Mechanisms of ventricular parasystole.

Eight cases of ventricular parasystole are reported. In all these cases, regardless of whether parasystole seems intermittent or "continuous," the presence of second degree entrance block of the Mobitz type I was suggested. Parasystole alternated with concealed extrasystolic bigeminy showing occasional reentrant extrasystoles. Such intermittent parasystole appears to originate in the reentrant path of extrasystoles. Reentrant extrasystolic bigeminy was seen in a comparatively rapid sinus rhythm, whereas parasystolic bigeminy was seen in a comparatively slow sinus rhythm. The difference between the interectopic intervals during parasystolic bigeminy and during (manifest or concealed) extrasystolic bigeminy was comparatively small so that occasionally the difference was not distinct; on such an occasion the case showed a seemingly "continuous" parasystole. These observations strongly suggest the possibility that most cases of parasystole, whether intermittent or "continuous," may be governed by incomplete entrance block of the second degree.     

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."     

Mechanisms of intermittent ventricular parasystole due to type II second degree entrance block

Three patients with intermittent ventricular parasystole are reported in whom the presence of second degree entrance block of type II or a type similar to that was shown. In all the patients, when a sinus beat occurred within a certain (the first) critical period after the preceding ectopic beat, the parasystolic focus was protected from this sinus impulse. When, on the other hand, a sinus beat occurred beyond another (the second) critical period after the ectopic beat, this sinus impulse reached and discharged the focus without an appreciable conduction delay. In one patient the second critical period was equal to the first one, while, in the other two, the second one was longer than the first one. In these two patients, when a sinus beat occurred between the two critical periods after the ectopic beat, this sinus impulse reached and discharged the focus after marked delay, and thereafter became a manifest or concealed re-entrant ventricular extrasystole. On the basis of these observations, an attempt was made to clarify the difference in mechanism between type I and type II second degree entrance block.     

Protection of the ventricular parasystolic focus due to interference of sinus and parasystolic impulses in the ventricular-ectopic junction

A 50-year-old man with intermittent ventricular parasystolic bigeminy is reported in whom the parasystolic focus was protected from late intervening sinus impulses. This is the first report to suggest the presence of protection due to interference in parasystolic bigeminy. The findings in this case suggest that when a sinus impulse falls in a late period of the parasystolic cycle, it travells so slowly along the ventricular-ectopic junction that it is unable to reach the parasystolic focus before the spontaneous occurrence of the next parasystolic impulse; as a result, the sinus impulse interferes with the next parasystolic impulse in the ventricular-ectopic junction. Thus it is suggested that the parasystolic focus is protected from the sinus impulse because of the interference and not because of an entrance block. This reinforces the concept of a second-degree entrance block as a mechanism of parasystole.     

Sites of entrance block and impulse formation in intermittent atrioventricular junctional parasystole.

The Wenckebach phenomenon of entrance block in intermittent atrioventricular junctional parasystole is reported for the first time in a 40-year-old woman. In this case the presence of dual pathways in the atrioventricular junction is demonstrated. One of them is a pathway without conduction disturbance. The other is a pathway containing both the ectopic focus and the site of second-degree entrance block. This site is located a considerably long distance above the focus. Entrance block occurs also at some site below the ectopic focus, which is a part of the pathway containing the focus. It is suggested that entrance block in this lower site might exist during the whole ectopic cycle.     

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.     

Differentiation between parasystole and reentry in concealed bigeminy.

There are two different theories to explain the mechanism of concealed bigeminy: one is '2:1 concealed reentry'; the other is 'irregular parasystole.' Two exemplary cases of the even-number variant of concealed bigeminy are presented. In case 1, the mechanism can be explained by an irregular parasystole due to a modulated parasystole; however, findings during temporary sinus arrest caused by vagal stimulation indicate that this case is not governed by a parasystole, but by a 2:1 concealed reentry. In case 2, the mechanism can be explained by a 2:1 concealed reentry without parasystole; however, findings during temporary sinus arrest indicate that this case is governed by an irregular parasystole due to a type-I second-degree entrance block. Thus, in cases of concealed bigeminy without pure ectopic cycles, it does not seem easy to explain the mechanism of concealed bigeminy on the theory of a modulated parasystole.     

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.     

Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug.

Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.     

Double ventricular parasystole. Supernormal phase of conduction as a mechanism of intermittent parasystole. Report of a case.

