Search Results (1,911)

Background and Objectives: Conduction disorders (CDs) and permanent pacemaker implantation (PPI) remain among the most common complications after transcatheter aortic valve implantation (TAVI). Given their potential impact on long-term outcomes, improved preprocedural identification of patients at high risk for new-onset CDs is increasingly important. We investigated whether selected preprocedural inflammatory and fibrotic biomarkers, along with echocardiographic indices of regional myocardial remodeling, were associated with new-onset CDs after TAVI. Materials and Methods: This single-center prospective observational study included 112 patients with severe aortic stenosis undergoing TAVI. Peripheral blood samples were obtained within 24 h before TAVI for measurement of inflammatory and fibrotic biomarkers, including interleukin-6 (IL-6), C-reactive protein (CRP), CRP-to-albumin ratio (CAR), procalcitonin, ferritin, lactate dehydrogenase, and transforming growth factor-β1. The primary outcome was the occurrence of new-onset CDs during the index hospitalization or within three months after TAVI. Results: New-onset CDs occurred in 58 patients (51.8%). IL-6 showed the strongest association with the outcome in univariable analysis (OR per 1-SD increase, 9.55; 95% CI 3.00–30.40; p < 0.001), remained associated after adjustment for selected clinical and procedural predictors in exploratory models (adjusted OR 10.70; 95% CI 2.43–47.07; p = 0.002), and demonstrated the highest, although moderate, discriminatory performance among the evaluated biomarkers (AUC 0.730; 95% CI 0.637–0.823). CRP and CAR were higher in patients with CDs and were significant in univariable analysis, but showed weaker and less consistent adjusted associations. Among echocardiographic markers, AB strain ratio ≥ 2 was the most consistent imaging correlate in exploratory biomarker–echocardiographic models. Conclusions: Elevated preprocedural IL-6 was the biomarker most consistently associated with new-onset CDs after TAVI. These findings suggest that higher preprocedural IL-6 levels may reflect patient-specific susceptibility to new-onset CDs after TAVI and could have potential value as an adjunctive biomarker, alongside echocardiographic assessment, for preprocedural risk evaluation, with further validation required in larger prospective studies. Full article

Background/Objectives: Prehospital identification of non-ST-elevation acute coronary syndrome remains unresolved, and available risk scores incorporate troponin categorically. We compared the discriminative performance of cardiac troponin I measured in a blood sample obtained at first prehospital medical contact, analysed as a continuous variable, against the HEART, GRACE, and TIMI scores for predicting 30-day major adverse cardiac events. Methods: We conducted a prospective cohort study in 333 adults with non-traumatic chest pain suggestive of non-ST-elevation acute coronary syndrome, which was attended by two physician-staffed advanced life support units. Venous blood was drawn at first medical contact and analysed later in the laboratory; the results were not available during patient care. All three scores used this same determination as their troponin component. The primary outcome was a composite of all-cause mortality, type 1 myocardial infarction, and unplanned coronary revascularisation at 30 days. Results: The primary outcome occurred in 82 patients (24.6%). Prehospital troponin discriminated better (area under the curve 0.916, 95% CI 0.875–0.952) than TIMI (0.817), GRACE (0.767), and HEART (0.721); all comparisons were p < 0.001. An exploratory rule-out threshold of 80 ng/L identified 61 patients (18.3%) with no events (sensitivity and negative predictive value 100%, exact 95% CI 95.6–100 and 94.1–100), whereas the ≥780 ng/L stratum showed an event rate of 69.4%. Conclusions: A blood sample obtained at first prehospital medical contact carries substantial prognostic information that clinical scores discard by categorising it. Because it was analysed subsequently in the laboratory, these findings do not evaluate a real-time strategy; they support development and validation of point-of-care devices. Full article

