from 35.08 ± 6.96% to 43.18 ± 8.42% (Δ +8.11%, p < 0.001), with reductions in left ventricular and atrial volumes. Loop diuretic dose decreased (median -10 mg/day furosemide equivalent, p < 0.001), and 26.3% discontinued diuretics. A lower prevalence of device-detected arrhythmias was observed at follow-up, from 34.2% to 6.6% (p < 0.001). Higher ARNI doses were associated with greater likelihood of clinical, functional, and structural response. Longer CRT duration reduced the probability of structural remodelling but not symptomatic or functional benefit. Conclusions: In patients with long-standing CRT, delayed ARNI initiation was associated with improvements in QoL, exercise capacity, cardiac remodelling, congestion status, and electrical stability. These findings suggest that CRT is not a therapeutic ceiling and that late ARNI initiation remains a valuable component of comprehensive GDMT.

Background: Sacubitril/valsartan is a cornerstone of guideline-directed medical therapy for heart failure with reduced ejection fraction (HFrEF), yet data regarding reverse remodeling after ARNI initiation in patients previously treated with cardiac resynchronization therapy (CRT) remain limited. This study evaluated echocardiographic reverse remodeling following sacubitril/valsartan initiation in a real-world cohort of CRT-treated patients and explored the association between treatment timing and remodeling response. Methods: This single-center retrospective pilot study included 188 patients with HFrEF treated with CRT who subsequently initiated sacubitril/valsartan. Patients were categorized into early (≤12 months after CRT, n = 112) and late (>12 months, n = 76) initiation groups. Echocardiographic parameters and functional status were assessed at baseline and at approximately 12 months. Reverse remodeling was evaluated using changes in left ventricular ejection fraction (LVEF), ventricular volumes, and clinical status. Multivariable logistic regression was used to explore factors associated with reverse remodeling (ΔLVEF ≥ 10%). Results: Sacubitril/valsartan therapy was associated with significant improvements in LVEF, left ventricular end-diastolic volume, left atrial volume, and NYHA functional class in both groups. The magnitude of improvement in echocardiographic parameters was similar between early and late initiation groups. In exploratory multivariable analyses, earlier ARNI initiation was associated with clinically meaningful reverse remodeling (ΔLVEF ≥ 10%) (OR 6.36, 95% CI 1.59–25.50, p = 0.009). SGLT2 inhibitor therapy was also associated with reverse remodeling (OR 5.76, 95% CI 1.86–17.87, p = 0.002), while a longer CRT-to-ARNI interval was associated with lower odds of response (OR 0.77 per year, 95% CI 0.62–0.96, p = 0.018). Analysis of CRT-to-ARNI interval as a continuous variable showed only a weak association with reverse remodeling, while receiver operating characteristic analysis did not identify a meaningful temporal threshold (AUC 0.497). Conclusions: Sacubitril/valsartan initiation after CRT was associated with significant reverse remodeling, including in patients who initiated therapy several years after CRT implantation, although the late-initiation subgroup was of limited size, and treatment intervals beyond the interquartile range (4.0–7.0 years) were sparsely represented. Absolute echocardiographic improvements were broadly similar between groups, and receiver operating characteristic analysis did not identify a discriminative temporal threshold (AUC 0.497), indicating no discriminative ability beyond chance. Exploratory multivariable analysis identified an association between earlier initiation and clinically meaningful reverse remodeling, but this finding was not supported by a clinically meaningful temporal threshold.

Background and Objectives: Healthcare-associated infections (HAIs) remain a relevant complication in coronary care units (CCUs), particularly among patients with cardiac dysfunction requiring invasive monitoring and prolonged hospitalization. In this setting, infection occurrence may reflect the cumulative interaction between baseline biological vulnerability and care-related exposure. This study aimed to explore whether a simple cumulative framework integrating these components can describe patterns of HAI occurrence and support early identification of patients at risk for severe infectious complications and sepsis. Materials and Methods: The retrospective cohort study included 870 consecutive adult patients admitted to a tertiary-care CCU. A four-component cumulative framework was constructed using reduced left ventricular ejection fraction (LVEF < 40%), diabetes mellitus, urinary catheterization, and CCU length of stay > 5 days. Each component contributed one point (range 0-4). HAIs were defined according to CDC/NHSN criteria and required microbiological confirmation. Associations between cumulative burden and infection occurrence were assessed using trend analysis and exploratory modeling. Results: HAI occurrence increased progressively across cumulative framework levels, demonstrating a stepwise pattern from low to higher vulnerability strata (p for trend < 0.001). A substantial proportion of infections clustered in patients with higher cumulative values, despite representing a minority of the cohort. Increasing cumulative burden was accompanied by higher observed infection occurrence, supporting a graded association between cumulative vulnerability and infection occurrence. Conclusions: In CCU patients, HAI occurrence appears to reflect the accumulation of biological vulnerability and care-related exposure during hospitalization. A simple cumulative framework may support early identification of patients requiring closer preventive attention and contribute to improved awareness of severe infectious complications in cardiac critical care. Prospective validation is warranted.

