Search Results (1,660)

Background: Myocardial infarction (MI) remains a leading cause of morbidity and mortality despite major advances in reperfusion and secondary prevention. Inflammation contributes throughout the MI continuum, from atherosclerotic plaque development and destabilization to myocardial injury, adverse ventricular remodeling, and recurrent cardiovascular events. Objective: This narrative review summarizes current evidence on inflammation across the MI continuum, focusing on inflammatory biomarkers, cardiovascular imaging, residual inflammatory risk, and emerging anti-inflammatory therapies. Methods: We reviewed current evidence on the pathophysiological and clinical relevance of inflammation in MI, with particular emphasis on circulating biomarkers, multimodality imaging, and inflammation-targeted therapeutic strategies. Results: High-sensitivity C-reactive protein remains the best-established biomarker of residual inflammatory risk, while interleukin-6, myeloperoxidase, suPAR, and GlycA provide complementary information. Advanced imaging, including coronary computed tomography-derived perivascular fat attenuation index, cardiac magnetic resonance, and positron emission tomography, may further characterize vascular and myocardial inflammation. Clinical trials support inflammation as a potentially modifiable component of cardiovascular risk; however, therapeutic benefit has been inconsistent across inflammatory targets, agents, and clinical settings. Canakinumab and low-dose colchicine have demonstrated cardiovascular benefit in selected secondary-prevention populations, although recent neutral trials highlight heterogeneity across clinical settings. Similarly, IL-6-targeted strategies have yielded mixed results, with the neutral ZEUS trial underscoring that biomarker reduction does not necessarily translate into cardiovascular benefit, while NLRP3-targeted approaches remain investigational. Conclusions: Integrating inflammatory biomarkers, multimodality imaging, and targeted therapies may improve risk stratification and support personalized secondary prevention. Further evidence is needed to define optimal patient selection and determine whether biomarker- or imaging-guided anti-inflammatory strategies improve clinical outcomes. Full article

Background: NT-proBNP is a mechanistically grounded biomarker of ventricular wall stress with established prognostic value in cardiac surgery, but its perioperative role in lung cancer resection remains incompletely characterised. Pulmonary resection imposes unique haemodynamic stressors—including one-lung ventilation-induced right ventricular afterload increase, permanent pulmonary vascular bed reduction, and ischaemia–reperfusion injury—that create a distinct biological context for natriuretic peptide elevation not represented in general surgical cohorts. Methods: A narrative review of the literature was conducted through systematic searches of PubMed, EMBASE/MEDLINE, and the Cochrane Library (January 2000–June 2026), supplemented by manual reference screening. Approximately 135 articles were included in the final synthesis. Results: Perioperative NT-proBNP elevation predicts postoperative atrial fibrillation, major adverse cardiovascular events, and long-term survival after lung resection, with effect sizes substantially exceeding those reported in general surgical populations. The PRESAGE trial established that NT-proBNP-guided prophylaxis reduces postoperative atrial fibrillation from 40% to 6% in high-risk patients. No thoracic surgery-specific NT-proBNP threshold has been prospectively validated in a multicentre setting, and approximately half the evidence base derives from BNP rather than NT-proBNP assays, precluding direct threshold synthesis. Surgical approach—particularly robot-assisted thoracoscopy—modulates postoperative biomarker elevation through OLV duration rather than inflammatory burden alone. The combination of NT-proBNP with high-sensitivity troponin identifies a dual-elevation subgroup with a MACE rate of 18.4%. Conclusions: NT-proBNP measurement is clinically actionable in thoracic surgery but requires assay-standardised, multicentre validation of population-specific thresholds stratified by resection extent and surgical approach. A dual biomarker strategy combining NT-proBNP with high-sensitivity troponin represents the most evidence-based perioperative risk stratification framework currently available. Full article

