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 multiple 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.     

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.     

Ventricular parasystole and ventricular couplets: A re-entry within the parasystolic focus?

We report a 62-year-old man with a persistent ventricular rhythm originating in a parasystolic focus associated with frequent ventricular couplets with fixed coupling. Both intravenous (IV) procainamide (1 g) and propafenone (70 mg IV) promptly suppressed only the second component of ventricular couplets, suggesting that re-entry rather than enhanced automaticity was the mechanism of ventricular couplets. On the contrary, the nonresponse of ventricular rhythm and ventricular couplets to verapamil (10 mg IV) suggested that triggered activity should not play a role in the genesis of this ventricular rhythm. The mechanisms of the ventricular couplets (rapidly discharging parasystolic focus vs. re-entry) are discussed.     

The effect of sinus rhythum on the periodicity and coupling interval of ventricular parasystolic rhythm

Ventricular parasystole was studied in three patients. Longperiods of the ECG were analysed allowing features of the ectopicmechanism to be deduced.The ECGs were recorded on magnetic tapeand analysed with the aid of special purpose and digital computers.Sinusrhythm was found to alter the periodicity of the ectopic rhythmand to adjust its phase relation–ship relative to sinusrhythm. These effects were more marked when the ectopic periodwas similar to the sinus period or its multiple. In one patientphase adjustment resulted in periods of bigeminy with fixedcoupling.The adjustment of periodicity and phase probably resultsfrom subthreshold stimuli due to sinus rhythm modifying thefunction of spontaneous depolarization of the ectopic pacemaker.     

Concealed ventricular extrasystoles due to interference and due to exit block.

Two cases of sinus rhythm with ventricular extrasystoles are reported in which extrasystoles arising from the same focus obey the rule of "comcealed bigeminy" and the "rule of bigeminy". In a comparatively rapid sinus rhythm, shortening of the sinus cycle favors the appearance of extrasystoles, and the extrasystoles obey the fule of "concealed bigeminy"; namely, sinus impulses intervene between extrasystoles in even numbers. The sinus impulses here include those both conducted and not conducted to the ventricles. Conversely, in a comparatively slow sinus rhythm, interectopic sinus impulses appear in odd numbers only, and the extrasystoles obey the "rule of bigeminy"; namely, lengthening of the sinus cycle favors the appearance of extrasystoles. From these observations, a new mechanism governing both of the rules is suggested as follows. Ectopic impulses arise following all the interctopic sinus beats, but they become concealed extrasystoles of two types. One of them is the "concealed extrasystole due to interference at the external end of the ventricular-ectopic (V-E) junction."The other is the "concealed extrasystole due to exit block within the V-E junction" because of refractoriness following stimulation. They alternate with each other. In the of "concealed begeminy", the last concealed extrasystole intervening between manifest extrasystoles is due to exit block, whereas in the "rule of bigeminy", it is due to interference.     

Modulation and suppression of parasystolic ventricular pacemakers

Using a three part model of canine false tendon in which an inexcitable gap intervenes between the proximal and distal region of Purkinje fibers, Jalife and Moe recently individualized a biological model of parasystole and showed how the electrotonic depolarization can modulate, entrain or annihilate pacemaker activity. We report the ECG of 9 patients with parasystole (as assessed by the direct recording of ectopic cycle length) in which the early nonparasystolic beats delayed whereas the late shortened the parasystolic cycle length. The phase response curve is specific for a given patient. In two cases a nonparasystolic impulse falling at a critical point in the ectopic cycle length was followed by the suppression of any parasystolic activity on the surface EKG. The recently described phenomenon called pace maker annihilation is thus discussed.     

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.     

Atrial parasystole and tachycardia. Modulation and automodulation of a parasystolic focus.

This report deals with a patient reflecting atrial parasystole and episodes of atrial tachycardia. The P' waves during tachycardia were identical to the parasystolic P' waves. Atrial parasystole was at times regular, as revealed by a precise mathematical relationship between the interectopic intervals, and on other occasions irregular. Irregularity was due to modulation, namely electrotonic influence exerted by the sinus impulses upon the parasystolic focus. Atrial tachycardia occurred only during the periods when atrial parasystole was modulated. Atrial tachycardia has been interpreted as due to automodulation, a situation where the propagated parasystolic impulse exerts an electrotonic influence on the ectopic focus itself, leading to a marked unexpected acceleration of the ensuing parasystolic discharge.     

