Partial atrioventricular canal defects (PAVC) are preferred to be repaired when diagnosed and before an operation would interfere with school. There were rare previous studies about partial atrioventricular canal defect operations in adult patients. In this single-center retrospective study, we mean to review the mid-term follow-up outcomes of late diagnosed and repaired partial atrioventricular canal defects in adult patients. 46 adult partial atrioventricular canal defect patients who underwent operation in West China Medical Center from 2009 to 2017 were included. Required data were obtained from operation notes, patient charts and the outpatient records. Among 46 patients, 10(21.7%)were male and mean age at operation was 37.6 ± 12.4 years. 11 patients had prior arrythmia, including 8 atrial fibrillations, 2 atrioventricular blocks and 1 left bundle branch block. There were 41 patients with tricuspid valve regurgitation and 22 underwent tricuspid valvuloplasty. All the patients had mitral regurgitation. 6 patients with valve incrassation and shrinkage underwent mitral valve replacement, and the rest underwent mitral repair surgery. There was one early death post operation and no more mortalities in the following follow-up years. According to the follow-up outcomes, heart function of the patients recovered significantly, dilation of atriums and ventricles, except for left atriums, were reversed to a large extent and all but one patients’ tricuspid valve regurgitations were reduced to mild and below. 4(8.7%) patients underwent reoperation and the main reasons were arrythmia and recurrent severe mitral valve regurgitation. Partial atrioventricular canal defect repair in adult patients can achieve good results. Compared with the results of patients underwent operations in preschool years, though delayed surgery timing seems to bring more preoperative complications and influences heart function, the mortality and reoperation rate are excellent.

Minimally invasive approaches such as perventricular closure of ventricular septal defects (VSD) have been applied for the surgical correction of congenital heart defects in order to avoid disadvantages related to median sternotomy with a cardiopulmonary bypass (CPB). However, reports remain scarce regarding combined perventricular closure of VSD and atrial septal defects (ASD) via minimally invasive approaches, such as lower ministernotomy. The authors have operated on 5 patients who were diagnosed with VSD in association with ASD, successfully realizing perventricular closure via lower ministernotomy. The proposed technique proved to be safe and effective.

Pericardiectomy is the final treatment for constrictive pericarditis. However, this greatest surgical approach is still very controversial. This study pursued to assess the outcomes in patients with recurrent chronic constrictive pericarditis undergoing reoperated pericardiectomy via median sternotomy versus left anterolateral thoracotomy and to explain which surgical approaches might be better for recurrent chronic constrictive pericarditis. A total of 24 patients were identified with recurrent chronic constrictive pericarditis and underwent reoperation with pericardiectomy between July 2003 and July 2015. The decision for this surgical approach was mainly dependent on the operating surgeon’s preference. Out of 20 patients, 16 patients underwent pericardiectomy via median sternotomy and 8 patients via left anterolateral thoracotomy pericardiectomy. Their data were obtained retrospectively from the case notes. Both groups of patients were similar in age, gender between two operations, and also in peripheral venous pressure, cardiac rhythm and New York Heart Association (NYHA) class distribution. The mortality rates were similar in both groups with one death (12.5%) due to low cardiac output syndrome in the left anterolateral thoracotomy group and two deaths (12.5%) in the median sternotomy group. All the deaths were associated with cardiac complications and happened in the perioperative period. NYHA functional class status enhanced in most of the patients. Patients in both groups had a similar and significant improvement in their NYHA status that improved from 3.4 ± 0.7 to 1.8 ± 0.1 (P = 0.001) in the left anterolateral thoracotomy group and reduced from 3.3 ± 0.6 to 1.9 ± 0.4 (P = 0.001) in the median sternotomy group. There was a significantly greater rate of pulmonary infection in the thoracotomy group than in the median sternotomy group (50% versus 25%, P = 0.02). Nevertheless, there was a significantly greater occurrence of wound infections in the median sternotomy group in 3 patients versus in one patient of the left anterolateral thoracotomy group (18.8% versus 12.5%, P = 0.02). Left thoracotomy incision was preferred to sternotomy in the current setting of this situation and was done safely without CPB. It avoided life-threatening sternal infection and it also has showed an equal as well las significant enhancement of NYHA status of the patients.

Copper is an essential trace element; however, its homeostasis is frequently disrupted in cardiovascular diseases, which are a leading cause of mortality worldwide. The recent discovery of cuproptosis—a copper-dependent form of regulated cell death (RCD)—has provided a crucial mechanistic link between this imbalance and cardiomyocyte loss. In this review, we synthesize the current understanding of how dysregulated copper metabolism and cuproptosis drive the pathogenesis of major cardiovascular conditions, including myocardial ischemia/reperfusion (I/R) injury, anthracycline-induced cardiotoxicity, atherosclerosis, diabetic cardiomyopathy (DCM), and sepsis-induced cardiac dysfunction, through pathways such as mitochondrial dysfunction, oxidative stress, and inflammation. We further evaluated emerging therapeutic strategies that target copper homeostasis—including chelators, chaperone inhibitors, and ionophores—and critically analyzed the translational challenges they face, such as off-target effects and preclinical model limitations. Advancing our knowledge of cardiac copper biology holds significant promise for the development of novel and precise therapeutic approaches for cardiovascular diseases.

Right ventricular dysfunction following surgical correction of tetralogy of Fallot (TOF) remains a major determinant of long-term morbidity and mortality in survivors. Despite advancements in surgical techniques, residual anatomical abnormalities – including pulmonary regurgitation, right ventricular outflow tract obstruction, abnormal coronary artery anatomy, scar formation, and tricuspid regurgitation – synergistically drive ventricular remodeling and functional decline. This review synthesizes evidence on the pathophysiological interplay of these anatomical substrates. Key imaging modalities, such as 3D late gadolinium enhancement cardiac magnetic resonance, and artificial intelligence tools enhance risk stratification for ventricular arrhythmias. We propose a hierarchical management framework prioritizing hemodynamic stabilization, electrophysiological substrate modification and individualized strategies for concomitant lesions considerations. This work aims to bridge anatomical insights with therapeutic innovations, offering a roadmap for improving longevity and quality of life in repaired TOF patients.

Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease (CHD). Although surgical correction of TOF is possible, patients often face challenges related to right ventricle dysfunction (RVD) post-surgery, which can significantly impact their long-term survival. The causes of RVD in TOF patients are complex, involving both the unique structural characteristics of the TOF heart and damage resulting from surgical interventions. Residual anatomical issues following TOF repair are often unavoidable, placing the RV under stress and leading to the activation of multiple molecular pathways. This review comprehensively outlines the causes of RVD in patients after TOF surgery, particularly focusing the molecular pathways that contribute to RVD, including established signaling pathways as well as emerging pathways identified through transcriptomic analysis of RV myocardium in TOF patients. We also highlight the features of these molecular pathways concerning RVD, as well as the influence of gender disparities on these molecular pathways. By interpreting the causes and molecular mechanisms underlying RVD after TOF surgery, this review provides new insights for managing RVD in repaired TOF, potentially paving the way for targeted therapies aimed at improving long-term outcomes for those affected by RVD.