A rare case of spontaneous double ventricular parasystole was studied in depth, together with a critical review of similar cases in the literature. The discussion was focused on 1) the variation of the shortest interectopic interval (SIEI), 2) entrance block and its failure, 3) supernormality as a mechanism of intermittence, and 4) effects of lidocaine and atropine on such an arrhythmia. In double ventricular parasystole a greater than usual variation in the SIEI tended to occur in one of the two parasystolic groups. If, however, such variations were too great in the face of otherwise parasystolic rhythm, presence of intermittence was confirmed. A temporary loss of the entrance block was deemed primarily responsible for the intermittency. That is to say, invasion, discharge, and resetting of one parasystolic focus by another parasystolic impulse during the supernormal phase of the ventricle was considered the cause of an intermittence. In a strict sense, this is the first report in the literature in which the supernormality was clearly indicated as one mechanism of intermittent ventricular parasystole. The advantage of the concept of double ventricular parasystole as compared to single parasystole in defining such a mechanism is stressed.     

Parasystole, reentry, and tachycardia: a canine preparation of cardiac arrhythmias occurring across inexcitable segments of tissue

A protected ectopic focus created in tissue excised from one heart was allowed to interact with the activity of the intact heart of another animal. The protected focus consisted of a Purkinje fiber in which a narrow central zone was rendered inexcitable. The model permitted us to study parasystole, modulated parasystole, reentry, and tachycardia in the same preparation. At moderate levels of electrotonic influence across the region of block, frequency scans revealed wide zones of pacemaker entrainment. The incidence and pattern of premature ventricular contractions generated were always a sensitive function of heart rate. Parasystolic patterns could be converted to apparent reentrant patterns by simple alteration of the atrial driving rate or the level of block. Suppression of pacemaker automaticity converted a modulated parasystole model to one of pure reentry. Reciprocation of the impulse across the inexcitable tissue segment generated a ventricular tachycardia that could be initiated and terminated by a single properly timed event. Our observations suggest that ectopic activity that behaves like parasystole and activity characteristic of what is commonly diagnosed as reentry, including tachycardia and idioventricular rhythms, may be a manifestation of a common mechanism whose arrhythmic expression differs as a continuous function of heart rate, level of block, or level of automaticity.     

The mechanisms of exercise provocation of supraventricular tachycardia

Treadmill exercise tests, electrophysiologic studies, and isoproterenol infusions were performed in 14 patients with exercise provocable supraventricular tachycardia to delineate the mechanisms of exercise provocation of paroxysmal supraventricular tachycardia. Treadmill exercise tests reproducibly provoked supraventricular tachycardia in all patients. Supraventricular tachycardia similar to that provoked by exercise occurred spontaneously during isoproterenol infusions in 9 of 11 patients tested. The specific supraventricular tachycardia diagnoses of all patients were atrial reentrant tachycardia (two patients), automatic atrial tachycardia (three), atrial flutter-fibrillation (one), atypical junctional tachycardia (two), and orthodromic atrioventricular (AV) reentrant tachycardia (six) as defined by electrophysiologic studies. Various mechanisms of exercise or isoproterenol induction of supraventricular tachycardia were identified. A critical heart rate and/or appropriate sympathetic state was found to provoke all instances of reentrant or automatic atrial tachycardia and atypical junctional tachycardia. A properly timed atrial premature beat provoked five of six cases of AV reentrant tachycardia and the only case of atrial flutter-fibrillation. The remaining case of AV reentrant tachycardia was induced by a ventricular premature beat. In conclusion, the mechanisms of exercise provocation of reentrant or automatic supraventricular tachycardia are multiple and include a critical sinus rate, increased sympathetic tone, and properly timed atrial or ventricular premature beats.     

A case reported of double parasystole-combined atrial and ventricular parasystole- (author's transl)]

Parasystole is an arrhythmia resulting from simultaneous activity of two independent impulse-forming foci, one of which is protected by the other. Ventricular parasystole which arises from an ectopic focus situated in ventricule is relatively common. On the contrary, supraventricular parasystole which is centered in the atria or atrioventricular junction, is extremely rare. Kaufmann and Rothberger studied first parasystole as an entity, and they reported the first case of atrial parasystole. However, the first correctly mentioned example of atrial parasystole was described by Jervell. In the previous paper, we described one observation on atrial parasystole and discussed on its consisting-mechanism. The occurrence of ventricular parasystole is not a rarity, since it has been estimated to be present once in every 1,200 electrocardiograms taken in a general hospital. In contrast, well-documented cases of atrial parasystole are exceedingly rare, and since the first case of it was reported by Kaufmann and Rothberger, only 25 cases have hitherto been reported. In the present paper is described and discussed a case of the extremely rare combination of atrial and ventricular parasystole with exit block and fusion phenomenon...     

