Parasystolic Rhythm Research Articles

The clinical and electrocardiographic characteristics of parasystolic idioventricular rhythm

The clinical and electrocardiographic characteristics of parasystolic idioventricular rhythm

Ventricular parasystolic couplets originating in the pathway between the ventricle and the parasystolic pacemaker: Mechanism of “irregular” parasystole

This article explains the mechanism of “irregular” parasystole. Two theories have been suggested: “electrotonic modulation” and “type I second degree entrance block.” This study attempts to clarify the mechanism of irregular parasystole in cases of true ventricular parasystole associated with ventricular parasystolic couplets. Cases associated with ventricular parasystolic couplets were selected from 37 clinical cases of true ventricular parasystole in which one or more pure parasystolic cycles with no intervening nonectopic QRS complexes were found. Of the 37 cases of true ventricular parasystole, ventricular parasystolic couplets were found in 4 cases. In none of the other 33 cases, ventricular parasystolic couplets were found. In all the cases coexisting with ventricular parasystolic couplets, the latter ectopic QRS complex of the couplet failed to reset the parasystolic rhythm. The above findings suggest that the latter ectopic QRS complex of the parasystolic couplet originated not in the parasystolic pacemaker but in the pathway between the ventricle and the parasystolic pacemaker. It seems that when a sinus impulse fell late in the parasystolic cycle, it passed through the site of second degree entrance block and that the parasystolic couplets originated from the reentrant pathway between the ventricle and the pacemaker. This strengthens our previous suggestion that the mechanism of irregular parasystole is governed by “type I second degree entrance block” and not by “electrotonic modulation.”

Modelling a parasystolic rhythm in a heart-transplant patient.

A parasystole from a heart-transplant patient is analysed using a beat-to-beat RR interval time series obtained from an electrocardiogram (ECG). The dysrhythmia, resulting from the co-existence of two pacemakers, the sinus node and an ectopic focus, presents distinctive regular patterns, with transitions from one pattern to another occurring abruptly. It is shown that the parasystolic rhythm can be simulated by a model involving two oscillators firing at fixed rates, under the restriction that neither is allowed to fire during the other's refractory period. It is found that the structure of the generated RR time series is essentially determined by the ratio of the periods of the two oscillators. In the case of a heart-transplant patient with a small heart-rate variability as a result of heart denervation, the model predicts the RR intervals with an error of less than 6% for an 80-beat sequence. From a physiological point of view, the results imply that the interaction between the two pacemakers in the heart is fairly weak, and hence the parasystole observed in the heart-transplant patient can be modelled as pure parasystole.

Effect of standing on ventricular parasystole: shortening of the parasystolic cycle length.

OBJECTIVE: To investigate the effect of standing on the parasystolic cycle length in cases of "true" ventricular parasystole. METHODS: Parasystolic cycle length and sinus cycle length were measured during lying...

Reduction of cerebral blood flow with induced tachycardia in rats and in patients with coronary artery disease and premature ventricular contractions.

A reduction of cerebral blood flow (CBF) was observed in experimental studies in rats immediately after the onset of parasystolic rhythm or with stable, but haemodynamically compromising, tachycardias. Based on these data and with a view to studying the effects of premature ventricular contractions (PVCs) on the cerebral circulation in humans, CBF was measured using the 133-Xenon inhalation method in 24 age matched human controls (group A1: age 58.5 +/- 6.2 years; group A2: 52.2 +/- 7.8 years) in nine coronary artery disease (CAD) patients without PVCs (B), in 11 CAD patients with frequent PVCs (> 300.h-1) (C) and in nine patients, after exclusion of CAD by angiography, also with frequent PVCs (> 300.h-1) (D). Holter monitoring was performed during the CBF measurement. CBF determined in the human control groups A1 and A2 was 79.9 +/- 9.9 ml.100 g.-1 min-1 and 81.5-13.0 ml. 100 g-1 min-1, respectively. CBF was 74.1 +/- 13.6 ml . 100 g.-1 min-1 (P = 0.267 vs A1) in group B, 65.8 +/- 11.8 ml.100 g-1 min-1 (P = 0.004 vs A1) in group C and 74.2 +/- 15.6 ml.100 g.-1 min-1 (P = 0.218 vs A2) in group D. The significant reduction of CBF in CAD patients with frequent PVCs suggests that arrhythmias have a significant impact on CBF. Non-CAD patients with frequent PVCs did not show significant CBF decreases in comparison with controls. One can hypothetize that an impairment of electrical postextrasystolic potentiation, due to premature ventricular depolarization, and hence myocardial dysfunction leads to CBF reduction in CAD patients. The CBF reduction with CAD could also reflect concomitant coronary and cerebral arteriosclerosis.