Background: The Heart Rate Recovery Index (HRRI), derived from post-exercise heart rate recovery (HRR), reflects autonomic function and cardiovascular performance. Whether HRRI reflects early myocardial dysfunction and left atrial remodelling in heart failure with preserved ejection fraction (HFpEF) has not been previously examined. The H₂FPEF score, which integrates clinical and echocardiographic parameters, is used to assess the likelihood of HFpEF. This study investigates the relationship between HRRI, H₂FPEF score, and echocardiographic markers of longitudinal systolic function, including mitral annular plane systolic excursion (MAPSE), as well as left atrial volume index (LAVI), in patients with preserved left ventricular ejection fraction. Methods: A prospective observational study included 241 patients referred for cardiac exercise testing at the Institute of Cardiovascular Diseases Timisoara and the Clinical County Hospital of Sibiu. HRRI was calculated as the ratio of heart rate acceleration time (AT) to deceleration time (DT) during exercise testing. A comprehensive echocardiographic assessment was performed on all patients. Statistical analysis involved univariate testing and multivariable logistic regression with stepwise selection. Results: HRRI was significantly lower in HFpEF patients compared with those without heart failure (1.97 ± 0.66 vs. 2.73 ± 1.08, p < 0.01). HRRI correlated significantly with exercise performance, age, H₂FPEF score, and echocardiographic markers of diastolic and longitudinal systolic dysfunction. ROC analysis identified an HRRI cut-off value of 2.25 for HFpEF detection (AUC = 0.748), while HRRI remained significantly associated with HFpEF after adjustment for the covariates included in the model. The combined HRRI–H₂FPEF score improved diagnostic discrimination compared with the H₂FPEF score alone (AUC 0.897 vs. 0.858), achieving an overall classification accuracy of 82.2%. Conclusions: In our study, HRRI is significantly reduced in HFpEF and distinguishes patients with and without heart failure. It shows associations with echocardiographic markers of diastolic and longitudinal systolic dysfunction, exercise capacity, and H₂FPEF score. Full article

Background and Objectives: Stenting isolated Medina 0,0,1 ostial side-branch lesions can result in geographic miss or protrusion into the main vessel. Drug-coated balloon (DCB) angioplasty avoids a permanent implant, but lesion-specific outcome data remain limited. We assessed procedural performance, bailout stenting, and 6- and 12-month outcomes after an intended DCB-only strategy. Materials and Methods: In this retrospective, single-center observational cohort study, we screened 170 patients who underwent coronary DCB treatment at a single center between 1 January 2023 and 31 July 2025. Thirty-one patients with de novo isolated Medina 0,0,1 lesions were included. The primary endpoint was 12-month target lesion failure (TLF), defined as cardiovascular death, target-vessel myocardial infarction, or clinically driven target lesion revascularization (TLR). Results: DCB-only strategy success was achieved in 29/31 patients (93.5%), post-DCB angiographic success in 29/31 (93.5%), and study-defined overall procedural success in 31/31 (100%). Final TIMI grade 3 flow after DCB was present in 30/31 patients; no flow-limiting dissection occurred. Two patients required bailout stenting, one because of deterioration to TIMI grade 2 flow and one because of residual stenosis >30% with recoil. Thirty patients were alive with documented follow-up at 12 months; one patient died from a non-cardiovascular cause at month 1. No TLF was recorded within 12 months. One clinically driven TLR for target-lesion restenosis occurred at month 20, outside the prespecified window. Conclusions: In this selected cohort, an intended DCB-only strategy avoided stent implantation in most patients and had a low bailout rate. The findings support procedural feasibility but do not establish comparative efficacy. Larger prospective studies are required. Full article

