Mechanism of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy. A theoretical model derived from the concepts of longitudinal dissociation and multilevel block in the reentrant pathway of extrasystoles.

A case of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy is presented. To explain the mechanism of such bradycardia-dependent appearance, a theoretical model is derived from the concepts of "longitudinal dissociation" and "multilevel block" in the reentrant pathway of extrasystoles. In the theoretical model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When manifest extrasystoles are not found for a long time, alternate sinus impulses pass through both pathways F and S, but become concealed extrasystoles because of insufficient conduction delay in the pathways. The other alternate sinus impulses are blocked in the pathways; in pathway F, the impulses are blocked at the entrance, while in pathway S, the impulses are blocked at a more distal level. When sinus cycles gradually lengthen, one of such alternate sinus impulses passes through the entrance of pathway F and, traveling very slowly, is blocked at a more distal level. The next sinus impulse is blocked at the entrance of pathway F; namely, 3:2 Wenckebach block occurs at the entrance of pathway F. Thus this sinus impulse enters only pathway S and passes through pathway S with enough conduction delay to become a manifest reentrant extrasystole.     

Mechanism of tachycardia-dependent appearance of ventricular extrasystoles in concealed bigeminy

A case of concealed ventricular bigeminy is reported in which the number of sinus QRS complexes intervening between two successive noninter-polated extrasystoles was always uneven. Coupling intervals of manifest extrasystoles to the preceding sinus QRS complexes were almost fixed and much longer than sinus QT intervals. Bradycardia-dependent disappearance of manifest bigeminy and tachycardia-dependent appearance of extrasystoles occurred in this case. Apparently, 2:1 block of sinus impulses occurred in the reentrant pathway, with markedly depressed conductivity. Concealed electrotonic conduction of blocked sinus impulses in the pathway of extrasystoles may have favored the appearance of the subsequent manifest extrasystoles without concealed conduction owing to two-level block. A possible explanation for the mechanism of such concealed bigeminy is presented, which uses the concepts of longitudinal dissociation and electrotonic inhibition in the reentrant pathway with markedly depressed conductivity.     

Mechanisms of concealed ventricular bigeminy: the concept of concealed conduction in the reentrant pathway

To clarify the presence of concealed conduction in the reentrant pathway of extrasystoles, 20 patients with ventricular extrasystoles were studied in whom two forms of interectopic periods were found in the same recording. One form is the XS1S2X period, in which two sinus QRS complexes (S1 and S2) intervene between an interpolated extrasystole (the first X) and the next extrasystole (the second X). The other is the XS2X or XS1X period, in which one sinus QRS complex intervenes between two extrasystoles. In all patients except one, the XX interval in the XS1S2X period was longer than that in the XS2X or XS1X period though shorter than twice the latter XX interval. This strongly suggests the presence of two-level block in the reentrant pathway of the extrasystoles. It appears that the sinus impulse S1 in the XS1S2X period invaded a large portion of the reentrant pathway and then was blocked at a distal site of the pathway; namely, that concealed conduction of the impulse S1 occurred in the pathway. It is suggested that such concealed conduction prolonged the conduction time of the following sinus impulse, S2, in the reentrant pathway, resulting in lengthening of the XX interval. The presence of three- or four-level block is also suggested. By the use of such multilevel block, mechanisms of concealed ventricular bigeminy are explained.     

Concealed (proximal) Wenckebach phenomenon with distal 2:1 exit block in the ectopic-ventricular junction.

The findings in two patients with interpolated ventricular extrasystoles showing 2:1 exit block are reported. In these patients the blocked impulses appear to penetrate into the ectopic-ventricular junction (or reentrant pathway) to a varying extent, and the coexistance of a distal 2:1 exit block and a proximal (concealed) Wenckebach phenomenon in the ectopic-ventricular junction is suggested.     

Ventricular Extrasystoles with Interpolation or Postponed Compensatory Pause during Atrial Fibrillation: Fact or Fiction?