Background/Objectives: Age may influence myocardial recovery after acute myocardial infarction (AMI) beyond changes in left ventricular ejection fraction (LVEF). We investigated age-related patterns in ischemic delay, admission biomarkers, biventricular function, myocardial deformation, and exploratory patterns of prescribed heart failure guideline-directed medical therapy (HF-GDMT) classes after primary percutaneous coronary intervention (PCI). Methods: This prospective frequency-matched cohort study included 90 AMI patients treated with primary PCI, stratified into younger (25–44 years; n = 30) and older (≥45 years; n = 60) groups. Clinical data, ischemic time, cardiac biomarkers, serial echocardiography at baseline, 6, and 12 months, and HF-GDMT intensity were analyzed. Results: Older patients had longer pain-to-balloon time (720 [480–1230] vs. 540 [420–660] min; p = 0.021), higher hs-cTnI (p = 0.045), and higher NT-proBNP (4776 [3013–5952] vs. 833.5 [95.7–1939.5] pg/mL; p < 0.001). Baseline and 12-month LVEF were similar between groups. Younger patients showed greater 12-month global longitudinal strain (GLS) improvement (−3.7 [−5.1 to −1.9] vs. −2.3 [−3.0 to −1.3] percentage points; p = 0.002), despite comparable absolute GLS. In exploratory post hoc analyses, prescribed HF-GDMT drug-class count showed an association with LVEF change primarily in older patients, who also had significantly lower baseline LVEF (ρ = 0.59; p < 0.001). Conclusions: In this prospective exploratory cohort, 12-month conventional systolic recovery assessed by LVEF and absolute GLS was comparable between age groups after primary PCI. However, the older comparator group had longer ischemic delay and higher admission biomarkers reflecting cardiomyocyte injury and myocardial wall stress, while younger patients showed greater longitudinal GLS improvement over time. These findings suggest that age-stratified recovery after AMI is better characterized by ischemic timing, baseline biomarker profile, and deformation trajectory than by LVEF alone. Because infarct size was not directly quantified, admission biomarker differences should not be interpreted as evidence of larger infarcts. Full article

Cardiovascular diseases are increasingly recognized as immune-inflammatory disorders in which adaptive immunity shapes tissue injury, repair, and long-term remodeling. T cells are central to these processes because they integrate antigen recognition, lineage-defining transcriptional programs, tissue trafficking, cytokine production, and immunological memory. In this Review, we synthesize current evidence on the Krüppel-like factor (KLF) family as a transcriptional framework linking T-cell biology to cardiovascular disease. KLF2 primarily regulates T-cell quiescence and trafficking, KLF10 supports regulatory T-cell suppressive function and immune-metabolic fitness, KLF4 contributes to inflammatory effector differentiation, and KLF13 regulates delayed inflammatory chemokine expression and, in thymocyte models, exerts a survival-restraining effect through apoptosis-related pathways. Across atherosclerosis, myocardial infarction, myocarditis, hypertension, and heart failure, these KLF-dependent programs may influence the balance between pathogenic effector responses and protective regulatory mechanisms. The strongest direct disease-specific evidence currently supports a role for KLF10 within the CD4⁺ T-cell lineage in experimental atherosclerosis, with complementary functional evidence implicating Treg–macrophage interactions, whereas the roles of KLF-dependent T-cell programs in other cardiovascular settings remain mechanistically compelling but less fully validated. Future progress will require disease-specific T-cell-restricted models, spatially resolved immune analyses, and cell-selective translational strategies to define the therapeutic relevance of the KLF–T-cell axis. Full article

