Background: Heart failure (HF) is the last stage in the progression of various cardiovascular diseases. Although it is documented that CD151 contributes to regulate the myocardial infarction, the function of CD151 on HF and involved mechanisms are still unclear. Method and results: In the present study, we found that the recombinant adeno-associated virus (rAAV)-mediated endothelial cell-specific knockdown of CD151-transfected mice improved transverse aortic constriction (TAC)-induced cardiac function, attenuated myocardial hypertrophy and fibrosis, and increased coronary perfusion, whereas overexpression of the CD151 protein aggravated cardiac dysfunction and showed the opposite effects. In vitro, the cardiomyocytes hypertrophy induced by PE were significantly improved, while the proliferation and migration of cardiac fibroblasts (CFs) were significantly reduced, when co-cultured with the CD151-silenced endothelial cells (ECs). To further explore the mechanisms, the exosomes from the CD151-silenced ECs were taken by cardiomyocyte (CMs) and CFs, verified the intercellular communication. And the protective effects of CD151-silenced ECs were inhibited when exosome inhibitor (GW4869) was added. Additionally, a quantitative proteomics method was used to identify potential proteins in CD151-silenced EC exosomes. We found that the suppression of CD151 could regulate the PPAR signaling pathway via exosomes. Conclusion: Our observations suggest that the downregulation of CD151 is an important positive regulator of cardiac function of heart failure, which can regulate exosome-stored proteins to play a role in the cellular interaction on the CMs and CFs. Modulating the exosome levels of ECs by reducing CD151 expression may offer novel therapeutic strategies and targets for HF treatment.

Disagreement exists regarding the long-term prognosis and recovery of left ventricular (LV) function in patients with fulminant myocarditis (FM). This study reported the outcome and LV ejection fraction (EF) changes in FM treated with Chinese protocol, and assessed whether global longitudinal strain (GLS) by two-dimensional speckle tracking echocardiography (2-D STE) could provide additional information. This retrospective study included 46 FM adult patients who applied timely circulatory support and immunomodulatory therapy with adequate doses of both glucocorticoids and immunoglobulins as core approaches and survived after acute phase. They all presented with acute onset of cardiac symptoms < 2 weeks. LV end-diastolic dimensions, LVEF and GLS at discharge and 2-year were obtained and compared. We then performed linear regression and ROC analysis to determine independent factors to predict normalization of GLS at 2-year. At 2 years, the survival was 100% in our cohort. And the GLS improved modestly (15.40 ± 3.89% vs 17.24 ± 2.89%, P = 0.002). At two years, a proportion of patients whose LV function remained abnormal, being 22% evaluated by EF (< 55%) and higher to 37% by GLS (< 17%). Moreover, GLS at discharge but not at presentation correlated with GLS at 2-year (r = 0.402, P = 0.007). The FM adult treated with Chinese protocol have good survival and modest improvement of LV function during 2-year.

Elevated serum high-sensitivity cardiac troponin (hs-cTn) levels are commonly observed in patients with fulminant myocarditis (FM) after the acute phase. This study aims to evaluate the relationship between elevated hs-cTnI levels at 30-day post-discharge and long-term cardiac structure and function. This study is a retrospective cohort study that selected FM patients hospitalized at Tongji Hospital in Wuhan from April 2016 to December 2022. All patients underwent serial monitoring of hs-cTnI levels. Patients were stratified into two groups based on hs-cTnI levels at 30 days post-discharge: the normal hs-cTnI (N-cTnI) group and the high hs-cTnI (H-cTnI) group. Left ventricular (LV) function and structure were assessed using 2-dimensional volume and speckle tracking strain echocardiography. Measurements were obtained at admission, discharge, and 6 months, 12 months, and annually thereafter post-discharge. Among 95 patients with analysable echocardiographic data (median age: 33 years; 42.11 % male), the N-cTnI group demonstrated significantly higher proportions of patients meeting cardiac function criteria during follow-up compared to the H-cTnI group: LV ejection fraction (LVEF) > 50 % (95 % vs. 72 %; P = 0.003), global longitudinal strain (GLS) > 16 % (68 % vs. 36 %; P = 0.002), and LV end-diastolic dimension < 5 cm (86 % vs. 65 %; P = 0.020). Given that the primary composite endpoint occurred in only 5 patients, statistical analyses focused on secondary composite endpoints. The incidence of secondary composite endpoints was significantly higher in the H-cTnI group than in the N-cTnI group (61.91 % vs. 16.98 %; P < 0.001). Multivariable Cox regression identified elevated hs-cTnI at 30 days post-discharge (HR: 5.365; 95 % CI: 1.876–15.344; P = 0.002) and LV-GLS at discharge (HR: 0.844; 95 % CI: 0.732–0.974; P = 0.021) as independent predictors of secondary composite endpoints. Delayed normalization of hs-cTnI after 30 days post-discharge may predict long-term deterioration of cardiac function and structural remodeling in patients with FM.

