Modeling Ventricular Parasystole a

Ventricular parasystole is a cardiac arrhythmia arising from competition between the normal sinus rhythm and an abnormal ectopic pacemaker located in the ventricles. Although this arrhythmia was identified as early as 1912 based on pulse pressure recordings,' cardiologists now identify parasystole from electrocardiographic (ECG) records. Since in classic (pure) parasystole it is assumed that the normal sinus pacemaker and the ectopic pacemaker fire independently of each other, the following features are predicted to be observed on the ECG:* (1) interectopic intervals are multiples of a common divisor; (2) there are varying coupling intervals between normal sinus beats and ectopic beats; and (3) fusion beats, differing in morphology from sinus and ectopic beats, arise from simultaneous activation of the ventricles by activity from both pacemakers. This definition for pure (ventricular) parasystole is limited and does not take into account the amazing variety of abnormal rhythms that can be found as a result of interactions between the sinus and ectopic pacemaker^.^,^ An important step in understanding the dynamics possible from the interactions between cardiac pacemakers was taken in 1976 by Jalife and Moe.' They analyzed the effects of the electrotonic spread of excitation across an inexcitable sucrose gap on the rhythm of a spontaneous pacemaker in Purkinje fiber. The effects of depolarizations on the pacemaker were characterized by a phase response curve (PRC), giving the dependence of the cycle length of the pacemaker as a function of the phase in the pacemaker cycle a t which the stimulus was delivered. Jalife, Moe, and c o l l e a g ~ e s ~ . ~ assumed normal sinus beats might act in a similar fashion to reset the period of a ventricular ectopic pacemaker, and that the resulting rhythms should be called modulated parasystole. A mathematical model of modulated parasystole4 showed several features, such as fixed coupling from the sinus to ectopic beats, that were previously thought to be inconsistent with a parasystolic mechanism. Subsequent investigators have constructed PRCs from clinical data.'-'' In a few cases, the PRCs