BACKGROUND:Gap junction remodeling is an important cause of ventricular arrhythmia in heart failure. However, it remains unclear whether renal denervation (RDN) regulates gap junction remodeling in heart failure. To explore the effect of RDN on gap junction remodeling in dogs with high-pacing-induced heart failure. METHODS:Fifteen dogs were randomly divided into control (n = 5), heart failure (HF) (n = 5), and RDN+HF (n = 5) group. A high-pacing-induced-heart failure model was established using rapid right ventricular pacing for 4 weeks. The RDN+HF group underwent surgical and chemical ablation of both renal arteries before 4 weeks rapid right ventricular pacing. After 4 weeks, echocardiography, High-Performance Liquid Chromatography-Mass Spectrometry test for norepinephrine and epinephrine, and pathological analysis were performed in the above 3 groups. Further, immunohistochemical staining was used to detect tyrosine hydroxylase, ChaT, connexin 43 (Cx43), and connexin 40 (Cx40). Connexin 43 and Cx40 expression was detected by western blotting. Transmission electron microscopy was used to observe the gap junction. RESULTS:Compared to the control group, myocardial fibrosis and sympathetic hyperactivity were observed in the HF group. Immunohistochemical staining and western blotting showed that Cx40 expression and Cx43 expression was significantly reduced in the HF group. Compared with the HF group, the RDN+HF group showed reduced sympathetic hyperactivity, Cx40 expression, Cx40/Cx43 ratio, and increased Cx43 expression. CONCLUSION:Renal denervation alleviates gap junction remodeling in high-pacing-induced heart failure dogs.

目的 探讨左心耳流速(LAAV)与心房颤动(AF)患者首次导管消融后复发的相关性.方法 回顾性分析2019年6月—2021年6月在新疆医科大学第一附属医院首次进行导管消融的AF患者.术前使用经食管超声心动图检查记录LAAV,评估患者的左心耳功能,收集患者的基本临床数据.并对纳入的患者随访1年.采用Cox风险比例模型来确定LAAV在AF复发中的预测价值.结果 研究共纳入268例患者,平均年龄(60.10±11.11)岁,49例患者出现AF复发.复发的患者多为持续性AF(P=0.001),45.左心耳开口深度较深[(28.06±7.09)mm vs(26.01±6.11)mm,P=0.04],LAAV 较低[(0.51±0.22)m/s vs(0.59± 0.22)m/s,P=0.033],通过ROC曲线分析显示LAAV=0.495 m/s对AF复发具有最佳的检验效能,并以此将患者分为LAAV正常组和LAAV减低组.通过Kaplan-Meier曲线分析发现,LAAV减低组与LAAV正常组相比,术后AF发生率明显升高(long-rank P=0.004),Cox 比例风险模型显示持续性 AF(HR=1.929,95％CI 1.017～3.658,P=0.044)、体重指数(HR=1.094,95％CI 1.005～1.192,P=0.038)、LAAV≤0.495 m/s(HR=1.947,95％CI 1.034～3.664,P=0.039)是影响AF复发的独立危险因素.在亚组分析中,无论阵发性AF患者还是持续性AF患者均未发现导管消融后AF复发的独立危险因素.结论 LAAV减低可能是导管消融后AF复发的潜在危险因素.

Hypertrophic obstructive cardiomyopathy (HOCM) is the most common type of hypertrophic cardiomyopathy, which is prone to left ventricular outflow obstruction and causes various adverse effects. It is also the main cause of sudden death in adolescents and athletes. Timely intervention is crucial for the prognosis of patients. Radiofrequency ablation has been widely used in the treatment of various arrhythmias, but it is still a new treatment method in HOCM. This article mainly reviews the clinical application progress of radiofrequency ablation in the treatment of HOCM patients.

