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Various mechanisms that cause deviations from the classical manifestations of a parasystolic rhythm are reviewed and illustrated by selected clinical electrocardiograms. They consist of: (1) Transient or continued fixed coupling of the ectopic beats, due to (a) synchronization of basic and parasystolic rhythms; (b) reversed coupling of the basic to the ectopic rhythm (unidirectional protection); (c) the operation of supernormal phase of excitability; and (d) intermittent parasystole, due to gap in the protection of the parasystolic center. (2) Irregularities in response to a regular parasystolic discharge may be caused by a second degree exit block, usually of Mobitz type II, rarely of type I. An electrophysiologic basis for the emergence and maintenance of parasystolic rhythms appears to be abnormal states of spontaneous diastolic (phase 4) depolarization in otherwise latent subsidiary cardiac pacemakers.

Eleven patients with tachycardia-dependent, bradycardia-dependent, or "pseudobradycardia-dependent" bundle branch block (BBB) alternans were studied. This classification is based on the following criteria: 1) When alternans is initiated by a sudden acceleration in ventricular rate, or it appears with aberration of the second beat after a pause, the alternans is tachycardia-dependent and results from a 2:1 bidirectional block in the affected bundle branch. 2) When alternans begins with the aberrant complex terminating a pause it is bradycardia-dependent; such an alternans results from alternating bundle branch cycle lengths and refractoriness, possibly produced by alternating transseptal retrograde penetration of the affected bundle branch. 3) In cases referred to as "pseudobradycardia-dependent BBB" alternans, a change from alternans to persiscardia-dependent BBB" alternans, a change from alternans to persistent BBB occurs as the cycle lengthens; however, the disappearance of BBB with further increase of the cycle length proves the tachycardia-dependence of the conduction defect.

A computer model of "modulated sinus parasystole" was devised in which two sinus pacemakers interacted electrotonically, entraining each other's periodicity according to their beat-to-beat phasic relationships. Depending on the preestablished rules, the model gave rise to various rhythm patterns that were similar to those recorded in patients with sinoatrial arrhythmias. The validity of the model in predicting clinically observed rhythm disturbances was tested in a case of sinoatrial extrasystolic activity. The sinoatrial origin of parasystolic discharges giving rise to various patterns of group beating in this case was diagnosed according to the following electrocardiographic criteria: premature P waves having contour identical to P waves of basic beats, variable coupling intervals, and absence of compensatory pauses (i.e., returning cycles having duration similar to that of the basic P-P interval). For the analysis, it was assumed that two distinct but closely apposed sinoatrial pacemaker centers were competing for activation of the heart. The model accurately simulated the arrhythmias in the electrocardiographic trace. The best fit was found when the two pacemakers interacted on the basis of "resetting" in one direction and electronic modulation in the other. In fact, under appropriate conditions, the model matched precisely all frequency-dependent patterns of extrasystolic activity observed in the trace. We conclude that the modulated parasystole hypothesis can readily explain the mechanism of sinus extrasystolic discharges whose returning cycle equals the basic P-P interval. Moreover, the model predicts that, when the rules for mutual entrainment between "dominant" and parasystolic sinus pacemaker are appropriate, the returning cycle can be shorter than the basic cycle.

Temporary coupled atrial stimulation slowed the ventricular rate by nearly 50% in an adolescent patient with intractable congestive heart failure and focal repetitive atrial tachycardia that was resistant to drug treatment. Because of the success with the temporary pacemaker, a specially designed permanent pacemaker was implanted to provide coupled atrial stimulation. The necessary electrophysiologic conditions for ventricular slowing by coupled atrial pacing are: (1) an atrial effective refractory period shorter than that of the atrioventricular junction, and (2) depolarization of the ectopic atrial pacemaker by the responses to coupled atrial stimulation. During a 4 year follow-up period the treatment resulted in elimination of the tachycardia, followed by return of the heart size to normal and complete clinical recovery. Coupled atrial stimulation can provide effective treatment in selected patients with disabling drug-resistant atrial tachycardia in whom this mode of therapy is shown to be effective by careful electrophysiologic studies.

Concealed intraventricular conduction is defined and the following classification of the manifestations of concealed conduction into the bundle branch system is proposed. 1. Trans-septal retrograde concealed intraventricular conduction responsible for (a) perpetuation of functional bundle branch block initiated by a premature supraventriculra impluse; (b) alternation of aberrant ventricular conduction in supraventricular bigeminy; (c) normalization of intraventricular conduction with acceleration or rate in bradycardia-dependent bundle branch block, and (d) prevention of the manifestation of Wenchbach periods of conduction in a bundle branch or fascicle. 2. Antegrade concealed intraventricular conduction responsible for (a) prevention of expected aberrant ventricular conduction when a short cycle follows a long one, and (b) exceptions to the "rule of bigeminy". 3. Retrograde concealed intraventricular conduction of a ventricular escape in association with unidirectional bundle branch or fasciular block responsible for (a) resumption of AV conduction in "paroxysmal AV block" with bundle branch block, and (b) facilitation (due to supernormality) of conduction in type II AV block due to bilateral bundle branch block. 4. Concealed intraventricular conduction of a premature ventricular impulse responsible for (a) initiation or termination of a re-entrant ventricular tachycardia; (b) resetting of an idioventricular pacemaker, and (c) pseudo-intraventricular or pseudo-AV block.

Electrophysiological and histological observations were made on the heart of the African lungfish. Impulse origin and propagation were studied using simultaneously recorded epicardial and pericardial electrograms. The primary pacemaker site in the lungfish was found to be at the sinus venosus at its junction with the left cardinal vein. Under a variety of circumstances, pacemaker function shifted to other sites. In response to stress, probably under vagal influence, the regular and rapid sinus venosus rate was generally superseded by an irregular and slower atrial pacemaker. Heart rate and sinoatrial and atrioventricular conduction times varied with changes in temperature [Q10=3.77, 2.55, and 5.46, respectively]. Although alterations in impulse formation and conduction did occur, the site of impulse formation and the patterns of conduction between heart chambers were usually fixed, implying the existence of an organized conduction system. Nonetheless, extensive histological study failed to disclose either organized nodal structures or specialized conduction pathways.