BACKGROUND: Tachycardia is a common arrhythmia in clinical practice, and its pathogenesis is mostly related to reentry. However, there are also a few tachycardia that are not related to reentry. Actively clarifying the pathogenesis of these non-reentry related tachycardia is of great significance for its treatment.
METHODS: A 55-year-old female patient presented with recurrent palpitations with a fastest heart rate of 180 beats/minute 10 years ago.
METHODS: Dual atrioventricular nodal non-reentrant tachycardia (DAVNNT).
METHODS: DAVNNT can be cured by radiofrequency ablation of atrioventricular nodal slow path modification.
RESULTS: The tachycardia has stopped.
CONCLUSIONS: DAVNNT is a rare disease in clinical practice. Its characteristic is not reentration-related arrhythmias, but the phenomenon of increased heart rate caused by electrical conduction down the double pathway of atrioventricular nodal tract and subsequent pathway. Electrophysiological examination helps to clarify the diagnosis and pathogenesis, and catheter ablation can cure the disease.

Physiologically, the atria contract first, followed by the ventricles, which is the prerequisite for normal blood circulation. The above phenomenon of atrioventricular sequential contraction results from the characteristically slow conduction of electrical excitation of the atrioventricular node (AVN) between the atria and the ventricles. However, it is not clear what controls the conduction of electrical excitation within AVNs. Here, we find that AVN pacemaker cells (AVNPCs) possess an intact intrinsic GABAergic system, which plays a key role in electrical conduction from the atria to the ventricles. First, along with the discovery of abundant GABA-containing vesicles under the surface membranes of AVNPCs, key elements of the GABAergic system, including GABA metabolic enzymes, GABA receptors, and GABA transporters, were identified in AVNPCs. Second, GABA synchronously elicited GABA-gated currents in AVNPCs, which significantly weakened the excitability of AVNPCs. Third, the key molecular elements of the GABAergic system markedly modulated the conductivity of electrical excitation in the AVN. Fourth, GABAA receptor deficiency in AVNPCs accelerated atrioventricular conduction, which impaired the AVN\'s protective potential against rapid ventricular frequency responses, increased susceptibility to lethal ventricular arrhythmias, and decreased the cardiac contractile function. Finally, interventions targeting the GABAergic system effectively prevented the occurrence and development of atrioventricular block. In summary, the endogenous GABAergic system in AVNPCs determines the slow conduction of electrical excitation within AVNs, thereby ensuring sequential atrioventricular contraction. The endogenous GABAergic system shows promise as a novel intervention target for cardiac arrhythmias.

BACKGROUND: During normal sinus rhythm, atrial depolarization is conducted from right atrium to left atrium through Bachmann\'s bundle, and a normal P wave axis which is measured on the frontal plane is between 0º and + 75º. The change of P wave polarity is helpful for the analysis of origin point.
METHODS: We report a patient with negative P wave in lead I. The characteristics of QRS complex in leads V1 to V6 are helpful to preliminarily differential diagnosis. The 12-lead electrocardiogram (ECG) with correct limb leads (right arm-left arm) placement shows sinus rhythm with complete right bundle branch block (RBBB).
CONCLUSIONS: The change of P wave polarity as well as characteristics of QRS complex can help identify limb-lead reversals.

暂无摘要。

BACKGROUND: The radiofrequency (RF) ablation target may be located at the compact atrioventricular node (AVN) region during so-called slow pathway (SP) RF ablation, potentially leading to transient or permanent atrioventricular block (AVB). However, related data are rare.
METHODS: Among 715 index consecutive patients who underwent RF ablation for atrioventricular nodal re-entry tachycardia, 17 patients subsequently experienced transient or permanent AVB and were included in this retrospective observational study.
RESULTS: Among the 17 patients, two patients (11.8%) developed transient first-degree AVB, four patients (23.5%) developed transient second-degree AVB, seven patients (41.2%) developed transient third-degree AVB, and four patients (23.5%) developed permanent third-degree AVB. During baseline sinus rhythm before the start of RF ablation, no His-bundle potential was recorded from the RF ablation catheter. During the so-called SP RF ablation that led to transient or permanent AVB, junctional rhythm with ventriculoatrial (VA) conduction block followed by subsequent AVB was observed in 14 of 17 patients (82.4%), and a low-amplitude, low-frequency hump-shaped atrial potential was recorded before the start of RF ablation in 7 of the 17 patients (41.2%). Direct AVB occurred in 3 of the 17 patients (17.6%), and a low-amplitude, low-frequency hump-shaped atrial potential was recorded before the start of RF ablation in all 3 patients.
CONCLUSIONS: The low-amplitude, low-frequency hump-shaped atrial potential recorded at the so-called SP region may reflect the electrogram of compact AVN activation, and RF ablation to this site heralds impending AVB even when a His-bundle potential is not recorded.

