Immunization with cardiac myosin in rats induced experimental autoimmune myocarditis, which significantly increased the incidence of ventricular arrhythmias to 46.1% compared to 13.1% in controls.
In a rat model of experimental autoimmune myocarditis, increased ventricular vulnerability and prolonged action potentials are associated with reduced expression of the Kv4.2 potassium channel.
Absolute Event Rate: 46.1% vs 13.1%
p-value: p=<0.0001
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.
Saito et al. (Tue,) conducted a other in Experimental autoimmune myocarditis (n=15). Immunization with purified cardiac myosin vs. Saline injection was evaluated on Incidence of ventricular arrhythmias induced by ventricular extrastimuli (p=<0.0001). Immunization with cardiac myosin in rats induced experimental autoimmune myocarditis, which significantly increased the incidence of ventricular arrhythmias to 46.1% compared to 13.1% in controls.