Globally, approximately three hundred million individuals undergo non-cardiac surgery each year. Perioperative mortality results from a complex interplay between patient-related factors and procedural variables, including both surgical and anesthetic aspects. Although cardiac surgery has a well-established risk profile for acute cardiovascular events, major non-cardiac surgery also carries significant—yet often underrecognized—cardiovascular risks. Approximately half of postoperative deaths following non-cardiac procedures are attributable to cardiovascular complications. Surgical and anesthetic stress responses may induce myocardial injury through several pathophysiological mechanisms. However, the absence of a universally accepted definition of perioperative myocardial injury complicates both diagnosis and management. Furthermore, these injuries frequently occur without symptoms, making them clinically silent and often undetected. Consequently, unexpected postoperative deaths may occur and may lead to allegations of medical malpractice. We conducted a narrative review of existing literature on perioperative myocardial injury and its implications for forensic investigation and medico-legal assessment. This paper highlights the importance of a comprehensive forensic evaluation of perioperative deaths, integrating clinical documentation, autopsy findings, histopathological evidence and ancillary investigations to support accurate medico-legal assessment, recognizing that no single element is sufficient to establish the cause of death in all cases. Four illustrative case studies are presented to demonstrate the medico-legal challenges associated with these events. A structured forensic investigation is essential for accurately determining the cause of death and for distinguishing preventable medical errors from unavoidable adverse outcomes within the context of complex perioperative care. Full article

Background: Management of high-grade carotid artery stenosis with concomitant ipsilateral parotid gland tumor presents a rare and challenging surgical condition. Due to the rarity of this dual pathology, standardized guidelines are lacking. Material and Methods: A retrospective study was conducted between January 2020 and May 2025. Six asymptomatic patients with significant carotid stenosis and coexisting ipsilateral Warthin’s tumor underwent simultaneous eversion CEA (carotid endarterectomy) and partial superficial parotidectomy/extracapsular enucleation via a single modified Blair’s incision. Results: Median follow-up was 43 months (range: 12–60 months). Postoperative and long-term survival at median follow-up was 100%, with a 5-year survival rate of 83.3% (one death at 50 months due to myocardial infarction). Disease-free survival at 5 years was 100% for Warthin’s tumor and 83.3% for carotid stenosis. No perioperative transient ischemic attacks (TIA), strokes, hematomas, salivary fistula or iatrogenic cranial nerve injuries occurred. Conclusions: In patients presenting with high-grade carotid stenosis and concomitant ipsilateral Warthin’s tumor, a simultaneous surgical approach is a feasible strategy. This approach eliminates the need for staged interventions, significantly reducing overall anesthetic risk, surgical burden, and healthcare resource utilization. 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

Cardiovascular disease causes the largest number of deaths across the world. The weak regenerative ability of adult hearts originates from limited cell proliferation and polyploidization of postnatal cardiomyocytes, which severely hinders tissue repair after myocardial injury. Fetal development represents a critical window during which maternal physiological and metabolic status can shape long-term offspring cardiac structure and function. Maternal exercise represents a safe nonpharmacological prenatal intervention that confers long-term benefits to offspring health. Available evidence indicates that maternal exercise enhances placental apelin secretion and elevates α-ketoglutarate (α-KG) levels in fetal brown adipose tissue, liver, and skeletal muscle. The apelin and α-KG signaling cascade participates in epigenetic regulation and confers protective effects on offspring metabolic health. Independent animal experiments have further validated that supplementation with either apelin or α-KG alleviates myocardial infarction (MI)-induced cardiac injury in adult mice, with α-KG showing direct evidence of reactivating cardiomyocyte proliferation. Nevertheless, it remains poorly elucidated whether maternal exercise could modulate fetal cardiomyocyte proliferative capacity in offspring through apelin- or α-KG-associated signaling. This narrative review integrates current evidence and proposes a testable framework in which maternal exercise influences fetal cardiac growth and regenerative potential through placental, metabolic, and epigenetic signaling. Because direct evidence remains limited, this model should be regarded as a hypothesis that requires further experimental validation. Full article

