Search Results (7,068)

Background: Breast and hematological cancer treatments, especially with anthracyclines, have been shown to be associated with an increased risk of cardiotoxicity (CTX). An accurate prediction of cardiotoxicity risk and early detection of myocardial injury may allow for effective cardioprotection to be instituted and tailored to reverse cardiac dysfunction and prevent the discontinuation of essential cancer treatments. Objectives: The PRoactive Evaluation of Function to Evade Cardio Toxicity (PREFECT) study sought to evaluate the ability of fast-strain-encoded (F-SENC) cardiac magnetic resonance imaging (CMR) and 2D echocardiography (2D Echo) to stratify patients at risk of CTX prior to initiating cancer treatment, detect early signs of cardiac dysfunction, including subclinical CTX (sub-CTX) and CTX, and monitor for recovery (REC) during cardioprotective therapy. Methods: Fifty-nine patients with breast cancer or lymphoma were prospectively monitored for CTX with F-SENC CMR and 2D Echo over at least 1 year for evidence of cardiac dysfunction during anthracycline based chemotherapy. F-SENC CMR also monitored myocardial deformation in 37 left ventricular (LV) segments to obtain a MyoHealth risk score based on both longitudinal and circumferential strain. Sub-CTX and CTX were classified based on pre-specified cardiotoxicity definitions. Results: CTX was observed in 9/59 (15%) and sub-CTX in 24/59 (41%) patients undergoing chemotherapy. F-SENC CMR parameters at baseline predicted CTX with a lower LVEF (57 ± 5% vs. 61 ± 5% for all, p = 0.05), as well as a lower MyoHealth (70 ± 9 vs. 79 ± 11 for all, p = 0.004) and a worse global circumferential strain (GCS) (−18 ± 1 vs. −20 ± 1 for all, p < 0.001). Pre-chemotherapy MyoHealth had a higher accuracy in predicting the development of CTX compared to CMR LVEF and 2D Echo LVEF (AUC = 0.85, 0.69, and 0.57, respectively). The 2D Echo parameters on baseline imaging did not stratify CTX risk. F-SENC CMR obtained good or excellent images in 320/322 (99.4%) scans. During cancer treatment, MyoHealth had a high accuracy of detecting sub-CTX or CTX (AUC = 0.950), and the highest log likelihood ratio (indicating a higher probability of detecting CTX) followed by F-SENC GLS and F-SENC GCS. CMR LVEF and CMR LV stroke volume index (LVSVI) also significantly worsened in patients developing CTX during cancer treatment. Conclusions: F-SENC CMR provided a reliable and accurate assessment of myocardial function during anthracycline-based chemotherapy, and demonstrated accurate early detection of CTX. In addition, MyoHealth allows for the robust identification of patients at risk for CTX prior to treatment with higher accuracy than LVEF. Full article

Hibiscus syriacus L. (HS), native to Eastern and Southern Asia, has been traditionally used in Asian herbal medicine for its anticancer, antimicrobial, and anti-inflammatory properties. Despite these recognized bioactivities, its potential cardioprotective effects, particularly in the setting of heart failure (HF), remain largely unexplored. This study aimed to investigate the effects of HS extracts and its bioactive constituents on angiotensin II (Ang II)-induced cardiac injury using an in vitro model with H9c2 rat cardiomyocytes. Cells exposed to Ang II were pretreated with HS extracts, and assays were performed to assess cell viability, reactive oxygen species (ROS) generation, protein synthesis, and secretion of inflammatory mediators, including tumor necrosis factor-alpha, interleukin 1β (IL-1β), and interleukin 6 (IL-6), as well as chemokine (CCL20) and HF-related biomarkers, such as brain natriuretic peptide (BNP) and endothelin-1. The results demonstrated that HS extracts significantly and dose-dependently attenuated Ang II-induced ROS accumulation and suppressed the secretion of pro-inflammatory cytokines, chemokines, BNP, and endothelin-1. Additionally, HS and its purified components inhibited Ang II-induced protein synthesis, indicating anti-hypertrophic effects. Collectively, these findings highlight the antioxidative, anti-inflammatory, and antihypertrophic properties of HS in the context of Ang II-induced cardiac injury, suggesting that HS may represent a promising adjunctive therapeutic candidate for HF management. Further in vivo studies and mechanistic investigations are warranted to validate its clinical potential. Full article

