Right ventricular dysfunction improves prediction of atrial fibrillation in hypertrophic cardiomyopathy: a cardiac magnetic resonance study

BackgroundAtrial fibrillation (AF) is a critical arrhythmia in hypertrophic cardiomyopathy (HCM), yet the role of right ventricular (RV) dysfunction in AF risk stratification remains underexplored. We aimed to evaluate the association between RV remodeling and incident AF in HCM patients.MethodsThis retrospective cohort study included 612 HCM patients who underwent cardiac magnetic resonance (CMR) at our institution (2016–2023). Incident AF was identified via electronic medical records or structured telephone interviews. RV function was assessed using CMR-derived parameters, including ejection fraction (RVEF), peak emptying rate (PER), and peak filling rate (PFR).ResultsAmong 612 patients (66.1% male), 72 (11.8%) had preexisting AF, and 29 (5.4%) developed new-onset AF over a median follow-up of 3.3 years. Patients with AF (preexisting or new-onset) exhibited older age and impaired RV function at baseline, including reduced RVEF, PER, and PFR (P < 0.05 for all). Multivariable Cox regression identified age, left atrial diameter (LAD), RVEF, and RV-PFR as independent predictors of new-onset AF. Adding RVEF and RV-PFR to a clinical model (age, NYHA class III/IV, LAD) significantly improved risk stratification (NRI: 0.80, P < 0.01; IDI: 0.07, P < 0.01).ConclusionsRV dysfunction is prevalent in HCM patients with AF and provides incremental prognostic value for predicting new-onset AF beyond traditional clinical markers. These findings underscore RV functional assessment as a critical tool in AF risk stratification for HCM patients

Enhancing Cardioprotection Through Neutrophil‐Mediated Delivery of 18β‐Glycyrrhetinic Acid in Myocardial Ischemia/Reperfusion Injury

Abstract Myocardial ischemia/reperfusion injury (MI/RI) generates reactive oxygen species (ROS) and initiates inflammatory responses. Traditional therapies targeting specific cytokines or ROS often prove inadequate. An innovative drug delivery system (DDS) is developed using neutrophil decoys (NDs) that encapsulate 18β‐glycyrrhetinic acid (GA) within a hydrolyzable oxalate polymer (HOP) and neutrophil membrane vesicles (NMVs). These NDs are responsive to hydrogen peroxide (H2O2), enabling controlled GA release. Additionally, NDs adsorb inflammatory factors, thereby reducing inflammation. They exhibit enhanced adhesion to inflamed endothelial cells (ECs) and improved penetration. Once internalized by cardiomyocytes through clathrin‐mediated endocytosis, NDs protect against ROS‐induced damage and inhibit HMGB1 translocation. In vivo studies show that NDs preferentially accumulate in injured myocardium, reducing infarct size, mitigating adverse remodeling, and enhancing cardiac function, all while maintaining favorable biosafety profiles. This neutrophil‐based system offers a promising targeted therapy for MI/RI by addressing both inflammation and ROS, holding potential for future clinical applications

Screening and Bioinformatics Analysis of Crucial Gene of Heart Failure and Atrial Fibrillation Based on GEO Database

Background and objectives: In clinical practice, we observed that the prognoses of patients with heart failure and atrial fibrillation were worse than those of patients with only heart failure or atrial fibrillation. The study aims to get a better understanding of the common pathogenesis of the two diseases and find new therapeutic targets. Materials and Methods: We downloaded heart failure datasets and atrial fibrillation datasets from the gene expression omnibus database. The common DEGs (differentially expressed genes) in heart failure and atrial fibrillation were identified by a series of bioinformatics methods. To better understand the functions and possible pathways of DEGs, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Results: We identified 22 up-regulated genes and 14 down-regulated genes in two datasets of heart failure and 475 up-regulated and 110 down-regulated genes in atrial fibrillation datasets. In addition, two co-upregulated (FRZB, SFRP4) and three co-downregulated genes (ENTPPL, AQP4, C1orf105) were identified. GO enrichment results showed that these common differentially expressed genes were mainly concentrated in the signal regulation of the Wnt pathway. Conclusions: We found five crucial genes in heart failure and atrial fibrillation, which may be potential therapeutic targets for patients with heart failure and atrial fibrillation

Neutrophil membrane-camouflaged nanoparticles alleviate inflammation and promote angiogenesis in ischemic myocardial injury

Acute myocardial infarction (AMI) induces a sterile inflammatory response, leading to cardiomyocyte damage and adverse cardiac remodeling. Interleukin-5 (IL-5) plays an essential role in developing eosinophils (EOS), which are beneficial for the resolution of inflammation. Furthermore, the proangiogenic properties of IL-5 also contribute to tissue healing following injury. Therefore, targeted delivery of IL-5 is an innovative therapeutic approach for treating AMI. It has been shown that conventional IL-5 delivery can result in undesirable adverse effects and potential drug overdose. In this study, we successfully synthesized a biomimetic IL-5 nanoparticle by camouflaging the IL-5 nanoparticle in a neutrophilic membrane. The administration of neutrophil membrane–camouflaged nanoparticles (NM-NPIL-5) in the in vivo model showed that these nanoparticles promoted EOS accumulation and angiogenesis in the infarcted myocardium, thereby limiting adverse cardiac remodeling after AMI. Our results also demonstrated that the NM-NPIL-5 could serve as neutrophil “decoys” to adsorb and neutralize the elevated neutrophil-related cytokines in the injured heart by inheriting multiple receptors from their “parent” neutrophils. Finally, the targeted delivery of NM-NPIL-5 protected the cardiomyocytes from excessive inflammatory-induced apoptosis and maintained cardiac function. Our findings provided a promising cardiac detoxification agent for acute cardiac injury