Publications by authors named "Gan-Xin Yan"

Objective: This study aimed to explore the impact of a combination of hyperuricemia (HUA) and excessive high-sensitivity C-reactive protein (hs-CRP) levels on the likelihood of developing cardiac conduction block (CCB). Additionally, it sought to assess whether the influence of uric acid (UA) on CCB is mediated by hs-CRP.

Methods: A prospective study was executed utilizing data from the Kailuan cohort, including 81,896 individuals initially free from CCB.

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During drug discovery, small molecules are typically assayed in vitro for secondary pharmacology effects, which include ion channels relevant to cardiac electrophysiology. Compound A was an irreversible inhibitor of myeloperoxidase investigated for the treatment of peripheral artery disease. Oral doses in dogs at ≥5 mg/kg resulted in cardiac arrhythmias in a dose-dependent manner (at Cmax, free ≥1.

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Mexiletine, a class Ib antiarrhythmic drug, exhibits its major antiarrhythmic effect via inhibition of the fast and late Na currents in myocardial tissues that are dependent on the opening of Na channels for their excitation. Through a comprehensive examination of mexiletine's therapeutic benefits and potential risks, we aim to provide valuable insights that reinforce its role as a vital therapeutic option for patients with ventricular arrhythmias, long QT syndrome, and other heart rhythm disorders. This review will highlight the current understandings of the antiarrhythmic effects and rationales for recent off-label use and address the mortality and proarrhythmic effects of mexiletine utilizing published basic and clinical studies over the past five decades.

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A 3-year-old boy with congenital ventricular septal defect underwent a closure procedure. Telemetry after the procedure reveals sinus arrhythmia with varying types of bundle branch blocks. Inverse decremental conduction in left posterior fascicle, related to preceding RP interval during sinus arrhythmia, underlies changes between right and left bundle branch blocks.

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Background: The QTc in sinus rhythm (SR) following direct current cardioversion (DCCV) of atrial fibrillation (AF) is commonly used as a baseline QTc for patients who require initiation of antiarrhythmic drugs for rhythm control. Inaccurate baseline QTc may cause drug-induced torsades de pointes.

Objectives: This study sought to assess time-dependent QTc changes following DCCV.

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Background: Macroscopic T wave alternans (macro-TWA) often heralds the onset of Torsades de Pointes in patients with QT prolongation. However, the mechanisms underlying macro-TWA remain unclear. We examined the cellular and ionic basis for macro-TWA in rabbits with left ventricular hypertrophy (LVH).

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Background: Atrial dissociation (AD) is described as the existence of two simultaneous electrically isolated atrial rhythms. Theoretically, detection of dual atrial rhythms with a sufficiently high rate by pacemaker can lead to automatic mode switching and associated pacemaker syndrome. Such a clinical observation has not been reported before in the literature.

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Background: On surface electrocardiographic (ECGs), it is difficult to differentiate I -mediated J waves, a repolarization phenomenon seen in J wave syndromes (JWS) from terminal QRS deflections that mimic J waves (pseudo J waves) in intraventricular conduction delay (IVCD), an abnormality in depolarization. We hypothesize that the difference between the "maximum QRS duration" inclusive of J point or terminal QRS deflections and the minimum QRS duration identified across a 12-lead ECG is significantly larger in I -mediated J waves, and can serve as a marker to make this distinction.

Methods: A retrospective analysis was performed on adults with ECGs consisting of one of the four following manifestations: J waves associated with hypothermia and early repolarization, and pseudo J waves associated with right bundle branch block (RBBB) and non-specific intraventricular conduction delay (NS-IVCD).

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Article Synopsis
  • Brugada syndrome (BrS) is linked to mutations in a cardiac sodium channel gene, but there is limited research on the genetic factors in patients experiencing their first arrhythmic events.
  • A large survey of 678 BrS patients across 14 countries identified 392 probands, with 23.5% having pathogenic or likely pathogenic (P/LP) variants, revealing differences in demographics and clinical features based on genotype.
  • Results showed that patients with P/LP variants were generally younger, more often female, and had a higher incidence of family history of sudden cardiac death, suggesting a complex interplay between genetics, age, gender, and ethnicity in BrS.
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Potassium is the predominant intracellular cation, with its extracellular concentrations maintained between 3. 5 and 5 mM. Among the different potassium disorders, hypokalaemia is a common clinical condition that increases the risk of life-threatening ventricular arrhythmias.

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Drugs that prolong QT may cause torsade de pointes (TdP). However, translation of nonclinical assessment of QT prolongation or hERG channel, targeted by QT-prolonging drugs, into clinical TdP risk has been insufficient to date. In this blinded study, we confirmed the utility of a Normalized TdP Score System in predicting drug-induced TdP risks among 34 drugs, including 28 with low, intermediate, and high TdP risks under the Comprehensive In Vitro Proarrhythmia Assay (CiPA) initiative plus six compounds with names blinded to the investigators, using the rabbit ventricular wedge assay.

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Mitochondrial dysfunction and oxidative stress play an important role in the pathogenesis of both atrial fibrillation (AF) and diabetes mellitus (DM). Wenxin Keli (WXKL), an antiarrhythmic traditional Chinese medicine, has been shown to prevent cardiac arrhythmias through modulation of cardiac ion channels. This study tested the hypothesis that WXKL can improve atrial remodeling in diabetic rats by restoring mitochondrial function.

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Brugada syndrome (BrS) is an inherited ion channel channelopathy predisposing to ventricular arrhythmias and sudden cardiac death. Originally believed to be predominantly associated with mutations in SCN5A encoding for the cardiac sodium channel, mutations of 18 genes other than SCN5A have been implicated in the pathogenesis of BrS to date. Diagnosis is based on the presence of a spontaneous or drug-induced coved-type ST segment elevation.

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