Chimeric antigen receptor T-cell therapy and bispecific T-cell engagers have transformed treatment of relapsed and refractory hematologic malignancies, achieving unprecedented response rates. However, their clinical adoption has revealed a complex spectrum of cardiovascular toxicities, differing in frequency and pattern between the two technologies. Manifestations range from common hemodynamic perturbations—hypotension and tachycardia—to severe events, including malignant arrhythmias, left ventricular dysfunction, myocardial infarction, and cardiogenic shock. These complications seem to have different pathophysiological pathways that are yet to be completely understood: on the one hand, they are frequently intertwined with cytokine release syndrome, the hallmark immune complication of T-cell-redirecting therapies, as seen with chimeric antigen receptor T-cell therapy; on the other, a substantial proportion of cardiovascular events—particularly with bispecific T-cell engagers—occur independently of cytokine release syndrome. Proposed cardiotoxic mechanisms include on-target, off-tumor antigen recognition and consequent damage; interleukin-6-driven systemic inflammation; and off-target, off-tumor antigen cross-reactivity. Effective management requires proactive baseline risk stratification, serial cardiac biomarker monitoring, and timely immunosuppressive intervention—primarily tocilizumab—to mitigate cytokine release syndrome-driven injury. Despite rapid clinical expansion, critical gaps remain: long-term cardiovascular outcomes are poorly characterized, validated surveillance protocols are lacking, and cardiovascular endpoints are rarely included in pivotal trials. This narrative review appraises the pathophysiology, clinical spectrum, and management of cardiovascular toxicities associated with these therapies, aiming to define this emerging cardio-oncology frontier, inform multidisciplinary care frameworks and propose a clinical management algorithm. Full article

Objective: The aim of this study was to evaluate the efficacy and safety of endovascular and hybrid treatment approaches in patients with aortic arch aneurysms. Materials and Methods. This retrospective study included 68 male and female patients with a confirmed diagnosis of either an aortic arch aneurysm or a descending thoracic aortic aneurysm with a short proximal landing zone (<1.5 cm) who underwent either hybrid or endovascular treatment at the Department of Vascular Surgery between January 2017 and December 2024. Study outcomes included a composite measure of technical success, a composite measure of in-hospital clinical success, and a composite measure of long-term treatment outcomes, including stroke, myocardial infarction, and aortic-related mortality. Results. All 68 patients were divided into two groups: Group I comprised patients who underwent endovascular treatment, whereas Group II included patients who underwent hybrid surgical treatment. The groups were comparable with regard to demographic and anatomical characteristics, clinical presentation, and comorbidities. The composite technical success rate (defined as successful target stent-graft deployment without conversion to open surgery and absence of type I or type III endoleaks) was comparable between the groups at the intraoperative stage (p = 1.000). The composite measure of in-hospital clinical success was achieved in 33 patients (94%) in Group I and 22 patients (67%) in Group II and was significantly higher in the endovascular group (adjusted p = 0.005). This difference was primarily attributable to a higher incidence of complications in the hybrid treatment group, including stroke (9%) and peripheral nerve injury (9%), associated with the open surgical component of the procedure. The mean follow-up duration was shorter in Group I (19.3 ± 10.4 months) than in Group II (63.9 ± 29.5 months), reflecting the fact that most patients in Group I underwent treatment during the later years of the study period. Although a difference in the composite long-term outcome measure was observed before adjustment (p = 0.031), this finding did not remain statistically significant after correction for multiple testing (adjusted p = 1.000). Conclusions. In this preliminary single-centre study, endovascular and hybrid approaches showed comparable technical efficacy in the early postoperative period. However, hybrid surgical treatment was associated with a less favourable safety profile during the early postoperative period, as reflected by the significantly lower in-hospital composite clinical success rate and longer hospital stay than in the endovascular group. These findings remained robust after correction for multiple testing. Long-term results should be interpreted with caution and require confirmation in larger prospective studies with longer and balanced follow-up periods. Full article