Simultaneous but separate intermittent and continuous ventricular parasystole

A 19 year old female with end-stage biventricular congestive cardiomyopathy and digitalis toxicity demonstrated double ventricular parasystole with separate but simultaneous intermittent and continuous parasystolic rhythms. The intermittent parasystolic focus, left ventricular in origin, showed failure of entrance block when conducted beats followed its ectopic beats at a critical compensatory interval. Each new parasystolic series was coupled to this interrupting conducted beat at an interval equaling the parasystolic cycle length. Even numbers of conducted beats intervened between ectopic beats during intermittency and odd numbers during uninterrupted parasystole. The mechanism of intermittency was explained by a concealed ventricular tachycardia with 3 3n1 exit block with the demonstration of occasional 3 3n2 Wenckebach exit block within a parasystolic interectopic interval.A second continuous parasystolic rhythm, right ventricular in origin, occurred at a later time without altering the first intermittent parasystolic rhythm.A 4% parallel and proportionate lengthening of both the sinus node and intermittent parasystolic cycle lengths was shown at an even later time.     

Noninvasive diagnosis of dual AV nodal physiology in patients with AV nodal reentrant tachycardia by adenosine triphosphate test

Atrioventricular nodal reentrant tachycardia (AVNRT) is a relatively common paroxysmal supraventricular tachycardia. This study investigated whether adenosine-5'-triphosphate (ATP) injection during sinus rhythm might be useful in the noninvasive diagnosis of dual AV nodal pathways. The study group consisted of 9 patients with slow/fast AVNRT and 11 control patients without antegrade dual AV nodal physiology (DAVNP). ATP (2.5 to 30 mg, in 2.5-mg increments was injected during sinus rhythm until signs of DAVNP (> or = 50 msec increase or decrease in AH or PR interval in two consecutive beats) or > or = second-degree AV block was observed. DAVNP was diagnosed by ATP test in all 9 patients with slow/fast AVNRT. DAVNP was observed by ATP test in 3 of the 11 control patients. Thus, the test had a sensitivity of 100% and specificity of 73%. ATP test given during sinus rhythm is useful for identifying patients with dual AV nodal pathways who are prone to AVNRT.     

Use of intravenous adenosine in sinus rhythm as a diagnostic test for latent preexcitation

In a proportion of patients with left free wall accessory connections, preexcitation is apparent only during atrial arrhythmias or atrial pacing (latent preexcitation). These patients may be at risk of a rapid ventricular response to atrial fibrillation despite the absence of preexcitation in sinus rhythm. The ability of intravenous adenosine to unmask latent preexcitation was evaluated in 22 patients with a history of documented supraventricular tachycardia and a normal electrocardiogram during sinus rhythm. Preexcitation was unmasked in response to adenosine in 4 patients: all 4 were shown to have latent preexcitation at electrophysiologic study. In 12 patients atrioventricular (AV) nodal conduction delay or block was induced without preexcitation after adenosine (first-degree AV block in 8, second-degree block in 4): at subsequent electrophysiologic study none of these patients was found to have latent preexcitation. Five patients had little or no PR prolongation in response to adenosine: of these, 2 were shown to have latent preexcitation at electrophysiologic study. Atrial fibrillation was induced in 1 patient and a narrow complex regular tachycardia in another after intravenous adenosine. Intravenous adenosine during sinus rhythm is capable of producing AV nodal conduction delay or block in 73% of patients with a history of supraventricular tachycardia: in these patients adenosine provides a diagnostic test that is both 100% sensitive and 100% specific for latent preexcitation. In those patients in whom adenosine does not produce AV conduction delay or block, further investigation is required to establish or refute the diagnosis of latent preexcitation.     

Coexistence of ventricular parasystole and ventricular couplets: mechanism and clinical significance.

