Modulated parasystole originating in the sinoatrial node.

Abstract

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-tobeat 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: (1) premature P waves having contour identical to P waves of basic beats, (2) variable coupling intervals, and (3) 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 electrotonic 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 retuming cycle can be shorter than the basic cycle. Circulation 74, No. 5, 945-954, 1986. In 1908, Wenckebach' first suggested that extrasystoles could arise from the sinoatrial region. In the electrocardiogram, such extrasystoles are characterized by premature P waves whose contour is identical to that of P waves associated with normal pacemaker activity, and by the absence of compensatory pauses. After the initial description, only a handful of clinical examples had been published,1 7 until 1967 when Schamroth' published the first case attributed to sinus parasystole. In that case, the ectopic atrial beats differed in contour from the sinus beats, and probably originated outside of the sinoatrial region. Yet the dominant sinoatrial pacemaker showed complete entrance block and, for that reason, the arrhythmia was termed "sinus parasystole."5 The case analyzed here is the first clinical ex-

Anatomy of the sinus node, av node, and his bundle of the heart of the sperm whale (Physeter macrocephalus), with a note on the absence of an os cordis

“…An alternative explanation that appeals to us is the concept of the sinus node and AV node functioning as coupled relaxation oscillators, originally suggested many years ago by Van der Pol (1926) and Van der Pol andVan der Mark (1927, 1928). This concept has been a subject of subsequent study by several others (Antzelevitch et al, 1982;Guevara and Glass, 1982;Jalife et al, 1986;Kirchhof et al, 1988;Sanchis et al, 1990) and of our own previous research in various contexts (Nadeau and James, 1966;Roberge et al, 1968;Urthaler et al, 1973;Katholi et al, 1977;James, 1983James, ,1990Meijler et al, 1984Meijler et al, ,1992Van der Tweel et al, 1986;Meijler and Janse, 1988;Wittkampf et al, 1988;Meijler and Fisch, 1989). For coupling of relaxation oscillators, a powerful sinus node could be a substantial advantage, particularly in large hearts.…”

Heart Rate Fragmentation: A New Approach to the Analysis of Cardiac Interbeat Interval Dynamics

“…For example, alternans phenotypes could be due to sinus node exit block or to very subtle atrial bigeminy with SVPBs originating near or even within the sino-atrial (SA) node (Geiger and Goerner, 1945). Another mechanism that could account for fragmentation would be modulated sinus node parasystole (Jalife et al, 1986), an arrhythmia in which two pacemaker sites in the SA area show bidirectional coupling and appear to “compete” for control of the heartbeat. Under certain parameter regimes, such coupling may induce a variety of alternating NN patterns (Jalife et al, 1986).…”

“…Another mechanism that could account for fragmentation would be modulated sinus node parasystole (Jalife et al, 1986), an arrhythmia in which two pacemaker sites in the SA area show bidirectional coupling and appear to “compete” for control of the heartbeat. Under certain parameter regimes, such coupling may induce a variety of alternating NN patterns (Jalife et al, 1986). The underlying electrophysiologic mechanisms to account for fragmentation may also involve perturbations of internal pacemaker “clocks” in the SA node (Lakatta et al, 2010).…”

Impact of Heart Rate Fragmentation on the Assessment of Heart Rate Variability

“…Thus, the counterintuitive increase in HF in the elderly seems to be the result but not the cause of increased HRF. Several mechanisms can be considered for the genesis of HRF [5], which include sinus node exit block, subtle atrial bigeminy originating near or within the sinoatrial (SA) node, modulated SA node parasystole caused by multiple interacting pacemaker sites in the SA node [16], and modulated periodicity of pacemaker clock in the SA node [17,18]. Thus, increased HRF may be a marker reflecting the age-related degeneration or pathologic impairment of the SA-node-atrial network for cardiac pacemaker function.…”