Heart failure with preserved ejection fraction (HFpEF) has a high prevalence and a low quality of life, and there are limited medications for the treatment of this disease. In recent years, disulfiram (DSF), an FDA-approved drug for the treatment of chronic alcohol addiction, has been found to have anti-inflammatory properties. The present study was designed to investigate the cardioprotective effects of DSF on patients with HFpEF and its mechanism using a model of HFpEF induced in mice fed a high-fat diet (HFD, 60% of calories from fat) and Nω-nitro-L-arginine methyl ester (L-NAME, 0.5 g/L in drinking water). The results showed that DSF effectively reversed the HFD + L-NAME-induced increases in left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), interventricular septal thickness, left ventricular mass, the ratio of peak early mitral diastolic velocity to peak late mitral diastolic velocity, the ratio of early mitral diastolic velocity to early diastolic velocity, as well as the reductions in the absolute value of global longitudinal strain (GLS), without affecting the left ventricular ejection fraction (LVEF). In addition, DSF notably attenuated the HFD + L-NAME-induced increase in blood pressure, exercise intolerance, cardiac hypertrophy, pulmonary edema, and elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels. Mechanistically, we found that DSF inhibited myocardial PANoptosis-like cell death, mainly by inhibiting the release of myocardial interleukin 1β (IL-1β), which inhibited transforming growth factor-β-activated kinase 1(TAK1)-mediated PANoptosis. Given the cardioprotective effects of DSF, its clinical use would be a novel strategy for the protection and treatment of cardiac injury in patients with HFpEF.

Hematocrit (HCT) has clinical significance in the prognosis of acute heart failure (AHF). This study investigated the association between HCT and 365-day all-cause mortality rate from the MIMIC-IV database. We also explored the specific inflection point for HCT that affects the varying clinical prognoses in patients with AHF.A total of 2,193 patients with AHF were extracted from the MIMIC-IV database. Patients were divided into 3 groups based on HCT levels at admission: low-HCT (< 30%), middle-HCT (30% - 40%), and high-HCT groups (≥ 40%). Ten variables were identified using the least absolute shrinkage and selection operator regression. In multivariable Cox regression, HCT was identified as an independent protective factor for 365-day all-cause mortality in patients with AHF (HR = 0.98, P = 0.004). The restricted cubic spline curve revealed a nonlinear relationship between the 2 (P nonlinear = 0.002), with inflection points at 30. According to the threshold effect analysis of HCT on mortality, patients in the low HCT group had a significantly higher mortality rate (HR = 0.92, P = 0.001). Finally, subgroup analysis revealed no interaction (P > 0.05).A negative association exists between HCT and 365-day all-cause mortality in patients with AHF. Low HCT (< 30%) was significantly associated with a higher mortality rate in patients with AHF.

Hypertrophic cardiomyopathy (HCM), recognized as the most prevalent inherited heart condition, is found in about 0.2% to 0.5% of the population globally. Recent years have witnessed a notable surge in HCM-related scholarly investigations. The aim of this study was to delineate the trajectory of HCM research over the preceding decade through a comprehensive bibliometric analysis. Utilizing the Web of Science Core Collection (WoSCC) database, we retrieved data on HCM-related studies conducted between 2013 and 2023. The acquired bibliographic data were methodically processed and examined using VOSviewer and CiteSpace software. A remarkable escalation in HCM-related publications was observed throughout the last decade. The United States emerged as the foremost contributor, amassing a total of 2,479 publications and exhibiting the most extensive international collaborative efforts. Mayo Clinic was recognized for its significant contributions and leadership in research collaborations within the HCM domain. Dr. Iacopo Olivotto stood out as a leading figure in the field, authoring 152 articles over this period. The decade was marked by robust transnational collaborations among countries, institutions, and authors. Notably, the publications 'Circulation,' 'JACC,' and 'European Heart Journal' recorded the most citations, receiving 30,736, 26,769, and 13,192 citations, respectively. Our study presents the first in-depth bibliometric and visual exploration of the global HCM research landscape, providing an invaluable reference for clinical researchers engaged in this field.

Acute myocardial infarction (AMI) impacts the regenerative capacity of hematopoietic stem and progenitor cells (HSPCs) following injury, but it remains unclear if these functional alterations persist beyond the initial ischemic event.A minimally invasive mouse model of recurrent myocardial infarction was established using echocardiography-guided coronary interventions. Bone marrow HSPCs were quantified and analyzed for proliferation by flow cytometry and BrdU incorporation. Peripheral blood leukocytes and inflammatory cytokines (IL-6, G-CSF) were measured by flow cytometry and ELISA. Bone marrow extracellular TGF-β1 was assessed by ELISA, and its functional role was evaluated through antibody-mediated inhibition.The minimally invasive infarction model was validated through electrocardiography, cardiac biomarkers, echocardiography, and cardiac pathology staining. Fourteen days post-I/R or sham treatment, bone marrow hematopoiesis returned to a steady state with no significant differences in Lin-Sca-1+c-Kit+ (LSK), hematopoietic stem cell (HSC), multipotent progenitor (MPP), and granulocyte/macrophage progenitor (GMP) cell numbers. However, after a secondary ischemic challenge, there was a dampened reactive hematopoiesis indicated by reduced HSPCs, compared to the first ischemic event. BrdU incorporation analysis showed decreased HSPC proliferation activity during the reparative phase after initial ischemic challenge, linking dampened hematopoiesis to decreased HSPCs proliferation. Additionally, early recurrent infarct mice had fewer neutrophils released in peripheral blood and lower serum IL-6 and G-CSF levels. Elevated TGF-β1 levels were detected in bone marrow extracellular fluid during the reparative phase of cardiac-ischemic injury, and inhibiting TGF-β1 reversed the dampened reactive hematopoiesis of HSPCs in an early recurrent MI setting.Our data suggest that initial myocardial ischemia challenges blunt bone marrow reactive hematopoiesis to subsequent ischemic stress, with decreased HSPC proliferation contributing to diminished regenerative capacity. TGF-β1 in bone marrow extracellular fluid may mediate this decreased HSPC proliferation.