BACKGROUND:While desmosomal junctions and gap junction remodeling are among the arrhythmogenic substrates, the fate of desmosomal and gap junctions in high-pacing-induced heart failure remains unclear. This aim of this study was to determine the fate of desmosomal junctions in high-pacing-induced heart failure.METHODS:Dogs were randomly divided into 2 equal groups, a high-pacing-induced heart failure model group (heart failure group, n = 6) and a sham operation group (control group, n = 6). Echocardiography and cardiac electrophysiological examination were performed. Cardiac tissue was analyzed by immunofluorescence and transmission electron microscopy. The expression of desmoplakin and desmoglein-2 proteins was detected by western blot.RESULTS:A significant decrease in ejection fraction, significant cardiac dilatation, diastolic and systolic dysfunction, and ventricular thinning occurred after 4 weeks in high-pacing-induced dog model of heart failure. Effective refractory period action potential duration at 90% repolarization was prolonged in the heart failure group. Immunofluorescence analysis and transmission electron microscopy demonstrated connexin-43 lateralization accompanies desmoglein-2 and desmoplakin remodeling in the heart failure group. Western blotting showed that the expression of desmoplakin and desmoglein-2 proteins was higher in heart failure than in normal tissue.CONCLUSION:Desmosome (desmoglein-2 and desmoplakin) redistribution and desmosome (desmoglein-2) overexpression accompanying connexin-43 lateralization were parts of a complex remodeling in high-pacing-induced heart failure.

Mitral valve disease is a common cause of heart failure and death. In the current issue of the Journal, Hasin et al. investigated the pathogenesis of functional mitral regurgitation and found that the reduced left ventricle (LV) rotational movement was independently associated with mitral regurgitation severity [ [1] Hasin T. Mann D. Welt M. Barrett O. Shalev A. Godfrey M. Kovacs A. Bogot N. Carasso S. Glikson M. Wolak A. Loss of left ventricular rotation is a significant determinant of functional mitral regurgitation. Int. J. Cardiol. 2021; 345: 143-149 Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar ]. This case report has inspired us to investigate mitral annular disjunction (MAD), a syndrome often being misdiagnosed as functional mitral regurgitation at its early stage, and its role in sudden cardiac death (SCD), which has been ignored and underestimated in clinics.

导管消融作为心房颤动的一线治疗方案,可显著改善患者预后.多项研究发现导管消融后并发症存在性别差异,女性患者术后并发症增加.现对心脏压塞、心房食管瘘、卒中事件、血管并发症、膈神经麻痹、肺静脉狭窄六种主要并发症阐述其性别差异及差异机制,增加对并发症性别差异的重视和预防,可优化导管消融的有效性和安全性,减轻心房颤动患者的公共卫生负担.

Background: The risk of ventricular arrhythmia in heart failure (HF) is extremely high. Desmosome remodeling is closely related to ventricular arrhythmia and is regulated by sympathetic signals. The high-pacing-induced HF dog model is a well-established HF model. This study investigated the relationship between changes in desmosomes and sympathetic nerve activity in a high-pacing-induced HF dog model.Methods: Beagles were randomly divided into a control group (sham HF, n=6), an HF group (sham sympathetic denervation [Sd] + HF, n=6), and an Sd-HF group (Sd + HF, n=6). HF and Sd-HF models were established by rapid right ventricular pacing (180 bpm for 3 days, 220 bpm for 3 days, 250 bpm for 3 weeks) and surgical/chemical renal sympathetic denervation, respectively. Echocardiography and cardiac electrophysiological examination were performed, and sympathetic activity was measured. Desmosomes were detected by transmission electron microscopy and immunofluorescence.Results: Sympathetic overactivity, electrical remodeling (effective refractory period [ERP] and prolonged action potential duration at 90% repolarization [APD90 ]), increased desmosomes (desmoglein 2 and desmoplakin 1+2 protein) in the HF model. Sympathetic denervation suppressed sympathetic overactivation by attenuating prolonged ERP and APD90 (P<0.05) and down-regulating the expression of desmoglein 2 and desmoplakin 1+2 (P<0.05). Moreover, immunofluorescence showed that Cx43 was co-localized with desmoglein 2 and desmoplakin 1+2, which were partially oriented parallel to the fiber direction in the HF model.Conclusions: High-pacing-induced HF promotes desmosome adhesion in dogs, possibly by the mediation of sympathetic overactivation.

Hypertrophic cardiomyopathy (HCM) is a cardiac disease characterized by left ventricular myocardial hypertrophy due to a mutation in the gene encoding myosin, or an unknown genetic variant, with a prevalence ranging from 1:500 to 1:200 in clinics [1]. HCM is most likely to cause left ventricular outflow tract (LVOT) obstruction, which is known as hypertrophic obstructive cardiomyopathy (HOCM). The treatment of HOCM is aiming to reduce left ventricular outflow tract pressure gradient and relieve symptoms.