Background: The left bundle branch pacing (LBBP) makes the ventricular depolarization closer to the physiological state and shortens QRS duration. The purpose of this study is to explore the ventricular systolic mechanical synchronization after LBBP in comparison with traditional right ventricular pacing (RVP) using two-dimensional strain echocardiography (2D-STE). Methods: Thirty-two patients who received LBBP (n = 16) or RVP (n = 16) from October 2018 to October 2019 and met the inclusion criteria were included in this retrospective study. Electrocardiogram (ECG) characteristics, pacing parameters, pacing sites, and safety events were assessed before and after implantation. Acquisition and analysis of ventricular systolic synchronization were implemented using 2D-STE. Results: In RVP group, ECG showed left bundle branch block patterns. At LBBP, QRS morphology was in the form of right bundle branch block, and QRS durations were significantly shorter than that of the RVP QRS (109.38 ± 12.89 vs 149.38 \ ± 19.40 ms, P < .001). Both the maximum time differences (TD) and SDs of the 18-segments systolic time to peak systolic strain were significantly shorter under
Targeting the adaptor protein (transforming growth factor-β (TGF-β)-activated protein kinase 1 (TAK1)-binding protein 1) (TAB1)-mediated non-canonical activation of p38α to limit ischemia/reperfusion (I/R) injury after an acute myocardial infarction seems to be attractive since TAB1/p38α interaction occurs specifically in very limited circumstances and possesses unique structural basis. However, so far no TAB1/p38α interaction inhibitor has been reported due to the limited knowledge about the interfaces. In this study, we sought to identify key amino acids essential for the unique mode of interaction with computer-guided molecular simulations and molecular docking. After validation of the predicted three-dimensional (3-D) structure of TAB1/p38α complex, we designed several peptides and evaluated whether they could block TAB1/p38α interaction with selectivity. We found that a cell-permeable peptide worked as a selective TAB1/p38α interaction inhibitor and decreased myocardial I/R injury. To our knowledge, this is the first TAB1/p38α interaction inhibitor.
Severe and moderate OSA with T2DM is marked by a delayed IGL peak following LSpO2. Nocturnal hypoxemia causes hyperglycemia in patients with OSA along with T2DM.
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