Low BMI has been reported to be associated with atrial fibrillation (AF) recurrence post-ablation, as well as with cardiovascular events and mortality. However, the previous studies have not fully accounted for baseline factors including age, nutritional status, anemia, and cardiac function. Thus, the potential risks inherent in patients with AF and low BMI remain unclear. AF patients who underwent primary ablation were enrolled. To exclude the effect of baseline factors including age, nutritional status, anemia and cardiac function, propensity score-matching was performed. The incidence of composite of heart failure (HF) hospitalization and all-cause death among the patients stratified by BMI was investigated. We finally analyzed 2396 patients. Low BMI was defined as < 18.5 kg/m2 and normal/high BMI as ≥ 18.5 kg/m2. The low and normal/high BMI groups consisted of 120 patients after 1:1 propensity score-matching, respectively. In propensity score-matched population, normal/high BMI had higher risk of late arrhythmia recurrence post-ablation than low BMI in persistent AF, while no significant difference in paroxysmal AF. Kaplan-Meier analysis showed incidence of the composite endpoint was significantly higher in patients with low BMI than those with normal/high in the overall and propensity score-matched populations (Log-rank P < 0.001 and P = 0.024, respectively). Cox proportional hazard analysis revealed low BMI had significantly and independently higher risk of the composite endpoint (HR = 2.43; 95% CI = 1.098-5.374). Despite a lower recurrence rate, patients with low BMI showed a paradoxically higher incidence of HF hospitalization and all-cause mortality, highlighting the need for further investigation into potential interventions targeting low BMI patients.

Myocardial ischemia-reperfusion injury (MI/RI) refers to the deterioration of cardiac function after restoring ischemic myocardium perfusion. Stem cell exosomes have produced unique advantages in treating MI/RI. However, the roles of exosomal microRNA-223-3p (miR-223-3p) from adipose-derived stem cells (ADSCs) on MI/RI are still unclear. This study aimed to investigate the effects of exosomal miR-223-3p from ADSCs on hypoxia/reoxygenation (H/R)-induced H9c2 cell injuries. Our findings indicated that the separated ADSC-derived exosomes (ADSC-Exo) were spherical, with a complete cell membrane, an average diameter of 110 nm, and CD9 and CD63 expression. ADSC-Exo increased the cell viability, proliferation, glutathione (GSH) level, and glutathione peroxidase 4 (GPX4) and miR-223-3p expression and decreased the apoptosis, reactive oxygen species (ROS), malondialdehyde (MDA), and Fe2+ levels and acyl-CoA synthetase long chain family member 4 (ACSL4) and transferrin receptor (TFRC) expression of H9c2 cells. Overexpressing exosomal miR-223-3p from ADSCs further strengthened the effects of ADSC-Exo on H9c2 cells. Overexpressing TFRC in H9c2 cells effectively reversed the effects of miR-223-3p overexpressed ADSC-Exo on H9c2 cells. In addition, miR-223-3p targeted and negatively regulated TFRC. This study confirmed that exosomal miR-223-3p from ADSCs alleviated H/R-induced ferroptosis of H9c2 cells by inhibiting TFRC, providing a novel target and pathway for the clinical treatment of MI/RI.

Two types of cryoballoon (CB) systems are currently available for catheter ablation of atrial fibrillation (AF). It is not clear how the difference between POLARx (Boston Scientific) and AFA-Pro (Medtronic) relates to myocardial injury and the incidence of early recurrence of fibrillation (ERAF).Patients (n = 137) who underwent catheter ablation for paroxysmal AF by 2 CB devices were included (AFA-Pro in 87; POLARx in 50). We assessed creatine kinase (CK)-MB pre and post-procedure, ERAF, and the number of atrial premature contractions (APCs) at Holter monitoring 1 month and 3 months after the procedure. The change ratio was defined by the following formula: (post-procedure/pre-procedure). ERAF is defined as the recurrence of AF within 90 days after the procedure.The 2 groups did not differ significantly in the number of CB applications or the percentage of touch-up applications by radiofrequency catheter. The CK-MB change ratio was considerably higher in the POLARx group than the AFA-Pro group (19.3 ± 21.6 versus 27.4 ± 21.3; P = 0.036). The incidence of ERAF was similar between the 2 groups (15% versus 24%; P = 0.23). Additionally, there were no significant differences in the number of APCs (120 [39-784] versus 147 [43-1039]; P = 0.70) or AF recurrence (3% versus 12%; P = 0.10).POLARx causes stronger myocardial injury than AFA-Pro but does not increase ERAF and APC numbers.