Triple ventricular parasystole

This presentation reflects the analysis of an electrocardiographic recording obtained from a patient with hypertensive heart disease. In the initial section of the tracing, fixed coupled monomorphic ectopic ventricular beats occurred in regular trigeminal rhythm. The pattern changed following an atrial extrasystole and several ventricular ectopic beats of various configuration occurred, often in sequence. Analysis demonstrated the presence of three independent parasystolic rhythms, two of which manifested with the character of intermittency, namely they were occasionally reset by extraneous impulses. The interplay of the sinus pacemaker with three parasystolic foci resulted in a very complex arrhythmic pattern. In some periods, however, two out of three ectopic rhythms were inapparent, and the third one manifested with fixed coupled complexes, so that a regular extrasystolic trigeminy ensued, and parasystole was not recognizable.

Failure of parasystolic impulses to appear on schedule: Exit block due to concealed conduction of sinus impulses

A 45-year-old patient free of any heart disease was admitted to the hospital with an electrocardiographic pattern of ventricular parasystole. The parasystolic rhythm was relatively fast, such that several consecutive ectopic complexes manifested. A later tracing reflected only isolated parasystolic complexes with long and fixed coupling intervals. The interectopic intervals, however, were once more in multiples of the parasystolic cycle as directly measured during the phases of undisturbed parasystolic rhythm. In the latter tracing, several scheduled parasystolic impulses did not yield a response, despite calculation suggesting that these impulses occurred outside the refractory period. In other words, an exit block was present. Analysis of the tracing suggests that the exit block was caused by concealed penetration of the sinus impulses into the ectopic-ventricular junction. That is, any sinus impulse penetrates into the junction and renders it refractory, in such a way that only parasystolic impulses that are relatively late within the sinus cycle may be conducted to the surrounding myocardium and result in a parasystolic complex.

Electrophysiologic mechanisms of ventricular arrhythmias

In this work the electrophysiologic mechanisms of ventricular arrhythmias have been briefly summarized. Ventricular arrhythmias can be caused either by pacemaker activity or by reentrant excitation. Enhancement of normal automaticity can generate a parasystolic rhythm in normal fibers. Abnormal automaticity may arise from fibers in which maximum diastolic potential has been reduced by a variety of interventions. Triggered activity is caused by either an early (EAD) or delayed (DAD) afterdepolarization and requires a prior normal action potential for initiation. While there is growing evidence that EAD-induced triggered activity plays a significant role in the Long QTU syndrome and Torsade de Pointes, no clinical arrhythmias has definitely been ascribed to DADs, although DADs have been recorded in man after acute digoxin intoxication. Ventricular arrhythmias can be also caused by reentrant excitation, which can be subdivided into reflection or circus movement reentry (CMR). In the reflection model impulses in both directions are transmitted over the same pathway. In the CMR three models can be differentiated: the ring model, which requires a fixed anatomical obstacle; the figure-eight model and the leading circle model, where functional rather than fixed anatomical obstacles are involved.