A Holter recording obtained from a patient with atrial fibrillation showed ventricular extrasystoles often in bigeminal rhythm. Most extrasystoles were followed by a long return cycle, and only in a few instances the postextrasystolic interval was short. The latter phenomenon was interpreted as a manifestation of poor retrograde concealed penetration of the ventricular impulse into the atrioventricular (A‐V) junction: accordingly, an ensuing relatively early fibrillation impulse reached the ventricular chamber, since it did not find the A‐V node refractory. These events are similar to what happens in interpolated ventricular extrasystoles occurring during sinus rhythm, the absent or minimal concealed retrograde penetration of the ectopic impulse into the A‐V node being necessary to permit anterograde conduction of the ensuing sinus impulse. Analysis of the recording also revealed that a very long (>2 second) interval between two consecutive narrow beats only occurred after an “interpolated” extrasystole. This was interpreted with the same mechanism underlying the “postponed compensatory pause” observed at times after interpolated ventricular extrasystoles during sinus rhythm: the minimal or nil penetration of the ventricular ectopic impulse into the A‐V junction, followed by conduction of an ensuing early atrial impulse, “shifts to the right” the A‐V nodal refractory period, preventing conduction of several further supraventricular impulses and generating a pause. Both interpolated ventricular extrasystoles and the phenomenon of “postponed compensatory pause” are, thus, conceivable during atrial fibrillation, although no definite demonstration is possible.     

Type A alternating Wenckebach periodicity in the re-entrant path of ventricular extrasystoles

A patient with ventricular extrasystoles is reported in whom Type A alternating Wenckebach periodicity in the re-entrant path of the extrasystoles is suggested for the first time. Namely, it appears that 2:1 exit block occurs at a proximal level in the re-entrant path and block of the Wenckebach form occurs at a distal level in the path. The presence of three-level block in the re-entrant path is also suggested in this patient.     

Mechanism of ventricular extrasystoles with fixed coupling. A theoretical model derived from the concept of longitudinal dissociation in the reentrant pathway of extrasystoles.

An electrocardiogram taken from a 29-year-old man with old myocardial infarction is presented as an exemplary case of ventricular extrasystoles with fixed coupling. To explain the mechanism of ventricular extrasystoles with fixed coupling, a theoretical model is derived from the concept of longitudinal dissociation in the reentrant pathway. In the model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When a sinus impulse is blocked in pathway F and passes only through pathway S, it becomes a manifest reentrant extrasystole because of marked conduction delay in pathway S. When the sinus rate does not exceed a certain value, such an impulse always becomes a manifest extrasystole with fixed coupling. Part of the impulse passing through pathway S enters pathway. F retrogradely. In some cases, thereafter, it reenters pathway S and initiates ventricular reentrant tachycardia. When, on the other hand, a sinus impulse passes through both of pathways F and S, it becomes a concealed reentrant extrasystole because of insufficient conduction delay in the pathways.     

2 or 3 level blocks in the Tawara node during atrial tachycardia]

In atrial flutter (or paroxysmal atrial tachycardia), the ventricular response is dependant on the passage through 3 superposed zones of conduction in the Tawara node, the zone of decremential conduction being the central zone N. When the ventricular response is between half and a quarter of the atrial rate there are two possible explanations: type B alternate Wenckebach period (mobitz I block in the central zone N, 2/1 block at the nodo-ventricular junction) or type A alternate Wenckebach period (Mobitz I block in the central zone N and 2/1 block at the atrio-nodal junction). These two responses may alternate in the same patient depending on the drug therapy or vagal activity due to a phenomenon similar to the "GAP" phenomenon. Inexactitudes in the working out of the arithmetic formulae may easily be explained by a certain degree of concealed conduction of blocked activation in one zone or more rarely by hisian extrasystoles. Type A alternate Wenckebach periods are always easier to construct than type B. Perfect 3/1 atrial flutter can only be explained by a type B alternate Wenckebach period with a 3/2 period with a 3/2 period in the N zone and a 2/1 block in the NH zone. When the ventricular rhythm is permanently very slow or when the RR intervals are greater than four times the atrial cycle, 3 zones of block are usually at issue (the third being located in the inferior part of the node or superior part of the bundle of His). Examples of 5/1, 6/1 flutter are thereby analysed. Rapid atrial pacing after termination of the atrial arrhythmia allows a better analysis of its mechanism and the successive reproduction of conduction defects in each zone of block.     

