Predictors for new-onset conduction block in patients with pure native aortic regurgitation after transcatheter aortic valve replacement with a new-generation self-expanding valve (VitaFlow Liberty™): a retrospective cohort study.

BACKGROUND: New-generation self-expanding valves can improve the success rate of transcatheter aortic valve replacement (TAVR) for severe pure native aortic regurgitation (PNAR). However, predictors of new-onset conduction block post-TAVR using new-generation self-expanding valves in patients with PNAR remain to be established. Therefore, this study aimed to identify predictors of new-onset conduction block post-TAVR using new-generation self-expanding valves (VitaFlow Liberty™) in patients with PNAR. METHODS: In this retrospective cohort study, patients were categorized into pacemaker and non-pacemaker groups based on their need for new postoperative permanent pacemaker implantation (PPI). Based on the postoperative presence of either new-onset complete left bundle branch block (cLBBB) or high-grade atrioventricular block (AVB), patients were further classified into conduction disorder and non-conduction disorder groups. Laboratory, echocardiographic, computed tomography, preoperative and postoperative electrocardiography, and procedural and clinical data were collected immediately after TAVR and during hospitalization and compared between the groups. Multivariate logistic regression analysis was performed incorporating the significant variables from the univariate analyses. RESULTS: This study examined 68 consecutive patients with severe PNAR who underwent TAVR. In 20 patients, a permanent pacemaker was fitted postoperatively. Multivariate logistic regression analysis revealed an association between the need for postoperative PPI and preoperative complete right bundle branch block (cRBBB) or first-degree AVB, as well as a non-tubular left ventricular outflow tract (LVOT). In addition, valve implantation depth and angle of aortic root were independent predictors of new-onset cLBBB or high-grade AVB developing post-TAVR. The predictive value of valve implantation depth and angle of aortic root was further supported by receiver operating characteristic curve analysis results. CONCLUSIONS: In patients with PNAR undergoing TAVR using self-expanding valves, preoperative cRBBB or first-degree AVB and a non-tubular LVOT were indicators of a higher likelihood of PPI requirement. Moreover, deeper valve implantation depth and greater angle of aortic root may be independent risk factors for new-onset cLBBB or high-grade AVB post-TAVR. Valve implantation depth and angle of aortic root values may be used to predict the possibility of new cLBBB or high-grade AVB post-TAVR.

High glucose induced endothelial cell reactive oxygen species via OGG1/PKC/NADPH oxidase pathway.

AIMS: Reactive oxygen species (ROS) caused by high glucose (HG) is involved in a lot of diseases including diabetes. However, the underlying mechanism of ROS induction by HG remains unclear. Emerging evidence has shown the 8-oxoguanine glycosylase (OGG1) is the main DNA glycosylase responsible for atherosclerosis, obesity, hepatic steatosis, and insulin resistance, and so on. Our aim was to explore the role of OGG1 on HG-mediated endothelial ROS. MAIN METHODS: Human umbilical vein endothelial cells (HUVECs) were exposed to HG (30 mM) for different time periods. HG predominantly inhibited OGG1 expression in a time-dependent manner measured by western blotting, qPCR and immunofluorescence. Additionally, HUVECs were cultured with a fluorescent probe, DCFH and DHE, after being subjected to HG. Cell chemiluminescence and flow cytometry results revealed that HG caused endothelial ROS activation. KEY FINDINGS: High glucose remarkably decreased endothelial OGG1 expression. The overexpression of OGG1 significantly reversed HG-mediated PKC and NADPH oxidase activities and ROS levels. Moreover, manipulated expression of PKC significantly contacted the role of OGG1 on NADPH oxidase activation. SIGNIFICANCE: These results suggest that OGG1 downregulation promoted HG-induced endothelial ROS production and might be a potential clinical treatment target of diabetics.