Modulated Parasystole Complicating Permanent Ventricular Pacing: The Different Influence of Spontaneous and Paced Impulses Upon the Parasystolic Rhythm

A case of modulated ventricular parasystole observed in a patient with a VVIM pacemaker is reported. Analysis reveals that the electronic influence (modulation) effected upon the parasystolic focus by the sinus impulses is different from that exerted by the paced impulses. Furthermore, fusion beats reflect an intermediate modulating effect according to the prevalence of the sinus or the paced wavefront.

Influence of sinus impulses on the parasystolic cycle length

Recently, it has been shown that in most clinical cases of parasystole, the parasystolic rhythm is not completely independent of the sinus rhythm. In this study, to disclose the mechanism of such “irregular” parasystole, parasystolic cycles with an intervening sinus QRS complex (XSX) were compared with their immediately adjacent pure parasystolic cycles without any intervening nonparasystolic QRS complexes (XX) in 10 cases of ventricular parasystole. In eight cases, the XSX interval was equal to or nearly equal to the adjacent pure XX interval; in one, the XSX interval was shorter than the XX interval; and in only one, the XSX interval was longer than the XX interval. In six cases in which the XSX interval was almost equal to the XX interval, calculated XSX intervals with a later intervening sinus QRS complex were obtained from the differences between the XSSX interval (ie, interectopic interval with two intervening sinus QRS complexes) and its adjacent XX interval. In five of the six cases, the calculated XSX interval was shorter than the XX interval. These observations suggest that in most cases of parasystole, early intervening sinus impulses do not change the parasystolic cycle, whereas late intervening sinus impulses shorten the parasystolic cycle. This suggests the presence of type I second-degree entrance block as the mechanism of “irregular” parasystole.

Concealed ventricular hexageminy

The authors report a case of concealed ventricular hexageminy in which, with a few exceptions, extrasystoles were separated by sinus beats conforming to the formula 6n - 1. Whenever an exception to this formula occurs, the intervening beats are not all of sinus origin, but include also a ventricular extrasystole that is different from those occurring in hexageminal distribution. The pattern is explained by a parasystolic rhythm modulated by sinus impulses, assuming a 3:1 ratio between the parasystolic cycle and the sinus cycle. Such a ratio would have to be associated with a trigeminal or concealed trigeminal distribution. There is, however, a 2:1 ectopic-ventricular block, leading to a change of the ectopic distributional pattern from theexpected concealed trigeminy to that of the concealed hesageminy.

Ventricular Tachycardia with Alternating Cycle Lengths: Self‐Entrainment of Parasystolic Rhythm?

A patient had ventricular tachycardia with cycle lengths consistently varying between 400 and 490 ms. Arrhythmias with a similar electrocardiographic pattern had been thought to result from the regular activity of an automatic pacemaker with either 3:2 exit block of the Wenckebach type or alternation in exit conduction times. However, the findings in our patient could also be explained by postulating the existence of modulated ventricular parasystole having 3:2 exit block or with alternating (short-long) exit conduction times. In either case, the action potentials elicited by the parasystole must have reached (with variable delays) the ventricular tissue beyond the zone of protection to produce electrotonic depolarizations which, in turn, were reflected back to the ectopic focus itself. This resulted in runs of 2:3 or 2:2 "self-entrainment" of the parasystolic pacemaker. Similar phenomena have been produced in biologic and mathematical models of modulated parasystole.

Parasystolic Accelerated Idioventricular Rhythms Producing Bidirectional Tachycardia Patterns

Two patients with digitalis toxicity had markedly irregular accelerated idioventricular rhythms that were parasystolic in nature. The relatively abrupt appearance of extrasystoles with different morphologies resulted in patterns of the so‐called rapid and “slow” bidirectional ventricular tachycardias.The parasystolic rhythms seemed to have been classic rather than modulated since nonparasystolic beats occurring in different moments of the cycle failed to affect the latter in the expected, predictable manner. It is possible for the existence of marked, spontaneous variations of the degree of automatic activity to interfere with the diagnosis of parasystolic modulation.

