ABSTRACT
We encountered a 44-year-old woman with acute eosinophilic myocarditis that showed positive immunostaining for interleukin-4 in the area of marked infiltration of eosinophils into the myocardium. When prednisolone alone proved ineffective, supplementary treatment with suplatast tosilate, an antiallergic selective Th2 cytokine inhibitor, improved the patient's inflammation, reduced the level of cardiac enzymes, and allowed for a reduction in corticosteroid dosage without any adverse effects.
Subject(s)
Anti-Allergic Agents/pharmacology , Arylsulfonates/pharmacology , Eosinophils/drug effects , Interleukin-4/antagonists & inhibitors , Myocarditis/drug therapy , Sulfonium Compounds/pharmacology , Th2 Cells/immunology , Acute Disease , Adult , Anti-Allergic Agents/administration & dosage , Anti-Inflammatory Agents/administration & dosage , Arylsulfonates/administration & dosage , Drug Administration Schedule , Drug Therapy, Combination , Female , Humans , Myocarditis/blood , Myocarditis/immunology , Myocarditis/pathology , Prednisolone/administration & dosage , Sulfonium Compounds/administration & dosage , Th2 Cells/drug effects , Time FactorsABSTRACT
The aims of this study were to evaluate the changes in the electrophysiological characteristics of the right atrium after the administration of flecainide and to clarify whether flecainide has a selective effect on human atrial tissue. Electrophysiological measurements were made in 38 patients, before and after intravenous administration of flecainide (2 mg/kg per 10 min). The effective refractory period of the right atrium (ERP-A), maximum conduction delay (Max.CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were studied in the patients who were divided into 2 groups based on whether repetitive atrial firing (RAF) was induced in the baseline study. Flecainide significantly prolonged the ERP-A (202+/-22 to 238+/-33 ms, p<0.001) and shortened Max.CD (77+/-17 to 63+/-32 ms, p<0.05) in the patients with RAF, but not in those without RAF in the baseline study. After flecainide administration, there were significant reductions in the RAFZ (43+/-22 to 13+/-19 ms, p<0.0001), FAAZ (51+/-22 to 28+/-26 ms, p<0.001) and CDZ (70+/-21 to 48+/-30 ms, p<0.01) in the patients with RAF. However, atrial fibrillation (AF) was induced by stimulation after flecainide in 2 patients without RAF in the baseline study. There was a significant negative correlation between the ERP-A in the baseline study and the change in the ERP-A upon flecainide administration (r=0.45, p<0.01). Flecainide may preferentially activate the substrate for AF and RAF, but that action is mainly based on the electrophysiological characteristics found in the baseline study.
Subject(s)
Anti-Arrhythmia Agents/pharmacology , Flecainide/pharmacology , Heart Atria/physiopathology , Atrial Fibrillation/drug therapy , Atrial Fibrillation/physiopathology , Electrocardiography , Electrophysiology/methods , Female , Heart Atria/drug effects , Heart Conduction System/drug effects , Humans , Male , Middle Aged , Regression AnalysisABSTRACT
Bepridil is effective for intractable cardiac arrhythmia, but in rare cases will induce torsades de pointes (TdP) associated with QT interval prolongation. Beta-blockers will effectively prevent TdP in some clinical settings, so the effect of beta-blocker on the change in QT interval, QT dispersion and transmural dispersion of repolarization (TDR) induced by bepridil was investigated in 10 patients (7 male, 3 female; 62+/-6 years old) with intractable paroxysmal atrial fibrillation. The QTc interval, QTc dispersion and TDR were measured before and after 1 month of administration of bepridil, and then a beta-blocker was added and the QTc interval, QTc dispersion and TDR re-measured 1 month later. Bepridil significantly prolonged the QTc interval (0.42+/-0.05 to 0.50+/-0.08; p<0.01), and increased both the QT dispersion (0.07+/-0.05 to 0.14+/-0.08; p<0.01) and TDR (0.10+/-0.04 to 0.16+/-0.05; p<0.01). The addition of a beta-blocker decreased the QTc interval (0.50+/-0.08 to 0.47+/-0.04; p=0.09) and significantly decreased both the QTc dispersion (0.14 +/-0.08 to 0.06+/-0.02; p<0.01) and TDR (0.16+/-0.05 to 0.11+/-0.04; p<0.001). Compared with the control, the combination therapy significantly prolonged the QTc interval, but did not increase either QTc dispersion or TDR, and so was effective in all patients with intractable AF. The findings suggest that beta-blocker reduces the increase in QT dispersion and TDR induced by bepridil, and combined therapy with bepridil and beta-blocker might thus be useful for intractable atrial fibrillation.