Background: Atrial fibrillation (AF) is associated with atrial remodelling, hemodynamic stress, and complex cardiopulmonary interactions. While natriuretic peptides and echocardiographic abnormalities are established markers of AF-related substrate, the contribution of spirometry changes, as a landmark of pulmonary impairment, remains less clearly defined. This study evaluated whether AF is associated with an integrated cardiopulmonary profile characterized by altered spirometry, increased NT-proBNP, and conventional echocardiographic markers of left atrial structure and function. Methods: We performed a retrospective, single-center observational study based on an existing clinical database of adult patients referred for 24 h 12-lead Holter ECG monitoring because of palpitations and/or chest pain. None of the included patients had a previously documented diagnosis of atrial fibrillation before Holter monitoring. Because a single 24 h Holter recording cannot establish spontaneous termination or long-term temporal pattern with certainty, AF documented for the first time during this recording is referred to throughout as “newly detected AF” rather than “paroxysmal AF”. During Holter monitoring, no ECG changes suggestive of myocardial ischemia were detected. From 536 records of patients without previously known AF who underwent 24 h 12-lead Holter ECG monitoring for palpitations and/or chest pain, 164 patients were retained for the main comparison, including 48 with newly detected paroxysmal AF and 116 without AF. Demographic, biochemical, spirometric, and echocardiographic variables were analyzed. The main respiratory parameters were forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and peak expiratory flow (PEF). NT-proBNP was the primary biomarker, while conventional left atrial structural and functional variables were used for echocardiographic assessment. Results: NT-proBNP was markedly higher in the AF group (684.5 vs. 62.3 pg/mL, p = 0.001), even when accounting for confounders like age, CKD, or CPD, showing by far the largest between-group difference among the biomarkers assessed (formal discrimination statistics such as ROC/AUC were not computed). The exploratory inflammatory markers assessed (hs-CRP, neutrophil/lymphocyte ratio, homocysteine) showed only modest, non-significant differences. Conventional echocardiographic parameters did not differ significantly between groups. In the strict complete-case comparison, spirometric indices did not reach statistical significance; however, preliminary project-level analysis showed lower FVC, FEV1, and PEF in AF patients, but without supporting the COPD diagnosis, and exploratory correlations suggested a relationship between spirometric performance and left atrial function. Conclusions: In this cohort, AF was most strongly associated with NT-proBNP, while the respiratory signal was weaker but directionally consistent with a broader cardiopulmonary phenotype. These findings do not support spirometry or NT-proBNP as stand-alone diagnostic tools for AF. However, when interpreted alongside traditional AF risk factors and symptoms, elevated NT-proBNP with concordant spirometric impairment may represent a hypothesis-generating additive signal supporting longer or repeated rhythm monitoring beyond 24 h in selected patients with suspected AF; this additive value was not formally tested against clinical models alone and requires prospective confirmation. Full article

Background: Intraoperative hypotension during major abdominal surgery is common and can result from changes in preload, afterload, or myocardial contractility. Recognising the underlying cause is essential for targeted haemodynamic management. Arterial dP/dt_max has been proposed as a surrogate marker for ventricular systolic function, but its behaviour during fluid and vasopressor administration under general anaesthesia remains not fully understood. This study evaluated changes in radial arterial dP/dt_max following protocol-guided fluid administration and norepinephrine boluses during intraoperative hypotension. Methods: This prospective observational study involved 88 adult patients undergoing elective major abdominal surgery with continuous radial arterial waveform monitoring. Hypotensive episodes were defined as a mean arterial pressure <65 mmHg persisting for at least 60 s and were managed according to a predefined algorithm based on stroke volume variation and dynamic arterial elastance. The primary outcome was the change in arterial dP/dt_max from baseline to 5 min after fluid administration. Linear mixed-effects models were used to account for repeated intervention episodes within patients. Results: A total of 502 protocol-guided intervention episodes contributed by 76 patients were included in the primary analysis: 228 fluid-treated episodes and 274 norepinephrine-treated episodes. Estimated mean arterial dP/dt_max increased from 517 mmHg·s⁻¹ (95% CI 477–557) at baseline to 631 mmHg·s⁻¹ (95% CI 591–671) at 5 min during fluid-treated episodes and from 575 mmHg·s⁻¹ (95% CI 536–615) to 647 mmHg·s⁻¹ (95% CI 608–686) during norepinephrine-treated episodes (both p < 0.001). A significant intervention-condition-by-time interaction was observed (F = 5.55, p = 0.019), indicating that temporal evolution of arterial dP/dt_max differed between the two algorithm-defined haemodynamic conditions. Conclusions: Radial arterial dP/dt_max increased after both fluid administration and norepinephrine, confirming its sensitivity to haemodynamic loading conditions. It should therefore be interpreted as an integrated haemodynamic variable influenced by ventricular performance, preload, and arterial properties rather than as a direct measure of intrinsic myocardial contractility. Full article