Concealed conduction in the reentrant pathway as a mechanism of stable ventricular quadrigeminy

This is the first report on the stable occurrence of ventricular quadrigeminy as a manifestation of concealed bigeminy in a case of fixed and late coupled ventricular extrasystoles. A 46-year-old man is reported in whom the period of ventricular bigeminy alternated with the period of ventricular quadrigeminy. Coupling intervals of the extrasystoles were fixed and much longer than sinus QT intervals. When the heart rate is decreased, the period of bigeminy changed to the period of quadrigeminy without gradual decrease in coupling of the preceding extrasystoles. Once such a change occurred, stable quadrigeminy is maintained for a period. These findings suggest the possibility that concealed electrotonic conduction of blocked impulses and interference of conducted impulses may occur in the reentrant extrasystolic pathway as a mechanism of stable ventricular quadrigeminy.     

Mechanism of supraventricular parasystole

Two patients with supraventricular parasystole (one atrioventricular and one auricular) are reported. In both patients, reentrant extrasystoles appeared to occur as the result of Mobitz type I second-degree entrance block. We believe that when a sinus impulse fell soon after the absolute refractory period of the pathway containing the parasytolic focus, it reached and discharged the focus after marked delay, and thereafter became a reentrant extrasystole. In interectopic intervals containing more than one sinus beat, the number of intervening sinus beats was always even, suggesting the presence of concealed reentrant extrasystolic bigeminy. The observations in the present report and in our previous patients with ventricular parasystole strongly suggest that most cases of parasystole, whether ventricular or supraventricular, or whether intermittent or "continuous," may be governed by second-degree entrance block.     

A cause of paired ventricular extrasystoles.

Eight patients with ventricular extrasystoles are reported in whom coupling intervals of the extrasystoles to the proceding sinus beats were variable and in whom paired ventricular extrasystoles were occasionally seen. In all patients, paired ventricular extrasystoles were initiated only by comparatively late coupled ventricular extrasystoles. However, the interval between the first and the second of these paired extrasystoles was always much shorter than the coupling interval of this first extrasystole to the preceding sinus beat, so that the latter extrasystole often interrupted the T wave of the first one, indicating the R-on-T phenomenon. In two patients there was a gap between the ranges of coupling intervals for single extrasystoles and for the first ones of paired extrasystoles. These observations suggest the presence of longitudinal dissociation in the reentrant pathway as one of the causes of paired ventricular extrasystoles.     

Intermittent ventricular parasystolic bigeminy accompanied by reentrant ventricular extrasystoles.

An extremely rare case of intermittent ventricular parasystolic bigeminy is presented, in which coexisting reentrant ventricular extrasystoles of sinus origin, showing mainly trigeminy, and those of ventricular parasystolic origin, showing a close coupling to the ventricular parasystolic beat, are demonstrated. Such a unique case has never been reported. Timely parasystolic exit block occurring just prior to the anterograde ventricular activation of the sinus impulse was considered to be of critical importance in developing the reentrant extrasystolic trigeminy.     

Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: Effects of slow pathway ablation and insights into the location of the reentrant circuit

BACKGROUND: The electrophysiologic mechanisms of different ventriculoatrial (VA) block patterns during atrioventricular nodal reentrant tachycardia (AVNRT) are poorly understood. OBJECTIVES: The purpose of this study was to characterize AVNRTs with different VA block patterns and to assess the effects of slow pathway ablation. METHODS: Electrophysiologic data from six AVNRT patients with different VA block patterns were reviewed. RESULTS: All AVNRTs were induced after a sudden AH "jump-up" with the earliest retrograde atrial activation at the right superoparaseptum. Different VA block patterns comprised Wenckebach His-atrial (HA) block (n = 4), 2:1 HA block (n = 1), and variable HA conduction times during fixed AVNRT cycle length (CL) (n = 1). Wenckebach HA block during AVNRT was preceded by gradual HA interval prolongation with fixed His-His (HH) interval and unchanged atrial activation sequence. AVNRT with 2:1 HA block was induced after slow pathway ablation for slow-slow AVNRT with 1:1 HA conduction, and earliest atrial activation shifted from right inferoparaseptum to superoparaseptum without change in AVNRT CL. The presence of a lower common pathway was suggested by a longer HA interval during ventricular pacing at AVNRT CL than during AVNRT (n = 5) or Wenckebach HA block during ventricular pacing at AVNRT CL (n = 1). In four patients, HA interval during ventricular pacing at AVNRT CL was unusually long (188 +/- 30 ms). Ablations at the right inferoparaseptum rendered AVNRT noninducible in 5 (83%) of 6 patients. CONCLUSION: Most AVNRTs with different VA block patterns were amenable to classic slow pathway ablation. The reentrant circuit could be contained within a functionally protected region around the AV node and posterior nodal extensions, and different VA block patterns resulted from variable conduction at tissues extrinsic to the reentrant circuit.     