Cardiovascular disease encompasses a wide group of conditions that affect the heart and blood vessels. Of these diseases, cardiomyopathies and arrhythmias specifically have been well-studied in their relationship to cardiac dyads, nanoscopic structures that connect electrical signals to muscle contraction. The proper development and positioning of dyads is essential in excitation–contraction (EC) coupling and, thus, beating of the heart. Three proteins, namely CMYA5, JPH2, and BIN1, are responsible for maintaining the dyadic cleft between the T-tubule and junctional sarcoplasmic reticulum (jSR). Various other dyadic proteins play integral roles in the primary function of the dyad—translating a propagating action potential (AP) into a myocardial contraction. Ca²⁺, a secondary messenger in this process, acts as an allosteric activator of the sarcomere, and its cytoplasmic concentration is regulated by the dyad. Loss-of-function mutations have been shown to result in cardiomyopathies and arrhythmias. Adeno-associated virus (AAV) gene therapy with dyad components can rescue dyadic dysfunction, which results in cardiomyopathies and arrhythmias. Overall, the dyad and its components serve as essential mediators of calcium homeostasis and excitation–contraction coupling in the mammalian heart and, when dysfunctional, result in significant cardiac dysfunction, arrhythmias, morbidity, and mortality. Full article

Background: Senescence, a state of permanent cell cycle arrest, is a complex cellular phenomenon closely affiliated with age-related diseases and pathological fibrosis. Cellular senescence is now recognized as a significant contributor to organ fibrosis, largely driven by transforming growth factor beta (TGF-β) signaling, such as in metabolic dysfunction-associated steatohepatitis (MASH), idiopathic pulmonary fibrosis (IPF), chronic kidney disease (CKD), and myocardial fibrosis, which can lead to heart failure, cystic fibrosis, and fibrosis in pancreatic tumors, to name a few. MASH is a progressive inflammatory and fibrotic liver condition that has reached pandemic proportions, now considered the largest non-viral contributor to the need for liver transplantation. Methods: We previously studied Oxy210, an anti-fibrotic and anti-inflammatory, orally bioavailable, oxysterol-based drug candidate for MASH, using APOE*3-Leiden.CETP mice, a humanized hyperlipidemic mouse model that closely recapitulates the hallmarks of human MASH. In this model, treatment of mice with Oxy210 for 16 weeks caused significant amelioration of the disease, evidenced by reduced hepatic inflammation, lipid deposition, and fibrosis, atherosclerosis and adipose tissue inflammation. Results: Here we demonstrate increased hepatic expression of senescence-associated genes and senescence-associated secretory phenotype (SASP), correlated with the expression of pro-fibrotic and pro-inflammatorygenes in these mice during the development of MASH that are significantly inhibited by Oxy210. Using the HepG2 human hepatocyte cell line, we demonstrate the induced expression of senescent-associated genes and SASP by TGF-β and inhibition by Oxy210. Conclusions: These findings further support the potential therapeutic effects of Oxy210 mediated in part through inhibition of senescence-driven hepatic fibrosis and inflammation in MASH and perhaps in other senescence-associated fibrotic diseases. Full article

Arrhythmogenic cardiomyopathies (ACMs) are a phenotypically and etiologically heterogeneous group of myocardial disorders characterized by fibrotic or fibro-fatty replacement of ventricular myocardium, electrical instability, and an elevated risk of sudden cardiac death. Initially identified as a right ventricular disease, ACMs are now recognized to include biventricular and left-dominant forms. Genetic causes account for a substantial proportion of cases and include desmosomal variants, non-desmosomal variants, and familial gene-elusive forms with no identifiable pathogenic mutation. Nongenetic etiologies, including post-inflammatory, autoimmune, and infiltrative mechanisms, may mimic the phenotype. In many patients, the disease remains idiopathic despite comprehensive evaluation. Cardiac magnetic resonance imaging has emerged as a key tool for identifying non-ischemic scar patterns and for distinguishing arrhythmogenic phenotypes from other cardiomyopathies. Emerging classifications propose the unifying concept of scarring cardiomyopathies based on shared structural substrates, although global consensus is evolving. Risk stratification remains challenging, particularly in patients without overt systolic dysfunction or identifiable genetic markers. Advances in tissue phenotyping, multi-omics, and artificial intelligence hold promise for improved prognostic assessment and individualized therapy. Full article