Background/Objectives: This study aimed to evaluate the prognostic role of the extracellular volume (ECV) assessed by cardiac magnetic resonance imaging (MRI) in relation to systolic dysfunction and unfavorable remodeling of the left ventricular (LV) at 24 weeks after myocardial infarction (MI) and revascularization. Methods: The study included 154 patients aged 56 ± 8 years who had been diagnosed with their first MI. Cardiac MRI was performed at 7–10 days and after 24 weeks, including assessment of indexed volumes, LV ejection fraction (LVEF), ECV, and patterns of ischemic and reperfusion injury. The study is registered in the international clinical trials registry with the number NCT04347434 (ClinicalTrials.gov). Results: Patients were divided into two groups after 24 weeks: group 1 (n = 24) with LVEF < 50% and group 2 (n = 130) with LVEF ≥ 50%. At 7–10 days, the scar mass in group 1 was 58.5 (39.5; 69.8) g vs. 17.1 (9.2; 29.7) g in group 2 (p < 0.001); microvascular obstruction was present in 23 cases (95.8%) vs. 55 (42.3%) (p < 0.001). After 24 weeks, inter-group differences increased (p < 0.05). Global ECV and remote myocardial ECV were significantly higher in patients with LVEF < 50% both at 7–10 days and after 24 weeks compared to those with LVEF ≥ 50% (p < 0.05). Infarct zone ECV did not differ between groups. Systolic dysfunction after 24 weeks was predicted by global ECV > 38.3% (p < 0.001) and remote myocardial ECV > 33.6% (p = 0.008). Predictors of an increase in end-diastolic volume index > 12% after 24 weeks in the subgroup of patients with initial systolic dysfunction were global ECV > 42.8% (p = 0.017) and remote myocardial ECV > 35.6% (p = 0.012). Conclusions: Global ECV and ECV of the remote myocardium, which exceed a certain level established by a cardiac MRI in the acute stage of MI, are among the predictors of LVEF < 50% and unfavorable LV remodeling in the medium term. Full article

Background: Multisystem inflammatory syndrome in children (MIS-C) was recognized in 2020 as a post-infectious hyperinflammatory condition occurring 2–6 weeks after SARS-CoV-2 infection. While large studies from Europe and North America have described its clinical spectrum and outcomes, evidence from the Middle East remains limited. MIS-C shares features with Kawasaki disease (KD), including persistent fever, mucocutaneous manifestations, and cardiac involvement, but differs in age distribution, gastrointestinal involvement, and patterns of cardiac injury. Objective: To map the reported Middle Eastern evidence on the clinical and laboratory phenotype, Kawasaki-like manifestations, cardiovascular involvement, management, short-term outcomes, and evidence gaps in children with MIS-C. Methods: A scoping review was conducted using the Arksey and O’Malley framework, guided by Joanna Briggs Institute methodology and reported according to PRISMA-ScR. PubMed/MEDLINE, Scopus, Web of Science, and the WHO COVID-19 database were searched for studies published from 1 December 2020 through 30 September 2025. Two reviewers independently screened records in Rayyan and charted data using standardized forms. Findings were synthesized descriptively; numerical ranges reflect values reported across selected contributing studies and are not pooled regional estimates. Results: Twenty-seven original clinical studies met the eligibility criteria, including case reports, case series, and observational cohorts from the UAE, Saudi Arabia, Qatar, Jordan, and multinational Middle Eastern collaborations. Across the included reports, affected children were generally older than the typical classic Kawasaki disease population. Gastrointestinal symptoms were commonly reported, and myocardial dysfunction was reported more frequently than coronary artery abnormalities. Most patients received intravenous immunoglobulin, often combined with corticosteroids. Short-term outcomes were generally favorable, but the evidence was heterogeneous and follow-up was limited. No meta-analysis was performed. Conclusions: The available Middle Eastern literature suggests that MIS-C commonly presents in school-aged children with gastrointestinal, mucocutaneous, and myocardial involvement. These patterns are descriptive rather than definitive because the evidence is predominantly retrospective, geographically uneven, and methodologically heterogeneous. The principal contribution of this review is to map the regional literature and identify priorities for prospective, standardized, multicenter studies and long-term follow-up. Full article

Brain-derived neurotrophic factor (BDNF) impacts parasympathetic nervous system function by increasing the excitability of cardioinhibitory parasympathetic neurons in the brainstem, ultimately lowering heart rate (HR) and heightening resting parasympathetic tone. Yet, whether BDNF and its high-affinity receptor—tropomyosin receptor kinase B (TrkB)—also act more distally, i.e., at the level of cholinergic-sensitive intrinsic cardiac ganglia (ICGs), remains unclear. Hence, we conducted morphological and functional studies in neural crest-specific BDNF knockout mice (ncBDNF KO), a model that selectively ablates BDNF signaling in neural crest-derived autonomic structures, including the intrinsic cardiac nervous system. ncBDNF mice exhibited a significant rise in resting heart rate with unchanged baseline contractile performance, thus supporting the role of endogenous BDNF in maintaining physiological parasympathetic restraint. When examining the ICGs, immunofluorescence analysis revealed a highly compartmentalized organization, with BDNF being predominantly confined to cholinergic neuronal somata and TrkB mainly clustered instead in S100-positive satellite glial cells, thus unveiling a previously unrecognized neuron–glia BDNF/TrkB ICG pattern. Next, we directly infused BDNF in Langendorff-perfused isolated WT mouse hearts and observed a rapid and reproducible bradycardic response that was abrogated by atropine but potentiated by neostigmine, hence attesting to the cholinergic nature of such bradycardia. Of note, BDNF maintained its positive inotropic effects under muscarinic blockade, as witnessed by the enhanced left ventricular developed pressure, maximal dP/dt, and rate-pressure product, congruent with direct BDNF-evoked myocardial TrkB agonism. Thus, ICGs are additional relevant relay stations interposed between BDNF/TrkB signaling and parasympathetic modulation of heart function. Although through different molecular paths, BDNF-mediated modulation of ICG firing can coordinate with the previously reported BDNF positive inotropy/lusitropy to adapt cardiac performance to increased workload and/or stress conditions. Full article

