Isolation of canine coronary sinus musculature from the atria by radiofrequency catheter ablation prevents induction of atrial fibrillation.

Background: The junction between the coronary sinus (CS) musculature and both atria contributes to initiation of atrial tachyarrhythmias. The current study investigated the effects of CS isolation from the atria by radiofrequency catheter ablation on the induction and maintenance of atrial fibrillation (AF).

Methods And Results: Using an optical mapping system, we mapped action potentials at 256 surface sites in 17 isolated and arterially perfused canine atrial tissues containing the entire musculature of the CS, right atrial septum, posterior left atrium, left inferior pulmonary vein, and vein of Marshal.

The role of coronary sinus musculature in the induction of atrial fibrillation.

Background: Coronary sinus (CS) musculature connects the right atria (RA) and the left atria (LA). However, the functional significance of the electrical junctions between the atria and the CS musculature is still unclear.

Objective: We investigated electrophysiological properties of the CS-atrial connections and their role in atrial fibrillation.

Relationship between autonomic nervous system activity during sleep and fasting glucose in Japanese workers.

Although autonomic nervous system activity is reportedly related to diurnal glucose tolerance impairment, the relationship with glucose tolerance during sleep is unclear. Since work styles have recently diversified, it is important to assess the effect of sleep on workers' health. Elucidation of the relationship between autonomic nervous system activity during sleep and glucose tolerance in workers may facilitate preventive measures against diabetes using non-pharmacological means (e.

Spontaneous electrocardiogram alterations predict ventricular fibrillation in Brugada syndrome.

Background: Patients with Brugada syndrome (BS) often have spontaneous changes in their electrocardiogram (ECG).

Objective: To evaluate the significance of ECG alterations, we investigated the relationships between the ECG and the occurrence of ventricular fibrillation (VF) in both patients and an experimental model of BS.

Methods: In study 1, we evaluated ECG alterations in BS patients with (VF+, n = 33) and without (VF-, n = 41) spontaneous VF.

Genotype-phenotype correlation in tissue models of Brugada syndrome simulating patients with sodium and calcium channelopathies.

Background: Genetic defects in the sodium channel or in the calcium channel have been identified in patients with Brugada syndrome (BS). However, the differences in their genotype-phenotype correlations are still unclear.

Objective: We evaluated the phenotypic differences and therapeutic effects between the sodium channel and calcium channel abnormalities in in vitro models of BS.

Epicardial ablation eliminates ventricular arrhythmias in an experimental model of Brugada syndrome.

Background: Although radiofrequency catheter ablation (RFCA) has been used to treat patients with Brugada syndrome (BS), it is difficult to eliminate polymorphic ventricular tachycardias (VTs) completely.

Objective: The purpose of this study was to determine the efficacy of RFCA in eliminating recurrent VTs in an experimental model of BS.

Methods: We optically mapped electrical activity on the epicardial (n = 9) or transmural (n = 8) surface in 17 arterially perfused canine right ventricle preparations.

Differential effects of cardiac sodium channel mutations on initiation of ventricular arrhythmias in patients with Brugada syndrome.

Background: Premature ventricular contractions (PVCs) do not occur frequently but can induce ventricular fibrillation (VF) in patients with Brugada syndrome. The effect of SCN5A mutation on the onset of ventricular arrhythmias is unknown.

Objective: The purpose of this study was to evaluate PVC morphology and onset of VF in patients with Brugada syndrome.

Fragmented QRS as a marker of conduction abnormality and a predictor of prognosis of Brugada syndrome.

Background: Conduction abnormalities serve as a substrate for ventricular fibrillation (VF) in patients with Brugada syndrome (BS). Signal-averaged electrograms can detect late potentials, but the significance of conduction abnormalities within the QRS complex is still unknown. The latter can present as multiple spikes within the QRS complex (fragmented QRS [f-QRS]).

Acute ischemia of canine interventricular septum produces asymmetric suppression of conduction.

Background: Acute ischemia depresses tissue excitability more rapidly in the epicardium than in the endocardium of the canine left ventricular (LV) free wall. However, the effects of acute ischemia on conduction in the interventricular septum (IVS), which is composed of right ventricular (RV) and LV endocardium and midmyocardium without epicardium, are less known.

Objective: The purpose of this study was to evaluate the hypothesis that the IVS exhibits transseptal differences in local tissue response to acute ischemia.

Repolarization heterogeneity in the right ventricular outflow tract: correlation with ventricular arrhythmias in Brugada patients and in an in vitro canine Brugada model.

Background: Brugada syndrome (BrS) is characterized by repolarization abnormality with ST-segment elevation in the right ventricular outflow tract (RVOT).