Fractional flow reserve (FFR) is a standard physiological index for guiding coronary revascularization, with a threshold of >0.80 typically used to defer intervention. However, due to its distinct anatomical and physiological features, the left anterior descending artery (LAD) often exhibits lower FFR values than non-LAD vessels for lesions of similar angiographic severity. These vessel-specific differences raise concerns about applying a uniform FFR cutoff across all coronary territories. Observational studies indicate that LAD lesions deferred at an FFR of 0.80 may have similar or better outcomes than non-LAD lesions do. LAD lesions also tend to show lower post-percutaneous coronary intervention FFR values, suggesting that vessel specific target thresholds may be more prognostically appropriate. Additionally, some evidence suggests that instantaneous wave-free ratio may offer greater prognostic value than FFR, specifically in LAD lesions, a trend not consistently seen in other arteries. In patients with acute myocardial infarction and multivessel disease, the prognostic relevance of non-culprit lesion FFR may vary by coronary territory, particularly in the LAD. This review outlines the physiological rationale and clinical evidence for vessel-specific interpretation of FFR, with a focus on the LAD, and explores its potential clinical implications and limitations. Full article

Background: Mobile health applications have emerged as a novel tool to support secondary prevention after myocardial infarction (MI) or percutaneous coronary intervention (PCI). However, the impact of app-based interventions on clinically meaningful outcomes such as hospital readmissions remains uncertain. Objective: To systematically evaluate the effectiveness of smartphone app-based interventions in reducing unplanned hospital readmissions among post-MI/PCI patients. Methods: A systematic search of PubMed was conducted for randomized controlled trials published between January 2020 and April 2025. Eligible studies evaluated smartphone apps designed for secondary cardiovascular prevention and reported on unplanned hospital readmissions. Risk ratios (RRs) and 95% confidence intervals (CIs) were pooled using a random-effects model. Subgroup analyses were performed based on follow-up duration and user adherence. Results: Four trials encompassing 827 patients met inclusion criteria. App-based interventions were associated with a significant reduction in unplanned hospital readmissions compared to standard care (RR 0.45; 95% CI: 0.23–0.89; p = 0.0219). Greater benefits were observed in studies with longer follow-up durations and higher adherence rates. Improvements in patient-reported outcomes, including health-related quality of life, were also documented. Heterogeneity was moderate. Major adverse cardiovascular events (MACEs) were reported in only two studies and were not analyzed due to inconsistent definitions and low event rates. Conclusions: Smartphone applications for post-MI/PCI care are associated with reduced unplanned hospital readmissions and improved patient-reported outcomes. These tools may play a meaningful role in future cardiovascular care models, especially when sustained engagement and personalized features are prioritized. Full article

Pathologies of the heart (e.g., ischemic disease, valve fibrosis and calcification, progressive myocardial fibrosis, heart failure, and arrhythmogenic disorders) stem from the irreversible deterioration of cardiac tissues, leading to severe clinical consequences. The limited regenerative capacity of the adult myocardium and the architectural complexity of the heart present major challenges for tissue engineering. However, recent advances in biomaterials and biofabrication techniques have opened new avenues for recreating functional cardiac tissues. Particularly relevant in this context is the integration of biomimetic design principles, such as structural anisotropy, mechanical and electrical responsiveness, and tissue-specific composition, into 3D bioprinting platforms. This review aims to provide a comprehensive overview of current approaches in cardiac bioprinting, with a focus on how structural and functional biomimicry can be achieved using advanced hydrogels, bioprinting techniques, and post-fabrication stimulation. By critically evaluating materials, methods, and applications such as patches, vasculature, valves, and chamber models, we define the state of the art and highlight opportunities for developing next-generation bioengineered cardiac constructs. Full article