Ivabradine reduces the heart rate by selectively inhibiting the If current of the sinoatrial node, mainly for the treatment of chronic heart failure with decreased left ventricular systolic function and inappropriate sinus tachycardia, but the inhibitory effect on the atrioventricular node is rarely reported. The patient was admitted to hospital mainly because of intermittent chest pain for 7 years, which worsened for 10 days. Admission electrocardiogram (ECG) considered sinus tachycardia, with QS wave and T wave inversion in II, III, aVF, V3 R-V5 R, V4 -V9 leads, and non-paroxysmal junctional tachycardia (NPJT) with interference atrioventricular dissociation. After treatment with ivabradine the ECG returned to normal conduction sequence. NPJT with interference atrioventricular dissociation is a fairly rare electrocardiographic phenomenon. This case reports for the first time that ivabradine is used in the treatment of NPJT with interference atrioventricular dissociation. It is speculated that ivabradine has a potential inhibitory effect on the atrioventricular node.

Tamoxifen, a selective estrogen receptor modulator, was initially used to treat cancer in women and more recently to induce conditional gene editing in rodent hearts. However, little is known about the baseline biological effects of tamoxifen on the myocardium. In order to clarify the short-term effects of tamoxifen on cardiac electrophysiology of myocardium, we applied a single-chest-lead quantitative method and analyzed the short-term electrocardiographic phenotypes induced by tamoxifen in the heart of adult female mice. We found that tamoxifen prolonged the PP interval and caused a decreased heartbeat, and further induced atrioventricular block by gradually prolonging the PR interval. Further correlation analysis suggested that tamoxifen had a synergistic and dose-independent inhibition on the time course of the PP interval and PR interval. This prolongation of the critical time course may represent a tamoxifen-specific ECG excitatory-inhibitory mechanism, leading to a reduction in the number of supraventricular action potentials and thus bradycardia. Segmental reconstructions showed that tamoxifen induced a decrease in the conduction velocity of action potentials throughout the atria and parts of the ventricles, resulting in a flattening of the P wave and R wave. In addition, we detected the previously reported prolongation of the QT interval, which may be due to a prolonged duration of the ventricular repolarizing T wave rather than the depolarizing QRS complex. Our study highlights that tamoxifen can produce patterning alternations in the cardiac conduction system, including the formation of inhibitory electrical signals with reduced conduction velocity, implying its involvement in the regulation of myocardial ion transport and the mediation of arrhythmias. A Novel Quantitative Electrocardiography Strategy Reveals the Electroinhibitory Effect of Tamoxifen on the Mouse Heart（Figure 9）. A working model of tamoxifen producing acute electrical disturbances in the myocardium. SN, sinus node; AVN, atrioventricular node; RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle.

