Simultaneous thoracoscopic surgery in patients with atrial fibrillation and early-stage lung cancer.

OBJECTIVES: Atrial fibrillation (AF) and early-stage lung cancer can both be treated under thoracoscopy. This study aims to evaluate the feasibility and safety of simultaneous thoracoscopic surgery for atrial fibrillation and early-stage lung cancer. METHODS: This was a single-center, retrospective study of 865 patients with paroxysmal or non-paroxysmal AF who underwent surgical ablation between October 2014 and December 2021. Patients were divided into two groups according to whether they have undergone simultaneous thoracoscopic early-stage lung cancer surgery and resulting in 24 pairs of patients. RESULTS: In total, 48 patients (24 matched pairs) were analyzed. The age was 63.71 ± 8.43 years. Procedure time and postoperative mechanical ventilation time were significantly lower in the group AF than group AFLC (Atrial fibrillation and lung cancer) (140.38 ± 27.53 vs. 230.79 ± 59.06 min, P<0.001; 5 vs 6.5 h, P = 0.002). There was no significant difference between the groups in terms of operative bleeding volume (90.00 ± 29.78 vs 85.83 ± 53.56 ml, P = 0.741), total postoperative drainage volume (1020.83 ± 516.5 vs 1406.25 ± 840.33 ml, P = 0.067), ICU (intensive care unit) length of stay (LOS) (43.5 vs 44 h, P = 0.33), hospitalization LOS (9.29 ± 1.92 vs 8.58 ± 1.98 days, P = 0.214) and incidence of freedom from AF or complications. CONCLUSIONS: Simultaneous thoracoscopic surgical AF ablation and early-stage lung cancer is safe and feasible. It can be used as an alternative method for coexisting atrial fibrillation and lung cancer with acceptable operative risks.

Downregulation of MYBL1 in endothelial cells contributes to atherosclerosis by repressing PLEKHM1-inducing autophagy.

MYBL1 is a strong transcriptional activator involved in the cell signaling. However, there is no systematic study on the role of MYBL1 in atherosclerosis. The aim of this study is to elucidate the role and mechanism of MYBL1 in atherosclerosis. GSE28829, GSE43292 and GSE41571 were downloaded from NCBI for differentially expressed analysis. The expression levels of MYBL1 in atherosclerotic plaque tissue and normal vessels were detected by qRT-PCR, Western blot and Immunohistochemistry. Transwell and CCK-8 were used to detect the migration and proliferation of HUVECs after silencing MYBL1. RNA-seq, Western blot, qRT-PCR, Luciferase reporter system, Immunofluorescence, Flow cytometry, ChIP and CO-IP were used to study the role and mechanism of MYBL1 in atherosclerosis. The microarray data of GSE28829, GSE43292, and GSE41571 were analyzed and intersected, and then MYBL1 were verified. MYBL1 was down-regulated in atherosclerotic plaque tissue. After silencing of MYBL1, HUVECs were damaged, and their migration and proliferation abilities were weakened. Overexpression of MYBL1 significantly enhanced the migration and proliferation of HUVECs. MYBL1 knockdown induced abnormal autophagy in HUVEC cells, suggesting that MYBL1 was involved in the regulation of HUVECs through autophagy. Mechanistic studies showed that MYBL1 knockdown inhibited autophagosome and lysosomal fusion in HUVECs by inhibiting PLEKHM1, thereby exacerbating atherosclerosis. Furthermore, MYBL1 was found to repress lipid accumulation in HUVECs after oxLDL treatment. MYBL1 knockdown in HUVECs was involved in atherosclerosis by inhibiting PLEKHM1-induced autophagy, which provided a novel target of therapy for atherosclerosis.

Immediate electrophysiological characteristics following modified thoracoscopic ablation via unilateral approach for non-valvular atrial fibrillation.