Modulation of Atrioventricular Junctional Parasystole During Atrial Pacing

In this report we describe a case of a 68-year-old man with atrioventricular junctional parasystole in whom atrial pacing caused marked changes in the arrhythmic pattern. During atrial pacing at a cycle length of 960 ms, the duration of the ectopic cycle length was influenced by the interval between the parasystolic and nonparasystolic beat. A shorter interval from nonparasystolic to ectopic beat prolonged the ectopic cycle length and a longer one shortened it. Pacing at a cycle length of 900 ms completely suppressed the parasystole. Both of these changes are most likely due to modulation and entrainment of the parasystolic rhythm. During spontaneous variation of the sinus cycle length over 24 hours of ambulatory ECG recording, modulation could not be confirmed; however, there was parallel variation of the ectopic and sinus cycle lengths which suggests that both pacemakers were under the influence of the autonomic nervous system.

Modulated ventricular parasystole manifesting as apparent Wenckebach exit block

Since Jalife and Moe 1 reported the experimental modulation of a parasystolic focus, it has become evident that a parasystolic rhythm may manifest with features different from those classically described. The modulated parasystolic cycle may become irregular as a result of influence exerted by the sinus beats, and the interectopic intervals may therefore not be mathematically related. 2–5 We present a case of modulated ventricular parasystole in which the typical diagnostic features of parasystole are lacking and in which the distribution of the ectopic beats suggests a Wenckebach form of ectopic-ventricular block.

Modulation of atrioventricular junctional parasystole: Electrocardiographic calculation of the phase-response curve

A parasystolic rhythm is classically described as the expression of a completely independent ectopic rhythmic focus, i.e., it is not affected in any way by the sinus or dominant rhythm. Nevertheless, clinical observations and recent experimental studies have shown that the parasystolic discharge may, under certain circumstances, be influenced by electrotonic modulation of the sinus rhythm. 1–8 This presentation reflects a case of atrioventricular (AV) junctional parasystole with features characteristic of modulation.

Incidence and clinical significance of repetitive ventricular response in patients without identifiable organic heart disease

We determined the incidence of repetitive ventricular response (RVR) after programmed electrical stimulation and the incidence of spontaneous ventricular arrhythmias during 24 hr Holter monitoring in 38 patients in whom extensive non-invasive and invasive diagnostic tests had excluded abnormalities suggestive of organic heart disease. A standardized stimulation protocol with single (S 1S 2) and double (S 1S 2S 3) extrastimuli during ventricular drive at cycle lengths of 600, 500 and 430 msec with a current strength below 5 mA at the right ventricular apex was employed. RVR occurred in 20 patients (58%) after S 1S 2 and in 30 patients (79%) after S 1S 2S 3 stimulation. Eighteen patients (47%) showed RVR with 2 echo beats and 1 patient had 3 echo beats. RVR was due to bundle branch reentry (BBR) in 20 patients independent of the mode of stimulation. RVR due to intraventricular reentry (IVR) was found in 17 patients (47%) only after S 1S 2S 3 stimulation. The incidence of both BBR and IVR was influenced by the basic ventricular driving rate, decreasing with shorter basic cycle lengths. 17 patients had no ventricular premature depolarizations (VPDs), 12 patients had uniform, 4 multiform (Lown III), 2 consecutive (Lown IVA) VPDs, and 1 patient had parasystolic rhythm. There was no relation to the incidence of repetitive ventricular response. We conclude that in patients without identifiable organic heart disease RVR with more than 2 consecutive beats is rarely found if single and double extrastimuli are employed during ventricular drive. Both bundle branch and intraventricular reentry with one or two echo beats are a common finding in this population without relation to the incidence of spontaneous ventricular arrhythmias.

