Chronic hypoxia is a common inducer of end-stage cardiovascular disease. In cells under hypoxia, the hypoxia-inducible factor-1 (HIF-1) plays a vital role in regulating downstream target genes. However, the mechanism of hypoxia in cardiomyocytes is still unclear. In this study, we aimed to identify novel downstream epigenetic targets of HIF-1α in cardiomyocytes under hypoxia. H9c2 cells were exposed to hypoxia condition, and quantitative real-time PCR analysis was performed to evaluate the expression of miR-20b-5p. The results indicated that the expression of miR-20b-5p was down-regulated in H9c2 cells under low oxygen condition. Meanwhile, HIF-1α overexpression further down-regulated the miR-20b-5p expression in H9c2 cells transfected with HIF-1α plasmids. In addition, Annexin-V-FITC/PI flow cytometry analysis suggested that overexpression of miR-20b-5p attenuated cell apoptosis under hypoxia condition in H9c2 cells. Western blot analysis showed that the hypoxia apparently increased Bax and cleaved-caspase-3, but decreased Bcl-2 expression in H9c2 cells, indicating that hypoxia-induced NF-κB signaling pathway activation is mediated by miR-20b-5p. Hypoxia-induced H9c2 cell apoptosis was reduced after HIF-1α knockdown as shown by the flow cytometry analysis. In conclusion, we identified that miR-20b-5p plays an important role in mediating cardiomyocytes apoptosis under hypoxia, which is mediated by the HIF-1/NF-κB signaling pathway.

This study was designed to investigate whether administration of digitalis could improve mechanical function of left atrial appendage (LAA) and left atrium prospectively in patients with atrial stunning. Fifty-four consecutive patients in whom atrial stunning was observed immediately after cardioversion of chronic atrial fibrillation (AF) were randomized into digitalis or control group for 1 week following cardioversion. Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were performed prior to, immediately following, 1 day after and 1 week after cardioversion to measure transmitral flow velocity and LAA flow velocity. Electrical cardioversion of AF elicited significantly slower left atrial appendage peak emptying velocity (LAA-PEV) and peak filling velocity (LAA-PFV) immediately following cardioversion in both groups. 1 day post cardioversion, there were no significant differences in transmitral E wave, A wave, E/A ratio, LAA-PEV, LAA-PFV or left atrial appendage ejection fraction (LAA-EF) between digitalis and control groups. 1 week post cardioversion, no significant differences were found in transmitral E wave, A wave, E/A ratio, LAA-PEV, LAA-PFV or LAA-EF between the two groups. The occurrence rates of spontaneous echo contrast were not significantly different between digitalis and control groups one day and one week post cardioversion. In conclusion, digitalis did not improve left atrial and appendage mechanical dysfunction following cardioversion of chronic AF. Digitalis did not prevent the development of spontaneous echo contrast in left atrial chamber and appendage. This may be due to the fact that digitalis aggravates intracellular calcium overload induced by chronic AF and has a negative effect on ventricular rate.

To analyze existing literature and understand how to balance the minimization of bleeding risk and ensuring adequate anticoagulation during coronary intervention treatment and long-term postoperative anticoagulation in hemophilia patients during the perioperative period, in order to provide guidance for healthcare professionals in developing effective treatment plans. This narrative review will analyze existing studies, case reports, and clinical guidelines to determine the most effective strategies for managing acute coronary syndrome in hemophilia patients. When evaluating the literature, factors such as patient age, medical history, and severity of the condition will be considered. The current management guidelines for acute coronary syndrome in hemophilia patients are not based on systematic evaluation and mainly rely on expert opinions. This article provides a comprehensive analysis of existing literature and recommends coagulation factor replacement therapy before anticoagulation and intervention treatment, as well as personalized anticoagulation treatment during the postoperative period for better management of hemophilia patients with acute coronary syndrome. These recommendations can help healthcare professionals develop more effective treatment plans for hemophilia patients.

The objective of this study was to evaluate the electrophysiologic characteristics of Crista terminalis (CT) and their implication in the pathogenesis of atrial tachycardia in rabbits. For this purpose, 27 New Zealand rabbits were used. Using standard glass microelectrode technique, cellular action potentials (APs) of CT and pectinate muscle (PM) were recorded in normal Tyrode's perfusion and Tyrode's perfusion with 4 μM isoproterenol. Longitudinal conduction velocity (V(L)) and transverse conduction velocity (V(T)) of CT were measured. As our data show, CT tissue had a trend of spontaneous phase IV depolarization. Conduction anisotropy (V(L)/V(T)) of CT was 4.53 ± 0.91. The duration of the AP of CT was longer than that of PM cells. APD(20) and APD(90) for CT were 28.1 ± 3.5 and 145.3 ± 7.1 ms; and for PM cells were 21.8 ± 4.1 and 125.3 ± 6.3 ms, respectively (all P values < 0.01). The early and delayed action depolarizations were recorded after isoproterenol perfusion. A fast paroxysmal irregular rhythm was recorded which could be arrested by 0.1 mmol/l Isoptin. It was, therefore, concluded that the latent autorhythmicity, trigger activity, and conduction properties of CT might provide the electrophysiologic basis for the occurrence and sustenance of atrial arrhythmia.