03253nas a2200301 4500008004100000022001400041245009200055210006900147260001200216300001200228490000700240520238200247653001702629653001202646653003102658653002402689653001702713653002402730653002702754653001002781653002902791100001902820700001702839700001702856700001702873700001402890856004702904 1995 eng d a0009-733000aEffects of pacing on stationary reentrant activity. Theoretical and experimental study.0 aEffects of pacing on stationary reentrant activity Theoretical a c12/1995 a1166-790 v773 a

It is well known that electrical pacing may either terminate or change the rate and/or ECG appearance of reentrant ventricular tachycardia. However, the dynamics of interaction of reentrant waves with waves initiated by external pacing are poorly understood. Prevailing concepts are based on simplistic models in which propagation occurs in one-dimensional rings of cardiac tissue. Since reentrant activation in the ventricles occurs in two or three dimensions, such concepts might be insufficient to explain the mechanisms of pacing-induced effects. We used numerical and biological models of cardiac excitation to explore the phenomena, which may take place as a result of electrical pacing during functionally determined reentry. Computer simulations of a two-dimensional array of electrically coupled FitzHugh-Nagumo cells were used to predict the response patterns expected from thin slices of sheep ventricular epicardial muscle, in which self-sustaining reentrant activity in the form of spiral waves was consistently initiated by premature stimulation and monitored by means of video mapping techniques. The results show that depending on their timing and shape, externally induced waves may collide with the self-sustaining spiral and result in one of three possible outcomes: (1) direct annihilation of the spiral, (2) multiplication of the spiral, or (3) shift of the spiral center (ie, core). Multiplication and shift of the spiral core were attended by changes in rate and morphology of the arrhythmia as seen by "pseudo-ECGs." Furthermore, delayed termination (ie, termination of the activity one to three cycles after the stimulus) occurred after both multiplication and shift of the spiral center. Both numerical predictions and experimental results support the hypothesis that whether a pacing stimulus will terminate a reentrant arrhythmia or modify its ECG appearance depends on whether the interactions between the externally induced wave and the spiral wave result in the de novo formation of one or more "wavebreaks." The final outcome depends on the stimulus parameters (ie, position and size of the electrodes and timing of the stimulus) as well as on the position of the newly formed wavebreak(s) in relation to that of the original wave.

10aAcceleration10aAnimals10aCardiac Pacing, Artificial10aComputer Simulation10aDeceleration10aElectrocardiography10aModels, Cardiovascular10aSheep10aTachycardia, Ventricular1 aDavidenko, J M1 aSalomonsz, R1 aPertsov, A V1 aBaxter, Bill1 aJalife, J uhttp://www.ncbi.nlm.nih.gov/pubmed/758623004137nas a2200313 4500008004100000022001400041245013200055210006900187260001300256300001200269490000700281520321100288653001203499653002403511653001003535653004003545653002703585653001403612653001203626653002903638100001403667700001403681700001603695700001703711700001203728700001903740700001703759856004703776 1995 eng d a0009-732200aNonstationary vortexlike reentrant activity as a mechanism of polymorphic ventricular tachycardia in the isolated rabbit heart.0 aNonstationary vortexlike reentrant activity as a mechanism of po c05/1995  a2454-690 v913 a

BACKGROUND: 

Ventricular tachycardia may result from vortexlike reentrant excitation of the myocardium. Our general hypothesis is that in the structurally normal heart, these arrhythmias are the result of one or two nonstationary three-dimensional electrical scroll waves activating the heart muscle at very high frequencies.

METHODS AND RESULTS: 

We used a combination of high-resolution video imaging, electrocardiography, and image processing in the isolated rabbit heart, together with mathematical modeling. We characterized the dynamics of changes in transmembrane potential patterns on the epicardial surface of the ventricles using optical mapping. Image processing techniques were used to identify the surface manifestation of the reentrant organizing centers, and the location of these centers was used to determine the movement of the reentrant pathway. We also used numerical simulations incorporating Fitzhugh-Nagumo kinetics and realistic heart geometry to study how stationary and nonstationary scroll waves are manifest on the epicardial surface and in the simulated ECG. We present epicardial surface manifestations (reentrant spiral waves) and ECG patterns of nonstationary reentrant activity that are consistent with those generated by scroll waves established at the right and left ventricles. We identified the organizing centers of the reentrant circuits on the epicardial surface during polymorphic tachycardia, and these centers moved during the episodes. In addition, the arrhythmias that showed the greatest movement of the reentrant centers displayed the largest changes in QRS morphology. The numerical simulations showed that stationary scroll waves give rise to monomorphic ECG signals, but nonstationary meandering scroll waves give rise to undulating ECGs characteristic of torsade de pointes.

CONCLUSIONS: 

Polymorphic ventricular tachycardia in the healthy, isolated rabbit heart is the result of either a single or paired ("figure-of-eight") nonstationary scroll waves. The extent of the scroll wave movement corresponds to the degree of polymorphism in the ECG. These results are consistent with our numerical simulations that showed monomorphic ECG patterns of activity for stationary scroll waves but polymorphic patterns for scroll waves that were nonstationary.

10aAnimals10aElectrocardiography10aHeart10aImage Processing, Computer-Assisted10aModels, Cardiovascular10aPerfusion10aRabbits10aTachycardia, Ventricular1 aGray, R A1 aJalife, J1 aPanfilov, A1 aBaxter, Bill1 aCabo, C1 aDavidenko, J M1 aPertsov, A V uhttp://www.ncbi.nlm.nih.gov/pubmed/7729033