In 78 consecutive patients with uniform ventricular ectopic complexes and without heart disease, ventricular couplets were present significantly more often when the coupling interval of ventricular ectopic complexes was variable than when it was fixed (P less than 0.04). In 69 consecutive patients with couplets, the prevalence of a variable coupling interval was significantly greater than that of (55 versus 14 cases; P less than 0.001). Among 55 patients with a variable coupling interval, ventricular parasystole was probable in 38 and possible in 17 patients. These results suggest that the association between ventricular couplets and parasystole is not coincidental. Of several possible mechanisms responsible for this association reentry within the parasystolic focus or its vicinity is the most probable. This may explain the observation that the couplets are seldom followed by consecutive ventricular ectopic complexes or ventricular tachycardia. If this hypothesis is correct, the clinical significance of ventricular couplets in the presence of ventricular parasystole may be similar to that of single reentrant ventricular ectopic complexes.     

Electrophysiological effects and clinical efficacy of propafenone in children with recurrent paroxysmal supraventricular tachycardia

Twenty-four patients aged 10.1 +/- 4.5 (mean +/- SD) years with recurrent paroxysmal supraventricular tachycardia underwent an electrophysiological study. Eleven patients had an overt and seven had a concealed accessory connection; six patients had no accessory connection. An orthodromic reciprocating tachycardia was inducible in 17 of 18 patients with an accessory connection, and an atrioventricular nodal reentrant tachycardia was inducible in four of six patients without accessory connection. After administration of propafenone, the sinus cycle length decreased. Intra-arterial, intranodal, and His-ventricle intervals and QRS duration increased. The atrial and ventricular effective refractory periods and anterograde and retrograde effective refractory periods of the atrioventricular node increased. The cycle length at which nodal second-degree block occurred increased. Of 18 patients with accessory connection, propafenone prolonged retrograde conduction in all, blocked anterograde conduction in five, and prolonged it in six. The drug terminated the orthodromic reciprocating tachycardia in all 17 patients and the atrioventricular nodal reentrant tachycardia in three of four patients. In three of four patients with atrioventricular nodal reentrant tachycardia and in 15 of 17 patients with orthodromic reciprocating tachycardia, the tachycardia was no longer inducible or nonsustained after propafenone. A follow-up of 26 +/- 10 months revealed that the drug when orally administered to all patients prevented recurrences of tachycardia in 15 of 18 patients with and in four of six patients without accessory connection. The results of short-term drug testing with propafenone predict the response to long-term oral therapy with this drug.     

Effects of exercise and standing on atrial parasystole: Prolongation and shortening of the parasystolic cycle length

In recently reported cases of ventricular parasystole, it was shown that after exercise the parasystolic cycle length is prolonged, in contrast to a shortening of the sinus cycle length, whereas during standing the parasystolic cycle length and the sinus cycle length both shortened. In this report, to explore whether the same features as occur in ventricular parasystole are seen in atrial parasystole, effects of exercise and standing on the parasystolic cycle length were investigated in two men with atrial parasystole. The atrial parasystolic cycle length was prolonged after exercise, whereas it shortened during standing, similar to what occurs in ventricular parasystole. This is the first report to show such changes of cycle length in atrial parasystole. These findings suggest that in atrial parasystole, as in ventricular parasystole, influences on the parasystolic cycle length do not always act in the same direction as those on sinus cycle length.     

The dual function of the A-V junction

The various electrocardiographic syndromes that develop as a consequence of abnormal dissociation of the two functions of the A-V junction can be summarized as follows (Table II):Acceleration of impulse formation in one or two pacemakers without any block in the A-V junction leads either to junctional rhythm with retrograde activation of the atria, or to isorhythmic A-V dissociation; when associated with retrograde block, the dissociation is incomplete with ventricular captures; when first- or second-degree antegrade block develops in addition, the captures tend to disappear and the A-V dissociation to become complete. An exit block of the junctional impulses may slow the manifest ventricular rate during the dissociation, and finally, an additional protective entrance block around the junctional pacemaker results in junctional parasystole. On the other hand, depression of junctional impulse formation without A-V block is one of the mechanisms responsible for the tachycardia-bradycardia syndrome.The basis of such a functional separation of the two properties of A-V junctional tissues appears to be a difference in structure and electrophysiologic behavior of cell elements that constitute the A-V junction.