The purpose of this study was to evaluate the electrical remodeling of the ventricular myocardium in the experimental autoimmune myocarditis (EAM) model in Lewis rats. EAM was induced by immunization with cardiac myosin. During the active myocarditis phase, the effective refractory period (ERP), the duration of the monophasic action potential (MAPD) was extracted from the left ventricular free wall, and the mRNA levels of Kv1.4, 4.2, 4.3 and L type Ca2+ channel were determined by RNase protection assays. The inducibility of ventricular arrhythmia was higher in EAM rats than in the control rat, and the direct relationship between the coupling intervals of the premature stimulus and the ventricular arrhythmia in EAM rats. The ERP was prolonged in EAM rats compared with the control group. The MAPDs determined as 20% and 90% repolarization time, were both longer in EAM rats than in the controls. The level of expression of Kv4.2 mRNA was reduced in EAM rats in comparison with the controls, whereas those of Kv1.4, 4.3 and the L type Ca2+ channel were unchanged. Ventricular vulnerability was higher in EAM rats than in the control rats, and some of the ventricular arrhythmias observed in the EAM group seemed to be based on triggered activity. The level of expression of Kv4.2 mRNA was significantly reduced, and this change was compatible with prolongation of the action potential duration. (Circ J 2002; 66: 97 - 103)

Post-repolarization refractoriness (PRR) is an important factor in determining conduction block and is the difference between the effective refractory period (ERP) and the duration of the monophasic action potential (MAPD). In the present study, conduction block in an artificial isthmus in the canine atrium was evaluated and the coupling interval of a premature beat, which caused the block, was defined as the block coupling interval (BCI). The usefulness of this value was also evaluated. Radiofrequency linear ablation was performed on the right atrial surface parallel to the atrioventricular groove in 5 mongrel dogs, and an artificial isthmus (8-10mm wide and 25-30mm long) was created. Fourteen simultaneous unipolar recordings were performed in the isthmus with a resolution of 1.2mm. Single extra-stimuli with basic drive train were delivered to induce conduction block in the isthmus and when it occurred, the coupling interval at the recording site just proximal to the site of the block was defined as the BCI. At the site of the block, the ERP and MAPD at each drive cycle length were measured. The PRR was calculated using 2 different formulae: (1) [ERP-MAPD], and (2) [BCI-MAPD]. It was found that each value was shortened in accordance with the shortening of the basic drive cycle length. In all basic drive trains, BCI>ERP>MAPD, and [ERP-MAPD] was always shorter than [BCI-MAPD]. In the shorter cycle length of basic drives, the difference between [ERP-MAPD] and [BCI-MAPD] was more prominent. In the artificial isthmus model in the canine atrium, BCI was always longer than the ERP measured at the same site as the block. Because the ERP may not directly reflect the block phenomenon, the electrophysiologic evaluation should use the BCI instead, as in the PRR evaluation.