Background: Atherosclerotic heart disease (AHD) remains a leading cause of global mortality and a major driver of fatal cardiac syndromes. Ischemic myocardial injury from AHD can lead to ventricular remodeling and myocyte loss, progressing to heart failure (HF) and, in advanced stages, cardiogenic shock (CS). However, long-term national mortality trends for deaths involving the combined burden of AHD, HF, and CS remain insufficiently characterized. Methods: Mortality data from 1999 to 2023 were obtained from the CDC WONDER Multiple Cause of Death database. Deaths involving CS (ICD-10 R57.0), HF (I50, I50.1, I50.9), and AHD (I25.1) in adults were identified. Age-adjusted mortality rates (AAMRs) per 1,000,000 population were calculated and stratified by sex, race/ethnicity, and geographic region. Temporal trends were analyzed using Joinpoint regression to estimate annual percent changes (APCs) and average annual percent changes (AAPCs). Autoregressive integrated moving average (ARIMA) modeling was used to forecast mortality trends through 2035. Results: A total of 15,631 deaths were attributed to AHD-associated HF and CS during the study period. Overall AAMRs increased significantly (AAPC 3.75%; 95% CI 3.32–4.29; p < 0.01). Mortality rates declined between 1999 and 2006 (APC −7.55%; 95% CI −13.15 to −5.23; p < 0.01), increased modestly from 2006 to 2013 (APC 3.94%; 95% CI −1.47 to 8.91), and rose sharply from 2013 to 2023 (APC 12.33%; 95% CI 11.27–14.46; p < 0.01). Males had higher AAMRs than females in 2023 (9.26 vs. 3.39 per 1,000,000). Non-Hispanic White individuals accounted for the highest number of deaths (11,878), followed by non-Hispanic Black individuals (1708), while non-Hispanic American Indian populations had the lowest counts (39). Regionally, the West (7.31) and South (5.92) exhibited the highest final AAMRs. State-level AAMRs ranged from 2.49 in Minnesota to 8.27 in Nevada. Conclusions: Mortality involving AHD, HF, and CS has risen substantially in the United States since 2013, with marked demographic and geographic disparities. These findings highlight a growing burden of advanced ischemic heart disease and heart failure and underscore the need for earlier intervention and improved access to advanced HF therapies to prevent progression to cardiogenic shock and death. Full article

Background: Myocardial ischemia–reperfusion during cardiac surgery is associated with complex metabolic alterations that reflect both myocardial injury and recovery. This prospective study aimed to characterize intraoperative lactate, pH, and bicarbonate dynamics in paired coronary sinus (CS) and peripheral blood samples and to explore whether these responses could be integrated into a composite marker of reperfusion-related metabolic burden (RMB). Methods: We prospectively studied 101 patients undergoing cardiac surgery with cardiopulmonary bypass. Simultaneous blood samples from the CS and peripheral circulation were obtained before aortic cross-clamping (T0), immediately after declamping (T1), and 10 min after reperfusion (T2). Temporal changes and transmyocardial gradients of lactate, pH, and bicarbonate were analyzed. RMB was calculated from standardized changes in these variables. As an exploratory analysis, associations with in-hospital mortality were evaluated using receiver operating characteristic (ROC) analysis. Results: Significant temporal variations in metabolic parameters were observed, with the most pronounced transmyocardial disturbances occurring at aortic declamping. Lactate demonstrated the largest gradient during early reperfusion, accompanied by transient acidosis and bicarbonate consumption. The RMB framework integrated these coordinated metabolic responses into a single measure of reperfusion stress. In exploratory outcome analyses, higher RMB values were observed among non-survivors, with the largest observed AUC for peripheral RMB measured 10 min after reperfusion (AUC 0.87). However, these estimates were based on only seven deaths and should be considered hypothesis-generating. Conclusions: Paired CS and peripheral sampling revealed dynamic metabolic adaptations during myocardial ischemia–reperfusion. The exploratory RMB framework integrates coordinated metabolic changes into a single descriptive measure of reperfusion-related stress. Its observed associations with in-hospital mortality remain preliminary and require confirmation through external validation and evaluation in larger independent prospective cohorts. 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