Wuhan Asia Heart Hospital

The liver, the largest internal organ in the human body, regulates multiple reactions and processes, including detoxification, regeneration, and immune defense. Liver diseases have emerged as a significant global public health issue. Numerous studies have indicated that the mitochondrial deacetylase SIRT3 has played various roles in the pathogenesis and pathological progression of liver diseases. Objectives: This review aims to explore the advances in the study of SIRT3 and liver disease and review possible mechanisms. Natural and chemical activators of SIRT3 are also discussed. The role of SIRT3 in the pathogenic mechanisms and therapeutic strategies of liver disease is summarized by reviewing Pubmed. SIRT3 alleviates liver diseases by regulating fatty acid metabolism, mitochondrial function, and immune-inflammatory response. Meanwhile, Withaferin A, lipoic acid, major royal jelly proteins, and berberine can activate SIRT3 or upregulate its expression, thereby alleviating liver damage. SIRT3 can effectively slow down the progression of liver disease and protect the liver from further damage. The use of SIRT3 as a pharmacological target for the treatment of liver disease is a potential therapeutic approach.

Metastatic intracardiac hepatoblastoma is an extremely rare entity. Metastasis pathways include lymphatic, hematogenous routes, direct, or transvenous spread. The multimodality imaging has enabled the identification of the etiology of intracardiac mass in many cases. The significant characteristics of indicating malignant cardiac tumors include irregular borders, vascular invasion, and rapid growth on echocardiography. Additionally, malignant cardiac tumors are characterized by heterogeneous enhancement, necrosis, and restricted diffusion on cardiac magnetic resonance (CMR).

The Fourth Universal Definition of Myocardial Infarction recommends high-sensitivity cardiac troponin (hs-cTn) as the preferred biomarker for diagnosing myocardial infarction. This study evaluated the analytical and clinical performance of a novel hs-cTnT chemiluminescence immunoassay (CLIA) developed by Mindray. Analytical performance characteristics including precision, sensitivity (limit of detection [LoD] and limit of quantification [LoQ]), imprecision profile, linearity, sample type comparison, method comparison, and potential interferences were assessed. Sex-specific 99th percentile upper reference limits (URLs) were established in 895 healthy individuals. Clinical diagnostic performance was evaluated in 559 patients with suspected acute myocardial infarction and compared with the Roche hs-cTnTassay. The Mindray assay showed excellent precision (repeatability CV≤1.99 %, within-laboratory precision CV≤6.11 %), superior sensitivity (LoD: 1.4 ng/L; LoQ: 2.4 ng/L), and linearity (r=0.9978), along with robust performance against common and immunological interferences. Using the manufacturer-claimed LoD of 2.0 ng/L, measurable values were found in 99.36 % of males, 83.26 % of females, and 91.48 % overall, meeting criteria for high-sensitivity assays. The derived sex-specific 99th percentiles were 18.6 ng/L (males), 9.6 ng/L (females), and 16.0 ng/L (overall). In the clinical cohort, the assay showed 100.0 % sensitivity, 83.3 % specificity, 80.0 % PPV, 100.0 % NPV, and an AUC of 0.988, comparable to the Roche Gen 5hs-cTnTassay. The Mindray hs-cTnT (CLIA) assay meets high-sensitivity assay criteria and demonstrates robust analytical and diagnostic performance, offering a reliable alternative to the Roche Gen 5 assay for clinical evaluation of myocardial injury.

Chronic total occlusion (CTO) of the coronary arteries can be managed using a retrograde strategy guided by bilateral angiography, substantially improving the likelihood of successful recanalization. To enhance procedural safety, hemodynamic support—such as intra-aortic balloon pump (IABP) counterpulsation—is frequently employed. Nevertheless, in patients presenting with concurrent femoral artery occlusion in the lower limbs, conventional access via the femoral route becomes unfeasible, significantly complicating intervention efforts. This report describes a case involving a patient with CTO alongside complete bilateral external iliac artery occlusion. In this instance, we achieved successful IABP insertion through the left brachial artery and performed bilateral coronary imaging via the right radial and right brachial arteries, ultimately accomplishing effective lesion recanalization. This alternative approach demonstrates a practical solution for individuals with CTO who have limited vascular access in the lower extremities.

This case report describes a patient with a history of mechanical aortic and mitral valve replacements who developed prosthetic valve stenosis years later and underwent a minimally invasive, thoracoscopic-assisted double valve re-replacement. Postoperatively, the patient developed a rare but life-threatening re-expansion pulmonary edema (RPE), which led to severe acute respiratory distress syndrome (ARDS), with rapid deterioration into refractory hypoxemia. Despite comprehensive conventional supportive management—including lung-protective ventilation, diuresis, anti-inflammatory therapy, and other measures—adequate oxygenation could not be maintained. Venovenous extracorporeal membrane oxygenation (VV-ECMO) was emergently initiated. With ECMO support, the patient's lungs were able to rest and recover. After 10 days of support, ECMO was successfully discontinued, and the patient eventually recovered and was discharged. This case aims to explore the pathophysiological mechanisms of RPE, management strategies for complications following minimally invasive cardiac surgery, and to emphasize the critical role of VV-ECMO in treating refractory respiratory failure, as well as the importance of multidisciplinary team (MDT) collaboration.

Abstract Background Dilated cardiomyopathy is a severe myocardial disorder characterized by ventricular dilation and systolic dysfunction. It is associated with poor prognosis due to complex and heterogeneous mechanisms involving immune dysregulation, cell death, and tissue remodeling. Identifying reliable molecular biomarkers and constructing effective diagnostic models remain urgent needs for early detection and targeted therapy. Methods We integrated bulk transcriptomic and single-cell RNA sequencing data from multiple public datasets to explore the molecular landscape of dilated cardiomyopathy. Differential gene expression, weighted gene co-expression network analysis, and machine learning algorithms were used to identify core genes associated with programmed cell death. A diagnostic risk model was established and validated across independent cohorts. Immune infiltration patterns and molecular subtypes were evaluated. Functional pathways and potential therapeutic compounds were explored through gene enrichment analysis, drug–gene interaction databases, and molecular docking. Key gene expression was confirmed by quantitative PCR and Western blot in mouse and human myocardial tissues. Results Eight core genes (AGTR2, GLI2, HRK, IL10, NQO1, NT5E, SFRP1, and STAT4) were identified as significantly altered in dilated cardiomyopathy. These genes demonstrated strong predictive capacity in the risk model across multiple datasets. Immune correlation analysis revealed their association with specific immune cell populations, indicating roles in inflammation and immune remodeling. Consensus clustering revealed distinct molecular subtypes with different immune infiltration profiles. Single-cell analysis showed cell-type–specific expression of core genes in fibroblasts and immune cells. Drug–gene prediction and docking identified several candidate compounds, including resveratrol and folic acid. Experimental validation confirmed consistent expression trends of selected genes at mRNA and protein levels in diseased tissues. Conclusions This study systematically identified key genes associated with programmed cell death in dilated cardiomyopathy and developed a robust diagnostic model. The findings reveal the interplay between immune regulation and cell death mechanisms and highlight novel molecular subtypes and drug targets. These results provide important insights for precise diagnosis and personalized treatment strategies in dilated cardiomyopathy.