Background: Risk stratification models are widely used in clinical research; however, their development becomes methodologically challenging in settings characterized by low outcome incidence. In coronary care unit (CCU) populations, healthcare-associated infections (HAIs) occur relatively infrequently, limiting the feasibility of conventional multivariable predictive modeling. Methods: A retrospectively assembled CCU cohort comprising 870 patients with 16 HAI events (1.8%) was used as an illustrative example to examine methodological constraints associated with low events-per-variable (EPV) ratios. The implications of limited event frequency for multivariable logistic regression were evaluated, including risks of overfitting, coefficient instability, and reduced reproducibility. As an alternative strategy, a prespecified cumulative additive framework integrating baseline vulnerability and exposure-related variables was conceptually and analytically explored. Results: With four candidate predictors and 16 outcome events, the resulting EPV was approximately four, indicating a high risk of instability for conventional multivariable modeling. The cumulative framework allowed structured cumulative stratification without coefficient optimization. Infection occurrence increased progressively across cumulative framework levels, illustrating a graded pattern of increasing HAI occurrence with accumulating vulnerability and exposure-related burden. Conclusions: In clinical datasets with limited outcome events, modeling strategies should be aligned with the informational capacity of the data. Cumulative additive frameworks may represent a pragmatic structural alternative to coefficient-based modeling approaches in rare-event clinical settings. The present work provides a structured methodological framework for risk stratification under low-events-per-variable conditions rather than proposing a novel clinical scoring system.

Background/Objectives: Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide and increasingly are recognized as a continuum of interconnected conditions rather than isolated entities. Methods: A structured narrative literature search was performed in PubMed, Scopus, and Google Scholar for publications from 2015 to 2025 using combinations of different keywords: “cardiovascular disease spectrum”, “multi-omics”, “precision cardiology”, “machine learning”, and “artificial intelligence in cardiology”. Results: Evidence was synthesized across seven major clusters of cardiovascular conditions, and across these domains, common biological pathways were mapped onto heterogeneous clinical phenotypes, and we summarize how multi-omics integration, AI-enabled imaging and digital tools contribute to improved risk prediction and more informed clinical decision-making within this spectrum. Conclusions: Interpreting cardiovascular conditions as components of a shared disease spectrum clarifies cross-disease interactions and supports a shift from organ- and syndrome-based classifications toward mechanism- and data-driven precision cardiology. The convergence of multi-omics, and AI offers substantial opportunities for earlier detection, individualized prevention, and tailored therapy, but requires careful attention to data quality, equity, interpretability, and practical implementation in routine care.

Background: Postprandial triglyceride (TG) metabolism represents a dynamic dimension of lipid physiology that complements conventional fasting lipid assessment. Although low-density lipoprotein cholesterol (LDL-C) remains the primary therapeutic target in cardiovascular prevention, residual cardiovascular risk persists in many individuals despite apparently adequate fasting lipid control. Because most individuals spend the majority of their waking hours in a fed state, postprandial TG responses may provide clinically relevant insight into metabolic flexibility, dietary exposure, and the efficiency of TG-rich lipoprotein clearance. Methods: This narrative review was conducted using a literature search guided by predefined themes, keywords, and databases, without following a formal systematic review protocol. Randomized controlled trials, observational studies, meta-analyses, and major reviews addressing postprandial lipid metabolism, dietary determinants, and cardiometabolic risk were included, with priority given to human studies. Results: Postprandial TG responses are strongly influenced by dietary composition, eating patterns, and metabolic health. Individuals with insulin resistance, type 2 diabetes, obesity, and metabolic-associated steatotic liver disease (MASLD) frequently demonstrate exaggerated or prolonged postprandial lipemia even when fasting TG concentrations appear acceptable. While circulating TGs serve as practical clinical markers of postprandial lipid handling, cholesterol-enriched remnant lipoproteins more closely reflect atherogenic burden. Nutritional interventions, weight management, and physical activity consistently improve postprandial TG dynamics, whereas pharmacologic therapy provides additional benefit in selected high-risk patients. Non-fasting TG measurements may provide additional insight into postprandial lipid metabolism and residual cardiovascular risk, although standardized protocols and validated clinical thresholds remain to be established. Conclusions: Postprandial TG metabolism provides clinically meaningful information beyond fasting lipid measurements and represents a useful adjunct for refining residual cardiovascular risk assessment. Although standardized protocols remain limited, integrating nutritional and clinical perspectives may support a more comprehensive and individualized approach to cardiometabolic prevention.