Background/Objectives: The effect of cardiac motion on dynamic positron emission tomography (PET) myocardial perfusion imaging (MPI) could distort the quantitative perfusion indices during acquisition, depending on direction, magnitude, and vascular territory. This study aimed to assess the impact of motion correction (MC) and its influences on quantitative perfusion indices using a comprehensive range of established statistical methods. Method: We retrospectively analyzed 171 patients’ data who underwent ¹³N-ammonia dynamic PET/CT-MPI. All the rebinned listmode data were transferred to the dedicated workstation for MC and quantification, yielding paired MC and non-motion correction (NMC) datasets for both phases. Frame-by-frame post-MC vectors were used to characterize motion magnitude and direction. Paired comparisons, directional analysis, association, agreement, accuracy, precision, and clinical reclassification were performed. Results: Motion occurred during both acquisition phases, but it was more frequent, more heterogeneous, and generally greater during stress, with the most notable displacement along the Y-axis. MC had a limited impact on the rest myocardial blood flow (MBF) but showed more significant effects on stress MBF, myocardial flow reserve (MFR), and non-invasive fractional flow reserve (niFFR) -like index, especially in the left anterior descending artery (LAD). Although MC and NMC values remained strongly associated for MBF and MFR, they were not fully interchangeable. The bidirectional reclassification of MFR and niFFR-like index showed that MC responded to the direction and magnitude of motion rather than a simple increase the values. Conclusions: MC exerts a structured, bidirectional, and motion-dependent influence on quantitative dynamic PET-MPI and has an impact beyond simple numerical adjustment. Full article

Objectives: Heart failure (HF) arises from multiple interrelated pathological processes. Among these, lysosomal impairment and loss of autophagic homeostasis are increasingly recognized as important contributors to myocardial damage and ventricular remodeling. This study sought to identify lysophagy-associated signature genes in HF and to define their biological roles, cellular origins, and potential diagnostic relevance. Methods: Bulk myocardial transcriptome datasets, including GSE16499, GSE57338, and GSE76701, were integrated with the human cardiac single-cell dataset GSE145154. Differential expression analysis was first performed to identify lysophagy-related differentially expressed genes (DEGs). Candidate hub genes were then screened using support vector machine-recursive feature elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) regression. Functional enrichment analysis, Gene Set Enrichment Analysis (GSEA), immune infiltration assessment, single-cell transcriptomic mapping, and regulatory network analysis were subsequently conducted. The expression profiles of the selected genes were validated in a murine HF model, and VAMP8 overexpression assays were performed in H9c2 cells. Results: Five hub genes, namely VAMP8, STX2, MCOLN1, DERL1, and PTP4A2, were consistently and markedly decreased in failing myocardial tissue. These genes were mainly linked to SNARE-dependent vesicle trafficking and lysophagy regulation. A diagnostic model incorporating these hub genes demonstrated good discriminatory performance in both the training dataset and a small independent validation cohort, supporting further evaluation of their potential diagnostic value. Single-cell analysis further indicated that these genes were primarily enriched in cardiac FOLR2⁺ tissue-resident macrophages (TRMs). Pseudotime and cell–cell communication analyses associated this module with FOLR2⁺ TRM cell states and predicted interactions with cardiac stromal cells. In the HF mouse model, the mRNA levels of all five hub genes were decreased, with concurrent reductions in VAMP8, MCOLN1 and DERL1 protein expression. In Ang II/LLOMe-induced H9c2 cells, VAMP8 overexpression was associated with reduced cardiomyocyte injury, attenuation of changes in the abundance of lysosome- and autophagy-related proteins, and fewer ultrastructural abnormalities, suggesting a potential cardioprotective effect. Conclusions: VAMP8, STX2, MCOLN1, DERL1, and PTP4A2 were identified as candidate molecular markers of HF that reflect alterations in a lysophagy- and vesicular-transport-related program associated with FOLR2⁺ tissue-resident macrophages. These findings provide new insights into immune-microenvironment remodeling in HF and suggest potential directions for mechanistic and therapeutic investigations. Full article