Objective: Although action potential (AP) heterogeneity is associated with induction of ventricular arrhythmias (VA) in BrS, clinical evidence and its experimental correlations are still absent and are the focus of this study.

Methods: We evaluated repolarization heterogeneity in 15 patients with BrS using body surface mapping and in 8 pairs of isolated canine RVOT and right ventricular anteroinferior (RVAI) preparations having drug-induced BrS using optical mapping.

Mechanism of U wave and polymorphic ventricular tachycardia in a canine tissue model of Andersen-Tawil syndrome.

Objective: Andersen-Tawil syndrome (ATS) is a channelopathy affecting inward rectifier potassium I(K1) with QT prolongation, large U waves, and frequent ventricular tachycardia (VT). Although ATS is clinically defined and genetically identified, its electrophysiological mechanism is still unclear, and thus, was the subject of the current study.

Methods And Results: We replicated the major electrophysiological features of ATS with cesium chloride (CsCl, at I(K1) blockade concentration of 5-10 mmol/l) in 23 isolated canine left ventricular tissues perfused arterially with Tyrode's solution having normal or low potassium concentrations, [K(+)](o).

Temperature modulation of ventricular arrhythmogenicity in a canine tissue model of Brugada syndrome.

Background: Fever promotes ventricular arrhythmias in Brugada syndrome (BrS). Hypothermia can induce BrS electrocardiogram (ECG) and arrhythmia. However, the mechanisms are unclear.

Analysis of action potentials in the canine ventricular septum: no phenotypic expression of M cells.

Objective: Transmural heterogeneity in the ventricular free wall, enhanced by the midmyocardial long action potential duration (APD) of M cells, plays an important role in the arrhythmogenesis of long QT syndrome. Although we observed dynamic expression of M cell phenotypes in the canine ventricular free wall, it is still unclear whether similar phenomena are present in the interventricular septum. This study evaluated transmural heterogeneity of APD in the septum.

Differences in arrhythmogenicity between the canine right ventricular outflow tract and anteroinferior right ventricle in a model of Brugada syndrome.

Background: The Brugada syndrome is characterized by ST-segment elevation on the ECG, especially in the right precordial leads sensitive to the right ventricular outflow tract (RVOT).

Objectives: The purpose of this study was to evaluate the hypothesis that right ventricular electrophysiologic heterogeneity caused arrhythmogenicity in the Brugada syndrome.

Methods: Action potentials (APs) were mapped on the epicardium of 14 RVOT preparations and on the transmural surfaces of 15 pairs of RVOT and right ventricular anteroinferior (RVAI) preparations isolated from canine hearts.

T wave alternans in an in vitro canine tissue model of Brugada syndrome.

Macroscopic T wave alternans (TWA) associated with increased occurrence of ventricular arrhythmias has been reported in patients with Brugada syndrome. However, the mechanisms in this syndrome are still unclear. We evaluated the hypothesis that TWA in Brugada syndrome was caused by the dynamic instability and heterogeneity of action potentials (APs) in the right ventricle.

Ventricular arrhythmia induced by sodium channel blocker in patients with Brugada syndrome.

Objectives: We administered pilsicainide chloride, a class Ic pure sodium channel blocker, to patients with Brugada syndrome (BS) and evaluated the occurrence of ventricular arrhythmia (VA) and T-wave alternans (TWA).

Background: Ventricular arrhythmia and TWA are sometimes induced by a sodium channel blocker challenge test in BS patients, but the significance of the induced VA and TWA is not known.

Methods: Pilsicainide was administered to 65 patients with BS (10 symptomatic and 55 asymptomatic patients), and the occurrence of VA, TWA, and change of electrocardiogram were evaluated.

Atrial fibrillation and atrial vulnerability in patients with Brugada syndrome.

Objectives: We sought to study atrial vulnerability in patients with Brugada syndrome.

Background: Atrial fibrillation (AF) often occurs in patients with Brugada syndrome, but atrial vulnerability in Brugada syndrome has not been evaluated.

Methods: The patient group consisted of 18 patients with Brugada syndrome.

[Two cases of acute lymphoblastic leukemia with cytoplasmic granules].

The presence of cytoplasmic granules in blastoid cells of patients with acute leukemia is generally accepted as a useful morphological marker for differentiation of myeloid leukemia from lymphoblastic leukemia. We diagnosed two cases of acute lymphoblastic leukemia(ALL) with cytoplasmic granulation. Surface marker analysis of leukemic cells revealed they were positive for CD10, 19, 20, 33, 34 and HLA-DR.