Ayaka Kawase

Widening of the Excitable Gap and Enlargement of the Core of Reentry During Atrial Fibrillation With a Pure Sodium Channel Blocker in Canine Atria

Background—This study aimed to assess the effects of pilsicainide, a pure sodium channel blocker, on electrophysiological action and wavefront dynamics during atrial fibrillation (AF). Methods and Results—In a newly developed model of isolated, perfused, and superfused canine atria (n=12), the right and left endocardia were mapped simultaneously by use of a computerized mapping system. AF was induced with 1 to 5 &mgr;mol/L acetylcholine. The antifibrillatory actions of pilsicainide on AF cycle length (AFCL), refractory period (RP), conduction velocity (CV), excitable gap (EG), and the core of the mother rotor were studied. The RP was defined as the shortest coupling interval that could capture the fibrillating atrium. The EG was estimated as the difference between the AFCL and RP. At baseline, multiple wavefronts were observed. After 2.5 &mgr;g/mL infusion of pilsicainide, all preparations showed irregular activity, and AF was terminated in 2 preparations. The AFCL and RP were prolonged, and CV was decreased significantly. The EG was widened (147%;P <0.01), and the core perimeter was increased (100%;P <0.01). Increasing the dosage either terminated AF (6 preparations) or converted to organized activity (ie, atypical atrial flutter) (4 preparations). On the maps, all “unorganized” AFs were terminated with the excitation of the core of the mother rotor by an outside wavefront, whereas in preparations with atrial flutter, pilsicainide did not terminate its activity. Conclusions—Widening of the EG by pilsicainide facilitates the excitation of the core of the mother rotor, leading to the termination of AF. In some experiments, pilsicainide converts AF to persistent atrial flutter.

Vortex cordis as a mechanism of postshock activation: Arrhythmia induction study Using a bidomain model

Introduction: The ventricular apex has a helical arrangement of myocardial fibers called the “vortex cordis.” Experimental studies have demonstrated that the first postshock activation originates from the ventricular apex, regardless of the electrical shock outcome; however, the related underlying mechanism is unclear. We hypothesized that the vortex cordis contributes to the initiation of postshock activation. To clarify this issue, we numerically studied the transmembrane potential distribution produced by various electrical shocks.

Predicting the recurrence of ventricular tachyarrhythmias from T-wave alternans assessed on antiarrhythmic pharmacotherapy : A prospective study in patients with dilated cardiomyopathy

Background: Microvolt T‐wave alternans (TWA) has been proposed as a useful index to identify patients at risk of ventricular tachyarrhythmias. Recent studies have demonstrated that antiarrhythmic drugs, such as amiodarone and procainamide, decrease the prevalence of TWA. In this study, we tested whether TWA in patients on antiarrhythmic pharmacotherapy significantly predicts the recurrence of ventricular tachyarrhythmias in patients with dilated cardiomyopathy.

Differences in sympathetic and vagal effects on paroxysmal atrial fibrillation: a simulation study.

The incidence of paroxysmal atrial fibrillation (AF) is affected by circadian variations in the vago-sympathetic balance. It is well known that both sympathetic and vagal effects increase the onset of paroxysmal AF, due to the shortened action potential duration. However, the reason why the vagally-mediated paroxysmal AF is maintained more than the adrenergically-mediated paroxysmal AF has remained unclear. In order to clarify this, we performed the following computer simulations. First, we constructed a homogeneous two-dimensional myocardial sheet (4.5 x 2.25 cm), using a bidomain ion channel model. The sympathetic and vagal effects were achieved by modifications of the ion channel conductance (Sympathetic effect: increased gSI and increased gK. Vagal effect: increased gK and increased gK1 with or without the dispersion of refractoriness). We found that the sympathetic effect shortened the action potential duration and flattened the restitution slope; therefore, this effect promoted spiral wave induction and restrained the spiral wave breakup. On the other hand, we found that the vagal effect also shortened the action potential duration and flattened the restitution slope; however, this effect promoted spiral wave breakup, due to the increase in both the IK1 and the dispersion of refractoriness. Overall, the differences between the sympathetic and vagal effects on the tendency toward spiral wave break-up may explain the reason why adrenergically-mediated paroxysmal AF terminates spontaneously and vagally-mediated paroxysmal AF tends to be maintained. In conclusion, our results may be helpful in understanding the difference in the action of sympathetic and vagal effects on paroxysmal AF.