Breast cancer is associated with systemic inflammation and increased cardiovascular risk, and anthracycline chemotherapy may contribute to persistent myocardial injury. This study aimed to evaluate acute changes in inflammatory cytokines and plasma redox status after the first anthracycline cycle and to assess long-term ventricular function after 10 years in women with breast cancer. We conducted a prospective study of 17 patients with breast cancer treated with anthracycline-based chemotherapy at Salvador Hospital, Santiago, Chile. Plasma cytokines were measured at baseline (day −7) and on day +3 after the first cycle using a MILLIPLEX Luminex^® assay. Echocardiographic assessment of left ventricular systolic and diastolic function, together with oxidative stress parameters, was performed at baseline and after 10 years of follow-up. Anthracycline exposure was associated with an acute increase in several cytokines related to inflammatory and vascular remodeling, including EGF, eotaxin, MCP-1, and VEGF. In addition, markers of redox imbalance suggested an acute pro-oxidant response after treatment. At long-term follow-up (10 years), left ventricular ejection fraction (LVEF) remained within the normal range in all patients. However, integrative echocardiographic assessment revealed impaired left ventricular relaxation, evidenced by significant reductions in the mitral inflow E/A ratio, and septal and lateral e′ velocities with respect to baseline, despite preserved estimated filling pressures. These alterations were accompanied by persistent oxidative stress, reflected by persistently elevated levels of lipid peroxidation markers, such as in vivo 8-isoprostanes. In this pilot cohort, anthracycline chemotherapy induced an early inflammatory and oxidative response that was not associated with overt long-term systolic dysfunction but was accompanied by persistent biochemical and diastolic alterations. These findings support the concept of a long-term subclinical cardiotoxic phenotype and highlight the potential value of combining echocardiographic assessment with circulating redox and inflammatory biomarkers to improve long-term cardiovascular surveillance in breast cancer survivors. Full article

Background: Patients with coronary artery disease (CAD) receiving dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) remain at risk of early adverse outcomes, including in-hospital mortality. Simple risk stratification based on routinely available variables may help identify higher-risk patients, but a limited number of outcome events constrains robust prediction-model development and validation. Aim: This exploratory study aimed to derive a preliminary, interpretable clinical score based on routinely available variables for risk stratification of all-cause in-hospital mortality in CAD patients receiving DAPT after PCI. In the clopidogrel-dominant practice setting of the participating centers, the score was conceived as a hypothesis-generating risk-enrichment framework rather than a validated treatment-selection tool or a surrogate measure of platelet reactivity. Methods: We analyzed a retrospective cohort of 1600 adults with CAD admitted between 2022 and 2024; 36 in-hospital deaths occurred. Twenty demographic, clinical, laboratory, and instrumental variables were evaluated. The primary outcome was all-cause in-hospital mortality during the index hospitalization. For exploratory score derivation, the dataset was randomly divided into a derivation subset (75%; n = 1200) and a hold-out assessment subset (25%; n = 400). Predictors were explored using univariable and multivariable logistic regression with stepwise selection. Continuous variables were categorized using Weight of Evidence binning, and an integer point score was derived. Performance was summarized using ROC analysis, AUC, sensitivity, specificity, and accuracy. Given the small number of deaths and the data-driven modelling workflow, all performance estimates were considered preliminary rather than definitive internal validation. Results: The exploratory six-variable score included age ≥ 57 years, estimated glomerular filtration rate < 45 mL/min/1.73 m², body mass index ≥ 25 kg/m², troponin I ≥ 100, prior myocardial infarction, and current smoking. In the derivation subset, each additional point was associated with higher odds of mortality (OR 1.39; 95% CI 1.29–1.51; p < 0.001), and the AUC was 0.654. A Youden-index threshold of approximately 6 points yielded sensitivity of 0.41, specificity of 0.80, and accuracy of 0.72. In the hold-out assessment subset, sensitivity was 0.53, specificity was 0.70, accuracy was 0.70, and AUC was 0.61. These estimates indicate modest discrimination and should be interpreted cautiously because only 36 outcome events were available. Conclusions: This exploratory clinical score showed modest discrimination for all-cause in-hospital mortality and should be regarded as a preliminary, hypothesis-generating risk-stratification approach. It is not sufficiently validated for routine prognostic classification, platelet-reactivity triage, or antiplatelet treatment selection. Model redevelopment using event-efficient methods, resampling-based internal validation, and subsequent external validation are required before clinical implementation. Full article