Mechanism of escape, extrasystolic, and parasystolic arrhythmias. Study on an electrical analogue.

A simple analogue of the heart consisting of a system of neon relaxation oscillators is presented. The analogue may display rhythm patterns similar to sinus rhythm, escape rhythm, isorrhythmic dissociation with synchronization, atrial extrasystoles, ventricular extrasystoles, and parasystole. The strict rules followed by these arrhythmias, as well as the deviations from the rules commonly followed by the equivalent heart arrhythmias, may be easily reproduced on the analogue. Such features are the Treppe phenomenon and captured beats in escape rhythm, fixed coupling intervals in extrasystoles, partial or complete atrioventricular block in very premature atrial extrasystoles, prolongation of the period following an atrial extrasystole, interpolated premature beats, complete compensatory pause and the rule of bigeminy in ventricular extrasystoles, slight instability of the parasystolic period, multiple length parasystolic periods slightly different from the exact multiples of the parasystolic idioperiod, preference of the parasystoles for certain phase in the sinus cycle, synchronization at a phase difference and fluctuation repeatedly and without interruption from a parasystolic to an extrasystolic rhythm and synchronization in escape rhythm with isorrhythmic dissociation. The mechanisms involved in these phenomena are discussed in detail. The striking similarity between the properties of the cardiac pacemakers and those of the relaxation oscillators on the one hand and betwen the rhythm patterns of the heart and those of the analogue on the other may permit the hypothesis that the mechanisms operating in the analogue may be used in analyzing and understanding heart arrhythmias.     

Antidromic reciprocating rhythm in Wolff-Parkinson-White syndrome precipitated by a ventricular extrasystole arising at the emergence of the preexcitation pathway

A 9 year old child was investigated for attacks of wide QRS complex tachycardia occurring exclusively during the daytime and favoured by exercise or stress, with ventricular extrasystoles of the same form occurring between attacks. Endocavitary investigation showed a concealed atrioventricular accessory pathway during sinus rhythm with anterograde 1/1 conduction up to 270/min; retrograde conduction was not so good with block occurring at 175/min. The spontaneous tachycardia was reproduced by catecholamine infusion: it was an antidromic reciprocating rhythm triggered by a ventricular extrasystole of identical form to that of a pure preexcitation complex and to that of the tachycardia complexes. Spontaneous termination of attacks always occurred when conduction from the ventricle to the atria stopped. The attacks could be induced by ventricular extrastimuli when they caused an increment in retrograde conduction time resulting from retrograde conduction up the nodohisian pathway and not the Kent bundle. The tachycardia could also be initiated by atrial extrastimuli providing pure pre-excitation could be obtained. In both cases, retrograde conduction of the nodohisian pathway had to be improved by catecholamines. When the patient was given betablocker therapy the attacks of tachycardia completely disappeared. The association of ventricular extrasystoles and antidromic reciprocating rhythm and their morphological identity suggest that these extrasystoles were in fact automatic activity of the Kent bundle. Escape phenomena as signs of passive automatism have been described in this conditions but, to our knowledge, extrasystoles suggesting an active automatic process have not been previously reported.     

Alternate Wenckebach conduction through the right bundle branch

This case report describes a patient with chronic chagasic myocarditis who presented with a unique tachycardia-dependent or phase 3 aberrant ventricular conduction. The electrocardiogram showed sinus tachycardia with sequences of alternate and progressive right bundle branch block, that is, Wenckebach periods of alternate beats. We postulated the existence of functional longitudinal dissociation in atrioventricular conduction axis, responsible for the alternant normal and Wenckebach beats.     

Concealed extrasystoles due to Wenckebach conduction delay within the reentry loop.

Long electrocardiographic strips were analyzed from an aged patient whose heart rhythm had periods of unifocal ventricular extrasystoles with fixed coupling intervals. Periods of gradual prolongation of the coupling interval finally led to omission of a ventricular premature beat. This sequence was repetitive and is considered to be the results of reentrant extrasystoles with a 3:2 Wenckebach type of conduction delay within the reentry loop. The mechanism of concealed conduction due to overlong propagation within the reentry loop is discussed.     

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.