Idiopathic recurrent sustained parasystolic ventricular tachycardia responsive to verapamil in a 15-year-old patient

A 15-year-old patient is presented with parasystolic ventricular tachycardia which was responsive to oral verapamil. We emphasize the value of verapamil in the treatment of this uncommon arrhythmia.     

A computer-based model of parasystolic activity modulated by ventricular activation in the open-chest dog

The modulated parasystole hypothesis proposed by Moe has been suggested as a common mechanism of a wide variety of arrhythmias. To represent the arrhythmic patterns defined by the model as an actual ECG trace, a "hybrid" experimental system was devised. The system consisted of the intact canine heart connected to a microcomputer that operated as the modulated parasystolic pacemaker. An intrinsic cycle length of the "ectopic" pacemaker was modulated by the phase-dependent effect of the activity of the intact heart in situ. Discharges in the "ectopic" pacemaker were transmitted to the right ventricle. The result was that the theoretically defined patterns of the ectopic activity were represented as real ECG traces. Some published examples of intermittent parasystole that had been attributed to other complex mechanisms were accurately reproduced when the estimated phase response curves were set in the "ectopic" pacemaker. A wide variety of clinical eCG tracings of ventricular arrhythmias may be reproduced by this hybrid experimental model.     

窦性心律下通过三维电压标测心肌梗死后瘢痕性室性心动过速

目的 介绍一种不需行拖带标测,而在窦性心律下可标测和消融心肌梗死后瘢痕性室性心动过速(室速)的方法.方法 两例男性患者,均在心肌梗死和冠状动脉再通治疗后出现室速.经胺碘酮治疗后出现甲状腺功能异常而停药.其中例1为前壁心肌梗死合并心尖部室壁瘤,在发作室速时心功能恶化伴顽固咳嗽;例2为下后壁心肌梗死,其临床室速有两种形态,室性早搏(室早)有多种形态.该两种情况占心肌梗死后室速的大部分,均不太适合常规的拖带标测.首先在窦性心律时在Carto系统指导下建立左心室的三维电解剖图,通过调整瘢痕区电压标准,使梗死边缘区三层结构清楚显示后,沿边缘区行起搏标测,通过特征电位和测量刺激至QRS间距来判定峡部区,然后以峡部区为中心,以垂直于边缘区的方向行连续线性消融,直至室速不能被诱发视为消融终点.结果 两例在消融前均可反复诱发室速,在经过几条垂直线消融后室速均不能被诱发,随访3个月室速也未复发.心功能和生活质量明显改善.但例1出现室壁瘤附壁血栓.结论 对大多数心肌梗死后瘢痕性室速患者,均可在窦性心律下标测到其关键峡部区,并以此为中心点沿着垂直于边缘区方向行线性消融,以室速不能被诱发做为急性期终点同样能得到较好的远期成功率,但术后1个月需保持华法林抗凝.     

Coupling interval, exit block, and periodicity of ventricular parasystolic rhythm.

The electrocardiograms in this study of parasystolic rhythm were tape recorded and then analysed with a special purpose hybrid computer. The rate of appearance of specific inter-ectopic intervals was shown to change significantly with small changes in either the sinus or parasystolic pacemaker period. Natural changes in the period of the ectopic pacemakers were observed over several hours. Changes amounting to 14% within 10 min and 18% overall were observed in one patient, and a gradual lengthening of 10% over 3 h in another. A previously undescribed form of exit block has been discovered in one patient where the block remained active for a given time only after propagation from the parasystolic focus. Different interectopic intervals were shown to contribute to specific and restricted coupling interval locations in diastole. Hence this form of exit block, by preventing some inter-ectopic intervals from propagating, limited the locations in diastole in which parasystolic ectopic complexes could appear. In this case later diastolic complexes were inhibited and hence fusion complexes were completely absent. Parasystolic rhythm, with and without the exit block described, was simulated successfully by a digital computer. The simulations aided our understanding of the clinical data.