Background/Objectives: Blunt cardiac injury (BCI) is a severe medical condition that may arise as a result of various traumas, including motor vehicle accidents and falls. The main objective of this study was to explore the role and underlying mechanisms of the TRPV4 gene in BCI. Elucidating the function of TRPV4 in BCI may reveal potential novel therapeutic targets for the treatment of this condition. Methods: Rats in each group, including the SD control group (SDCON), the SD blunt-trauma group (SDBT), the TRPV4 gene-knockout control group (KOCON), and the TRPV4 gene-knockout blunt-trauma group (KOBT), were all freely dropped from a fixed height with a weight of 200 g and struck in the left chest with a certain energy, causing BCI. After the experiment, the levels of serum IL-6 and IL-1β were detected to evaluate the inflammatory response. The myocardial tissue structure was observed by HE staining. In addition, cardiac transcriptome analysis was conducted to identify differentially expressed genes, and metabolomics studies were carried out using UHPLC-Q-TOF/MS technology to analyze metabolites. The results of transcriptomics and metabolomics were verified by qRT-PCR and Western blot analysis. Results: Compared with the SDCON group, the levels of serum IL-6 and IL-1β in the SDBT group were significantly increased (p < 0.001), while the levels of serum IL-6 and IL-1β in the KOBT group were significantly decreased (p < 0.001), indicating that the deletion of the TRPV4 gene alleviated the inflammation induced by BCI. HE staining showed that myocardial tissue injury was severe in the SDBT group, while myocardial tissue structure abnormalities were mild in the KOBT group. Transcriptome analysis revealed that there were 1045 upregulated genes and 643 downregulated genes in the KOBT group. These genes were enriched in pathways related to inflammation, apoptosis, and tissue repair, such as p53, apoptosis, AMPK, PPAR, and other signaling pathways. Metabolomics studies have found that TRPV4 regulates nucleotide metabolism, amino-acid metabolism, biotin metabolism, arginine and proline metabolism, pentose phosphate pathway, fructose and mannose metabolism, etc., in myocardial tissue. The combined analysis of metabolic and transcriptional data reveals that tryptophan metabolism and the protein digestion and absorption pathway may be the key mechanisms. The qRT-PCR results corroborated the expression of key genes identified in the transcriptome sequencing, while Western blot analysis validated the protein expression levels of pivotal regulators within the p53 and AMPK signaling pathways. Conclusions: Overall, the deletion of the TRPV4 gene effectively alleviates cardiac injury by reducing inflammation and tissue damage. These findings suggest that TRPV4 may become a new therapeutic target for BCI, providing new insights for future therapeutic strategies. Full article

Background/Objectives: Acute kidney injury (AKI) worsens outcomes in COPD exacerbation (COPDe), yet limited data compare the demographics and mortality risk factors of COPDe admissions with and without AKI. Understanding this association may enhance risk stratification and management strategies. The aim of this study was to identify demographic differences and mortality risk factors in COPDe admissions with and without AKI. Methods: We conducted a retrospective cohort study using the National Inpatient Sample (NIS) from 1 January 2016 to 1 January 2021. Patients aged ≥ 35 years with a history of smoking and a diagnosis of COPDe were included. Patients with CKD stage 5, end-stage kidney disease (ESKD), heart failure decompensation, urinary tract infections, myocardial infarction, alpha-1 antitrypsin deficiency, or active COVID-19 infection were excluded. Baseline demographics were analyzed using descriptive statistics. Multivariate logistic regression analysis was used to measure the odds ratio (OR) of mortality. Statistical analyses were conducted using IBM SPSS Statistics V.30, with statistical significance at p < 0.05. Results: Among 405,845 hospitalized COPDe patients, 13.6% had AKI. These patients were older, had longer hospital stays, and included fewer females and White patients. AKI was associated with significantly higher mortality (OR: 2.417), more frequent acute respiratory failure (OR: 4.559), intubation (OR: 10.262), and vasopressor use (OR: 2.736). CVA, pneumonia, and pulmonary hypertension were significant mortality predictors. Hypertension, CAD, and diabetes were associated with lower mortality. Conclusions: AKI in COPDe admissions is associated with worse outcomes. Protective effects from certain comorbidities may relate to renoprotective medications. Study limitations include coding errors and retrospective design. Full article