Annihilation, entrainment and modulation of ventricular parasystolic rhythms

Annihilation and one-to-one entrainment of modulated parasystolic rhythms in humans has not been previously discussed. In 9 nonmedicated patients, it was possible to measure the intrinsic, parasystolic ectopic cycle length given by the intervals between 2 consecutive parasystolic beats without any interposed nonparasystolic beat. The corresponding values varied between 960 and 2,350 ms (corresponding to rates between 62 and 26 beats/min). In addition, modulation could be determined, because nonparasystolic beats falling during the initial 59 % of the cycle prolonged the parasystolic cycle length (by 12 to 37.5%), whereas those that fell later in the cycle shortened it (by 9 to 25 %). Plotting this prolongation or shortening as a function of the temporal position of the nonparasystolic beats in the cycle yielded biphasic response curves, of which 7 were symmetric and 2 asymmetric. In 2 patients, episodes of concealed one-to-one entrainment were initiated by late nonparasystolic (sinus) beats and, later on, terminated by early ventricular extrasystoles. In 2 other patients (and in 2 separate occasions) nonparasystolic beats, falling in part of the cycle located in between those of maximal delay and acceleration, produced pacemaker annihilation (cessation of automatic activity for the remaining monitoring time). Parasystolic annihilation and concealed entrainment may be one of the causes that can explain the large, spontaneous, day-to-day variability in the incidence of ectopic ventricular beats reported in Holter recordings. Nevertheless, future prospective studies performing interventions that can change the sinus and ectopic rates are required to corroborate our finding.

Second degree entrance block with supernormal conduction in intermittent ventricular parasystole

A patient with intermittent ventricular parasystole is reported in whom the presence of second degree entrance block with supernormal conduction was suggested for the first time. In this patient, ventricular extrasystoles with variable coupling frequently occurred. The QRS configuration of the extrasystoles was different from that of the parasystolic beats. When extrasystoles did not occur, the parasystolic beat was never seen because the conducted sinus impulse always reset the parasystolic rhythm. When an extrasystole occurred 0.52 sec or more after the preceding sinus beat, this extrasystolic impulse also reset the parasystolic rhythm. On the other hand, when an extrasystole occurred between 0.47 and 0.51 sec after the sinus beat, the parasystolic focus was protected from this extrasystolic impulse. When, however, an extrasystole occurred in a short terminal portion of the T wave of the preceding sinus beat, this extrasystolic impulse reset the parasystolic rhythm again, suggesting entrance block failure during the supernormal phase.

Triggered ventricular rhythms in 1-day-old myocardial infarction in the dog.

Triggered activity developed in depolarized Purkinje fibers (maximum diastolic potential -59.3 +/- 9.9 mV) during superfusion with normal Tyrode's solution in 84% of subendocardial preparations from 1-day-old canine infarct. Triggered activity occurred when a delayed afterdepolarization attained threshold potential and spontaneously terminated after a subthreshold delayed afterdepolarization. Triggered activity was initiated either by stimulated beats or by the background slow Purkinje automaticity. When multiple stimulated beats were required, the amplitude of the afterdepolarization increased and the coupling interval decreased when the stimulation frequency and/or the number of stimulated beats increased. Varying degrees of entrance and exit block around sites of triggered activity were common, and some triggered activity manifested as a parasystolic rhythm. In preparations showing subthreshold delayed afterdepolarizations, both epinephrine (2.5 x 10(-6) M) and increasing [Ca++]o, (from 2.7 to 8.1 mM) increased the amplitude of afterdepolarizations and resulted in triggered activity. On the other hand, verapamil (2.2 x 10(-6) M) resulted in exit block around sites of triggered activity and/or completely suppressed afterdepolarizations and triggered activity. Isochronal mapping of endocardial activation during the initiation and perpetuation of triggered activity elucidated a focal site of origin from Purkinje fibers overlying the infarct and showed no evidence of a circus movement of excitation. The in vitro triggered activity may explain the spontaneous multiform ventricular rhythms seen in the intact heart.