BACKGROUND: Thoracoscopic ablation has emerged as an effective therapy for patients with long-standing persistent Atrial fibrillation (LsPAF). We aimed to investigate the immediate electrophysiological characteristics following modified ablation with 3 circular and 3 linear lesions in the thoracoscopic procedure via a unilateral approach. METHODS: Between May 2015 and October 2018, 40 patients underwent the one-stage hybrid procedure for LsPAF. Isolation of the pulmonary veins (PV) and left atrium posterior wall (LAPW), excision of the left atrial appendage (LAA), and high-density endocardial mapping and individualized percutaneous catheter ablation for AF termination were performed. RESULTS: The modified thoracoscopic procedure may enable successful PV and LAPW isolation and LAA removal. Endocardial electrophysiological examination showed 6 out of 40 (15%) patients with a right PV gap, 3 (7.5%) patients with incomplete roof lesions, and 8 (20%) patients with incomplete Dallas lesions. A total of 44 driving areas were mapped and ablated. Thirty-five patients achieved procedural AF termination. After a mean follow-up period of 26 months, the success rate of a single procedure was 85%. Cox regression analysis demonstrated that the failure of procedural AF termination may be a risk factor in atrial tachyarrhythmia recurrence. DISCUSSION: Endocardial electrophysiological examination is a necessary partner to thoracoscopic ablation. Our modified thoracoscopic ablation and driving areas-based ablation contribute to high rates of procedural AF termination, which may lead to reduced recurrence rate. The hybrid procedure may be an effective strategy for the management of LsPAF.

The Mei mini-maze procedure.

Atrial fibrillation is a common clinical arrhythmia with high morbidity and a risk of stroke. The Cox-maze IV procedure that uses radiofrequency energy for ablation is established as an effective way to eliminate atrial fibrillation. Compared to the Cox-maze IV procedure, the video-assisted Wolf mini-maze procedure is associated with reduced surgical trauma, but still requires bilateral thoracotomies, and the ablation line connecting the right and left pulmonary vein isolations cannot be created with a bipolar ablation clamp. We have developed a novel video-assisted mini-maze technique that uses a unilateral (left chest) thoracoscopic approach (the Mei mini-maze procedure).

MicroRNA-15a inhibition protects against hypoxia/reoxygenation-induced apoptosis of cardiomyocytes by targeting mothers against decapentaplegic homolog 7.

Myocardial ischemia/reperfusion (I/R) injury is a major pathological process in coronary heart disease and cardiac surgery, and is associated with aberrant microRNA (miR) expression. Previous studies have demonstrated that inhibition of miR-15a expression may ameliorate I/R­induced myocardial injury. In the present study, the potential role and underlying mechanism of miR­15a in hypoxia/reoxygenation­induced apoptosis of cardiomyocytes was investigated. Myocardial I/R was simulated in cultured H9c2 cells by 24 h hypoxia followed by 24 h reoxygenation. Using recombinant lentivirus vectors, the inhibition of miR­15a was indicated to significantly reduce cardiomyocyte apoptosis and release of lactate dehydrogenase and malondialdehyde. Conversely, upregulated miR­15a expression was pro­apoptotic. Mothers against decapentaplegic homolog 7 (SMAD7) was identified by bioinformatics analysis as a potential target of miR­15a. Luciferase reporter assays and western blotting for endogenous SMAD7 protein indicated that miR­15a inhibited SMAD7 expression via its 3'­untranslated region. Nuclear levels of nuclear factor­κB (NF­κB) p65 were increased by miR­15a expression and decreased by miR­15a inhibition, which is consistent with the possibility that the inhibition of SMAD7 by miR-15a results in NF­κB activation. These findings suggested that the therapeutic effects of miR­15a inhibition on I/R injury may potentially be explained by its ability to release SMAD­7­dependent NF­κB inhibition. This may provide evidence for miR­15a as a potential therapeutic target for the treatment of cardiac I/R injury.

Coarctation of the aorta associated with agenesis of left common carotid artery and left subclavian artery.

We describe the case of a 10-year-old boy with coarctation of the aorta complicated by innominate artery stenosis and agenesis of left common carotid artery and left subclavian artery. The patient was treated with an interposition graft between the ascending and descending aorta. The right subclavian was revascularized with another graft from the interposition graft to the distal right subclavian. This is a rare case of the combination of coarctation of the aorta and other vascular malformations.