(1) Background: Comparison of clinical outcomes between patients with moderate-severe aortic valve stenosis and those with mild or no aortic valve stenosis undergoing surgical revascularization for critical limb threating ischemia (CLTI). (2) Methods: Single center retrospective analysis of consecutive patients undergoing surgical lower limb revascularization with femoro-distal bypass for critical ischemia between 2016 and 2022. All patients were evaluated preoperatively by echocardiographic examination and divided into two cohorts: group A with moderate-severe aortic valve stenosis (AVA-cm² < or =1.5 cm²) and group B with mild or absent stenosis (AVA-cm² > 1.5 cm²). Primary outcomes were major limb amputation and mortality between the two groups. The rate of major cardiovascular events (stroke, myocardial infarction, sudden cardiac death) and change in “preoperative functional status” were the secondary outcomes. Descriptive statistics for continuous variables were performed by calculating means, standard deviation (SD) medians, and interquartile range (IQR) while, for categorical variables, frequencies and percentages were performed. Intergroup comparison tests, for continuous variables, were performed by t-test or corresponding nonparametric tests (Mann-Whitney test) while, for categorical variables, Chi-square test was used. Evaluation of cut-offs for the variable AVA-fx-cm², in terms of predictive of outcome outcomes, was calculated by ROC curves. Comparison between clinical and outcome variables was performed using logistic regression models. A total of 316 patients were analyzed and divided in two groups: 50 (16%) patients with moderate or severe aortic valve stenosis (group A) and 266 (84%) with no or mild aortic valve stenosis (AVA > 1.5 cm²). Patients in group A were significantly older than those in group B (78 years vs. 74 years, p value = 0.005); no other significant comorbidity differences were found between the two groups. The mean follow-up was 1178 days (SD 991 days; 2–3869 days). There were no statistically significant differences between group A and group B in terms of major amputation rate (20% vs. 16.5%; p = 0.895) and overall mortality (48.0% vs. 40.6%; p = 0.640). In the total cohort, the statistically significant variables associated with the major amputation were systemic perioperative complication (OR 5.83, 95% CI: 2.36, 14.57, p < 0.001), bypass-related complication within 30 days of surgery (OR 2.74, 95% CI: 1.17, 6.45, p = 0.020), surgical revascularization below the knee (OR 7.72, 95% CI: 1.53, 140.68, p = 0.049), and the presence of a previous cardiovascular event (OR 2.65, 95% CI: 1.14, 6.26, p = 0.024). In patients undergoing surgical revascularization for CLTI, no significant difference in major amputation rate and overall mortality was found between subjects with mild or no aortic valve stenosis and those with moderate/severe stenosis. As expected, overall mortality was higher in older patients with worse functional status. A significantly higher rate of limb amputation was found in those subjects undergoing subgenicular revascularization, early bypass failure, or previous cardiovascular event. Full article

Objectives: To assess the clinical and inflammatory outcomes of patients with calcified coronary arteries treated with rotational atherectomy (RA), compared to those with other intervention procedures. Methods: We conducted a systematic search of PubMed (Medline) and Embase. This review followed the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines and applied the PICO criteria. Results: A total of 110 articles were analyzed, comprising 2,328,417 patients with moderate to severe coronary calcified lesions treated with RA, conventional percutaneous coronary intervention (PCI), or other advanced interventions. The pooled incidence of short- to mid-term major adverse cardiovascular events (MACEs) was 6% (95% CI 4–7%), increasing to 17% (95% CI 15–21%) at 6 months. Mortality was 2% (95% CI 1–3%) within 6 months, rising to 7% (95% CI 6–9%) thereafter. RA significantly increased the risk of long-term MACEs, mortality, total lesion revascularization (TLR), bleeding, and fluoroscopy time, and was borderline associated with an increased risk of short-term myocardial infarction and a reduced risk of coronary dissection. RA and other invasive procedures showed similar risks for short-term MACEs, mortality, total vascular revascularization (TVR), stent thrombosis, heart failure, stroke, and inflammation. Conclusions: RA is linked to higher long-term risks of MACEs, mortality, TLR, bleeding, and fluoroscopy time compared to other interventions. While RA shows comparable outcomes for short-term MACEs and mortality with other procedures, it may slightly reduce the risk of coronary dissection. These findings underscore the importance of careful patient selection and weighing long-term risks when considering RA for calcified coronary lesions. Full article

Cardiac devices have transformed the management of heart failure, ventricular arrhythmias, ischemic cardiomyopathy, and valvular heart disease. Technologies such as cardiac resynchronization therapy (CRT), conduction system pacing, left ventricular assist devices (LVADs), and implantable cardioverter-defibrillators have contributed to abated global cardiovascular risk through action onto pathophysiological processes such as mechanical unloading, electrical resynchronization, or hemodynamic optimization, respectively. While their clinical benefits are well established, their long-term molecular and structural effects on the myocardium remain under investigation. Cardiac devices dynamically interact with myocardial and vascular biology, inducing molecular and extracellular matrix adaptations that vary by pathology. CRT enhances calcium cycling and reduces fibrosis, but chronic pacing may lead to pacing-induced cardiomyopathy. LVADs and Impella relieve ventricular workload yet alter sarcomeric integrity and mitochondrial function. Transcatheter valve therapies influence ventricular remodeling, conduction, and coronary flow. Understanding these remodeling processes is crucial for optimizing patient selection, device programming, and therapeutic strategies. This narrative review integrates the current knowledge on the molecular and structural effects of cardiac devices, highlighting their impact across different disease settings. Full article

Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder with significant racial and ethnic disparities in prevalence, disease severity, and outcomes. Cardiovascular complications, including pericarditis, myocarditis, valvular disease, and conduction abnormalities, contribute to increased morbidity and mortality in SLE patients. This study examines racial and ethnic disparities in cardiovascular outcomes among hospitalized SLE patients in the United States. Methods: This retrospective study utilized the National Inpatient Sample (NIS) database from 2016 to 2021 to analyze hospitalizations of adult patients (≥18 years) with a primary or secondary diagnosis of SLE. Patients were stratified into racial/ethnic groups: White, Black, Hispanic, Asian, Native American, and Other. Primary outcomes include major adverse cardiovascular events (MACEs), which are a composite of in-hospital mortality, myocardial infarction (MI), sudden cardiac death, and other SLE-related outcomes including cardiac, pulmonary, and renal involvement. Statistical analyses included multivariable logistic regression models adjusted for demographic, socioeconomic, and hospital-related factors to assess racial disparities. Results: The study included 514,750 White, 321,395 Black, and 146,600 Hispanic patients, with smaller proportions of Asian, Native American, and Other racial groups. Black patients had significantly higher odds of in-hospital mortality (OR = 1.17, 95% CI = 1.08–1.26, p < 0.001) and sudden cardiac death (OR = 1.64, 95% CI = 1.46–1.85, p < 0.001) compared to White patients. Asian patients also exhibited increased mortality risk (OR = 1.37, 95% CI = 1.14–1.63, p = 0.001) as compared to Whites. Conversely, Black (OR = 0.90, 95% CI = 0.85–0.96, p = 0.01) and Hispanic (OR = 0.87, 95% CI = 0.80–0.96, p = 0.03) patients had lower odds of MI. Racial disparities in access to care, socioeconomic status, and comorbidity burden may contribute to these differences. Conclusion: Significant racial and ethnic disparities exist in cardiovascular outcomes among hospitalized SLE patients. Black and Asian individuals face higher in-hospital all-causes mortality and sudden cardiac death risks, while Black and Hispanic patients exhibit lower MI rates. Addressing social determinants of health, improving access to specialized care, and implementing targeted interventions may reduce disparities and improve outcomes in minority populations with SLE. Full article

Myocardial infarction (MI) remains one of the most common cardiovascular diseases and a leading cause of morbidity and mortality worldwide. In recent years, natural polymeric patches have attracted increasing attention as a promising therapeutic platform for myocardial tissue repair. This study explored the fabrication and evaluation of screen-printed electrodes (SPEs) on chitosan film as a novel platform for cardiac patch applications. Chitosan is a biodegradable and biocompatible natural polymer that provides an ideal substrate for SPEs, providing mechanical stability and promoting cell adhesion. Silver ink was employed to enhance electrochemical performance, and the electrodes exhibited strong adhesion and structural integrity under wet conditions. Mechanical testing and swelling ratio analysis were conducted to assess the patch’s physical robustness and aqueous stability. Silver ink was employed to enhance electrochemical performance, which was evaluated using cyclic voltammetry. In vitro, electrical stimulation through the chitosan–SPE patch significantly increased the expression of cardiac-specific genes (GATA-4, β-MHC, troponin I) in bone marrow mesenchymal stem cells (BMSCs), indicating early cardiogenic differentiation potential. In vivo, the implantation of the chitosan–SPE patch in a rat MI model demonstrated good tissue integration, preserved myocardial structure, and enhanced ventricular wall thickness, indicating that the patch has the potential to serve as a functional cardiac scaffold. These findings support the feasibility of screen-printed electrodes fabricated on chitosan film substrates as a cost-effective and scalable platform for cardiac repair, offering a foundation for future applications in cardiac tissue engineering. Full article