BACKGROUND: There is currently no particularly effective strategy for patients with persistent atrial fibrillation accompanying heart failure with preserved ejection fraction (HFpEF), especially with recurrent atrial fibrillation after ablation. In this study, we will evaluate a new treatment strategy for patients with persistent atrial fibrillation who had at least two attempts (≧2 times) of radio-frequency catheter ablation but experienced recurrence, and physiologic conduction was reconstructed after atrioventricular node ablation or drug therapy, to control the patient\'s ventricular rate to maintain a regular heart rhythm, which is called His-Purkinje conduction system pacing (HPCSP) with atrioventricular node ablation.
RESULTS: This investigator-initiated, multicenter prospective randomized controlled trial aimed to recruit 296 randomized HFpEF patients with recurrent atrial fibrillation. All the enrolled patients were randomly assigned to the pacing group or the drug treatment group. The primary endpoint is differences in cardiovascular events and clinical composite endpoints (all-cause mortality) between patients in the HPCSP and drug-treated groups. Secondary endpoints included heart failure hospitalization, exercise capacity assessed by cardiopulmonary exercise tests, quality of life, echocardiogram parameters, 6-minute walk distance, NT-ProBNP, daily patient activity levels, and heart failure management report recorded by the CIED. It is planned to compete recruitment by the end of 2023 and report in 2025.
CONCLUSIONS: The study aims to determine whether His-Purkinje conduction system pacing with atrioventricular node ablation can better improve patients\' symptoms and quality of life, postpone the progression of heart failure, and reduce the rate of rehospitalization and mortality of patients with heart failure.
BACKGROUND: ChiCTR1900027723, URL: http://www.chictr.org.cn/edit.aspx?pid=46128&htm=4.

Spontaneously depolarizing nodal cells comprise the pacemaker of the heart. Intracellular calcium (Ca2+) plays a critical role in mediating nodal cell automaticity and understanding this so-called Ca2+ clock is critical to understanding nodal arrhythmias. We previously demonstrated a role for Jph2 (junctophilin 2) in regulating Ca2+-signaling through inhibition of RyR2 (ryanodine receptor 2) Ca2+ leak in cardiac myocytes; however, its role in pacemaker function and nodal arrhythmias remains unknown. We sought to determine whether nodal Jph2 expression silencing causes increased sinoatrial and atrioventricular nodal cell automaticity due to aberrant RyR2 Ca2+ leak.
A tamoxifen-inducible, nodal tissue-specific, knockdown mouse of Jph2 was achieved using a Cre-recombinase-triggered short RNA hairpin directed against Jph2 (Hcn4:shJph2). In vivo cardiac rhythm was monitored by surface ECG, implantable cardiac telemetry, and intracardiac electrophysiology studies. Intracellular Ca2+ imaging was performed using confocal-based line scans of isolated nodal cells loaded with fluorescent Ca2+ reporter Cal-520. Whole cell patch clamp was conducted on isolated nodal cells to determine action potential kinetics and sodium-calcium exchanger function.
Hcn4:shJph2 mice demonstrated a 40% reduction in nodal Jph2 expression, resting sinus tachycardia, and impaired heart rate response to pharmacologic stress. In vivo intracardiac electrophysiology studies and ex vivo optical mapping demonstrated accelerated junctional rhythm originating from the atrioventricular node. Hcn4:shJph2 nodal cells demonstrated increased and irregular Ca2+ transient generation with increased Ca2+ spark frequency and Ca2+ leak from the sarcoplasmic reticulum. This was associated with increased nodal cell AP firing rate, faster diastolic repolarization rate, and reduced sodium-calcium exchanger activity during repolarized states compared to control. Phenome-wide association studies of the JPH2 locus identified an association with sinoatrial nodal disease and atrioventricular nodal block.
Nodal-specific Jph2 knockdown causes increased nodal automaticity through increased Ca2+ leak from intracellular stores. Dysregulated intracellular Ca2+ underlies nodal arrhythmogenesis in this mouse model.

Heart failure (HF) combined with persistent atrial fibrillation (AF) often coexist and may promote the pathological conditions of cardiac dysfunction, leading to poor prognosis. Cardiac resynchronization therapy (CRT) combined with atrioventricular junction ablation (AVJA) is a highly effective treatment for HF patients with underlying AF who either have failed or are not suitable for catheter ablation. The CRT-AVJA combination therapy can improve clinical outcomes in HF patients. Currently, clinical CRT methods are categorized into biventricular pacing (BVP) - based and conduction system pacing (CSP) - based methods. These procedures have inherent advantages and disadvantages, in addition to their considerable differences in clinical applications. This article aims to review the clinical progress of AVJA combined with different CRT strategies for treating HF patients with persistent AF and propose that conversion CRT strategy (BVP/CSP-CRT) combined with AVJA may be a perspective alternative. Meanwhile, we generalize that 7 categories of HF patients with persistent AF may need to consider the CRT-AVJA combination therapy.