Background: Cardiorespiratory fitness (CRF) is a powerful predictor of cardiovascular morbidity and mortality. The cardiopulmonary exercise test (CPET) is considered a gold standard in assessing CRF. Patients with myocarditis are recommended to abstain from exercise because of the risk of sudden cardiac death (SCD). Therefore, the clinical benefit of exercise‐based cardiac rehabilitation (CR) has not been previously established in this population. Objective: The aim of this study is to assess the CRF of myocarditis and the safety and effectiveness of an exercise‐based CR program in these populations. Method: A total of 70 consecutive patients with a diagnosis of myocarditis admitted to Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology between October 2021 and December 2024 were enrolled in the current study. CPET was performed within 3–6 months of hospital discharge. The exercise‐based CR program was performed for 3 months. The protocol included biomarker analysis, CPET, and standard‐of‐care echocardiography (including resting left ventricular ejection fraction and global longitudinal strain [GLS]). Data were collected at admission and 3 months after discharge. Results: A total of 70 patients with myocarditis were enrolled. Among them, 47 patients completed the rehabilitation program and had complete follow‐up assessments, including cardiopulmonary exercise testing, and were included in the final analysis. In comparison with NFM, patients with FM were more often female, and had higher levels of creatine kinase (CK), lactate dehydrogenase (LDH), urea nitrogen (UN), N‐terminus probrain natriuretic peptide (NT‐proBNP), fasting blood glucose (FBG), and white blood cell (WBC). For FM, echocardiography revealed more frequently signs of left ventricular (LV) dysfunction in the form of a reduced ejection fraction ( p < 0.01), and lower GLS ( p < 0.01) in contrast to NFM. CPET results showed that FM patients had markedly lower exercise capacity, impaired ventilatory efficiency, and pulmonary function ( p < 0.05). After the 3‐month exercise‐based CR program, both groups demonstrated significant improvements in peak VO ₂ , peak workload, and MVV. However, no significant between‐group differences were observed in the magnitude of improvement in CRF. Conclusion: CRF was substantially impaired in patients recovering from myocarditis, particularly among those with fulminant presentations. Participation in a structured 3‐month exercise‐based CR program was feasible and was associated with favorable changes in exercise capacity and cardiopulmonary performance. Trial Registration: Chinese Clinical Trial Registry: ChiCTR2400088436

Acute myocardial infarction (AMI) carries a high short-term risk of death, even after percutaneous coronary intervention (PCI). Glucose variability (GV), measured by the glucose coefficient of variation (GluCV), is a potential risk factor for adverse outcomes. This study investigates GluCV's predictive value for in-hospital mortality in AMI patients undergoing PCI. This study involved 2325 AMI patients who were admitted to the ICU and underwent PCI from the MIMIC-IV database. Patients were categorized into quartiles based on GluCV: <0.13, 0.13–0.20, 0.20–0.29, and ≥0.29. Multivariable logistic regression and Restricted cubic spline (RCS) analysis were employed to analyze the relationship between GluCV and in-hospital mortality. Mediation analysis was used to evaluate the role of GluCV in the relationship between disease complexity and severity. Among the 2325 patients, 203 (8.7 %) died during hospitalization. Higher GluCV was associated with increased in-hospital mortality. Adjusted odds ratios for mortality were 1.35 (95 % CI: 0.71–2.55), 1.91 (95 % CI: 1.04–3.51), and 3.32 (95 % CI: 1.83–6.02) for the second, third, and fourth groups, respectively. RCS analysis indicated a linear relationship between Log GluCV and mortality risk, with each 1 SD increase in Log GluCV associated with a 1.70-fold increase in mortality. Subgroup analysis showed a stronger relationship between GluCV and mortality in patients younger than 70. Mediation analysis indicated that GluCV partially mediates the effect of comorbidities on organ dysfunction. GluCV is an important predictor of in-hospital mortality in AMI patients undergoing PCI. Managing GV to minimize fluctuations may improve patient prognosis.