To determine the effects of sensory-perceptual stimulation (videogame playing) on neuropsychological performance, measures of reaction time (RT), visual sensitivity, cognition, and affect were obtained from 60 healthy 60- to 79-year-old individuals before and after their 11-week participation in videogame (VG) playing, movie viewing, or as controls. Only RT demonstrated an activity specific change, being significantly faster at posttesting for the VG subjects. The RT results indicate that the central nervous system of elderly people can be modified by activation procedures. We speculate that VG playing may improve efficiency of cell assemblies stimulated by visuomotor activities common to both VG playing and RT.

The purpose of this study was to demonstrate errors in activation time maps created using the time derivative method on fractionated unipolar electrograms, to characterize the epicardial distribution of those fractionated electrograms, and to investigate spatial methods of activation time determination. Electrograms (EGs) were recorded using uniform grids of electrodes (1 or 2 mm spacing) on the epicardial surface of six normal canine hearts. Activation times were estimated using the time of the minimum time derivative, maximum spatial gradient, and zero Laplacian and compared with the time of arrival of the activation wave front as assessed from a time series of potential maps as the standard. When comparing activation times from the time derivative for the case of epicardial pacing, spatial gradient and Laplacian methods with the standard for EGs without fractionation, correlations were high (R2 = 0.98, 0.98, 0.97, respectively). Similar comparisons using results from only fractionated EGs (R2 = 0.85,0.97,0.95) showed a lower correlation between times from the time derivative method and the standard. The results suggest an advantage of spatial methods over the time derivative method only for the case of epicardial pacing where large numbers of fractionated electrograms are found.

The electrophysiologic efects of amiodarone were examined in 13 dogs that received 30 g amiodarone orally during 3 weeks and compared with 13 control dogs that did not receive amiodarone. Longitudinal and transverse epicardial conduction velocities were estimated with a square array of 64 closely spaced electrodes and a computer-assisted acquisition and analysis system. Amiodarone caused a rate-dependent decrease in conduction velocity with a slightly greater effect in the longitudinal direction of propagation. Rate-related depression of conduction velocity developed rapidly after abrupt shortening of the pacing cycle length; 67% of the change occurred between the first two beats of the rapid train, and little change occurred after the 10th beat. Recovery from use-dependent depression of conduction velocity was exponential with a mean time constant of 447±+172 msec in the longitudinal direction and 452±265 msec in the transverse direction. Repolarization intervals, defined as the interval between the activation time and the repolarization time in the unipolar electrograms, correlated highly with refractory period determinations in the absence and presence of amiodarone at each cycle length tested. The increase in repolarization intervals and refractory periods resulting from amiodarone treatment did not vary with cycle length. Amiodarone treatment also resulted in a significant rate-related reduction in systolic blood pressure. The systolic blood pressure in the group that received amiodarone decreased by a mean of 50±23% between steady-state pacing cycle lengths of 1,000 and 200 msec, whereas the corresponding decrease in the control group was 21±32% (p < 0.05). Plasma and myocardial amiodarone and desethylamiodarone levels were comparable to those observed clinically. We conclude that long-term amiodarone administration causes rate-dependent reductions in conduction velocity and blood pressure and causes rateindependent increases in repolarization intervals. (Circulation 1989;79:948-958) Amiodarone is an effective, widely used antiarrhythmic drug.1 Reduction of conduction velocity may be an important antiarrhythmic effect of amiodarone. Previous investigations showed that amiodarone decreases sodium current,2 reduces the maximum upstroke velocity of the action potential (VmX)3-6 and prolongs QRS duration,7-9 but its effects on myocardial conduction velocity have not been reported.

QTI is not a robust index of local recovery time on the cardiac surface. QTI distributions were affected by the position of the zero potential line, which is unrelated to local recovery times. However, similarities in the patterns of QTI and recovery times in some regions may help explain the frequently reported predictive value of QT dispersion. Preliminary results indicate STT area may be a better index of recovery time and recovery time dispersion on the epicardium than QTI.

Discrepancies between observed and predicted modes of initiation of ventricular tachycardia and between spontaneous and induced rhythms could result in inappropriate guidance and subsequent failure of antiarrhythmic treatment.