Background/Objectives: Cardiac resynchronization therapy (CRT) and angiotensin receptor–neprilysin inhibitors (ARNIs) are cornerstone therapies for patients with heart failure with reduced ejection fraction (HFrEF). However, nearly 30% of patients show no significant response to CRT alone. The potential of ARNI to enhance CRT outcomes—especially in non-responders—is an emerging field of interest. The objective of this review is to systematically evaluate and synthesize the available evidence on the clinical outcomes of combining CRT with ARNI therapy in patients with HFrEF. Methods: We conducted a comprehensive search of PubMed, Scopus, and Google Scholar up to September 2024, using the keywords “CRT and ARNI” and “cardiac resynchronization therapy and sacubitril/valsartan”. We included retrospective and prospective clinical studies, observational studies, and review articles reporting on patients with HFrEF treated with both CRT and ARNI. Studies not in English, animal studies, and those without full-text availability were excluded. Study selection and data extraction were performed in duplicate by independent reviewers, using PRISMA guidelines for transparency. The final selection included 8 studies published in the last four years, summarized by design, population, outcomes, and statistical significance. Results: The reviewed studies suggest that ARNI therapy, when combined with CRT, may contribute to improvements in left ventricle ejection fraction (LVEF), NYHA functional class, and ventricular remodeling, particularly in CRT non-responders. Some studies also report a potential reduction in ventricular arrhythmias and implantable cardioverter-defibrillator (ICD) interventions. However, outcomes varied across subgroups, and the influence of ARNI timing relative to CRT implantation remains inconclusive. Limitations: Heterogeneity in study designs and small sample sizes in some included studies limited the ability to conduct a meta-analysis. This review is not registered. Conclusions: ARNI therapy shows promise in enhancing CRT response in patients with HFrEF, particularly in non-responders. Further large-scale, prospective studies are needed to clarify optimal patient selection and treatment sequencing.

The electrical ventricular storm (VES) is defined as multiple sustained ventricular arrhythmias arising in a short time, often refractory to standard antiarrhythmic treatment. The three pillars of the physiopathogenesis of the VES are autonomic dysfunction, triggers, and an altered ventricular substrate. Incessant or highly recurrent ventricular arrhythmia impacts the hemodynamic status by worsening heart failure and increasing mortality. A stepwise, team-based, and tailored therapeutic approach is required to stop ventricular arrhythmia and regain the hemodynamic and electric stability of the patient. The authors focused on describing all currently available therapeutic approaches for VES, intending to establish the best VES therapeutic approaches. This process involves considering the patient’s specific condition, responses to previous treatments, and the potential risks and benefits of each approach. The options range from adjusting antiarrhythmic therapy to reprogramming of the ICD, sedation, epidural anaesthesia, stellate ganglia anaesthetic block, and the use of ECMO or left ventricular assist devices and radiofrequency catheter ablation. Particular attention is paid to the detailed management of genetic primary arrhythmia syndromes like long-QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome and Wolff–Parkinson–White syndrome, early repolarisation syndrome, right ventricular arrhythmogenic dysplasia, and idiopathic ventricular fibrillation. After overcoming the acute events of VES and obtaining hemodynamic stability, the treatment should shift toward an optimal balance of heart failure therapy, controlling the substrate by revascularisation procedures and resolving other pathology-generating ventricular arrhythmias. This article provides a comprehensive overview of ESV’s current management options using the most efficient strategies known to date.