Background and Objectives: Soluble suppression of tumorigenicity-2 (sST2) is a biomarker associated with myocardial stress, inflammation, and fibrosis. Although elevated sST2 levels have demonstrated prognostic significance in heart failure and acute coronary syndromes, their clinical relevance in patients undergoing percutaneous coronary intervention (PCI) remains incompletely defined. This study aimed to evaluate the association between baseline serum sST2 levels and long-term clinical outcomes in an unselected real-world cohort of patients undergoing PCI. Materials and Methods: A total of 758 consecutive patients with coronary artery disease who underwent PCI between September 2015 and November 2017 were enrolled. Baseline serum sST2 levels were measured before PCI, and patients were stratified according to the median value (28.3 ng/mL). The primary endpoint was major adverse cardiac and cerebrovascular events (MACCEs), defined as a composite of cardiac death, nonfatal myocardial infarction, and nonfatal stroke. Multivariable Cox proportional hazards models and receiver operating characteristic analyses were performed to assess the association of sST2 with clinical outcomes and its discriminatory ability. Results: During a median follow-up of 28.3 months, MACCEs occurred in 19 patients (2.5%). Patients with higher sST2 levels had significantly higher rates of MACCEs (4.2% vs. 0.8%, p = 0.005) and all-cause mortality (11.9% vs. 2.6%, p < 0.001) than those with lower sST2 levels. Although the association between elevated sST2 and MACCE was attenuated after multivariable adjustment (adjusted hazard ratio, 3.28; 95% confidence interval, 0.91–11.83; p = 0.070), receiver operating characteristic analysis demonstrated moderate predictive performance for MACCE (AUC, 0.723) and all-cause mortality (AUC, 0.763). The optimal cutoff value for predicting MACCE was 52.2 ng/mL. Conclusions: Elevated baseline serum sST2 levels were associated with adverse long-term clinical outcomes in an unselected, real-world cohort of patients undergoing PCI. Further studies are warranted to clarify its prognostic role in this population. Full article

Septic cardiomyopathy is a common complication of sepsis that significantly contributes to hemodynamic instability and adverse clinical outcomes. Despite increasing understanding of its pathophysiology, there is still no specific biomarker that reliably reflects myocardial function during sepsis. Growth differentiation factor-15 (GDF-15) is a cytokine induced by cellular stress associated with inflammation, oxidative stress, and cardiovascular damage. However, the relationship between GDF-15 and echocardiographic markers of septic myocardial dysfunction remains poorly understood. The aim of this study was to examine the association of serum concentrations of GDF-15 and high-sensitivity troponin I (hs-TnI) with echocardiographic parameters of systolic and diastolic myocardial function in patients with sepsis. This prospective observational study included 50 patients with sepsis treated in the Intensive Care Unit of the Osijek Clinical Hospital Center between 2023 and 2025. GDF-15 and hs-TnI concentrations were measured at admission and during follow-up, while transthoracic echocardiography was performed at the same time points to assess myocardial function. Single concentrations of GDF-15 were not significantly associated with most conventional echocardiographic parameters, but showed a positive association with the E/A ratio. In multivariable analysis adjusted for illness severity (SOFA score), admission GDF-15 was independently associated with left ventricular longitudinal systolic function (MAPSE). Changes in GDF-15 during hospitalization were associated with echocardiographic measurements of longitudinal myocardial function obtained at admission and follow-up, including mitral annular plane systolic excursion (MAPSE), tricuspid annular plane systolic excursion (TAPSE), tissue Doppler systolic velocity (S′), and isovolumetric relaxation time (IVRT). In contrast, hs-TnI did not show a consistent association with echocardiographic parameters. These findings suggest that serial GDF-15 assessment may provide additional insight into myocardial functional changes during sepsis and complement the echocardiographic evaluation of septic cardiomyopathy. Full article