Type A alternating Wenckebach periodicity in the reentrant pathway of interpolated ventricular extrasystoles

A 67-year-old man with interpolated ventricular extrasystoles is reported in whom alternate sinus QRS complexes were followed by interpolated ventricular extrasystoles with progressively lengthening coupling intervals until one of these alternate sinus complexes failed to be followed by an extrasystole. This is the first report to suggest the presence of type A alternating Wenckebach periodicity in the reentrant pathway of interpolated ventricular extrasystoles. It is suggested that 2:1 block occurred at a proximal level in the reentrant pathway, while Wenckebach block occurred at a distal level in the pathway.     

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.     

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.     

Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms.

OBJECTIVE--A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms. MATHEMATICAL MODEL--The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism. CLINICAL OBSERVATION--To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (> 1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability < 200 ms) over a wide range of RR intervals (> 700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39.3%) in whom coupling interval/RR diagrams were not definitive. CONCLUSION--These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms.     

A subvariant of concealed bigeminy.

A subvariant of the "even variant" of concealed bigeminy was studied in two patients. The typical pattern consisted of two types of sequences of conducted sinus beats between extrasystoles. One pattern was bigeminal, i.e., alternating sinus beats and extrasystoles. Between bigeminal sequences were intervals in which there were more than one conducted sinus beat between extrasystoles. In such longer sequences, the numbers of sinus beats were almost invariably even. In the bigeminal sequences, the coupling intervals progressively diminished for each successive extrasystole in the sequence. The proposed explanation for the subvariant was based on a reentry loop in which there were three sites of block: proximal, intermediate, and distal. Block was postulated to take place at the proximal site after those extrasystoles with the shortest coupling intervals, at the intermediate site after odd-numbered conducted sinus beats in the non-bigeminal sequences, and at the distal site ("concealment") after the even-numbered sinus beats in these longer sequences.     

QT dispersion in sinus beats and ventricular extrasystoles in normal hearts.

OBJECTIVE--Recent studies have suggested that QT interlead variability (dispersion) on the surface electrocardiogram may have potential as a measure of recovery time dispersion. To test this hypothesis further QT dispersion occurring in sinus beats was compared with that in ventricular extrasystoles. DESIGN--Simultaneous electrocardiograms were recorded at 50 mm/s during sinus rhythm in a drug free state while ventricular extrastimuli were introduced by programmed right ventricular stimulation at different coupling intervals. QT dispersion, defined as the difference between the maximum and minimum QT, was calculated separately for the extrasystoles and preceding and following sinus complexes. To correct for the influence of the number of measurable leads on QT dispersion, an "adjusted" QT dispersion calculated as QT dispersion/square root of the number of measurable leads, was used to compare sinus complexes and extrasystoles. PATIENTS--Nine patients were studied who were undergoing electrophysiological study for investigation of palpitation and were found to have electrically normal ventricles. RESULTS--At all coupling intervals tested "adjusted" QT dispersion was significantly greater in the ventricular extrasystoles than in either the preceding or following sinus complexes. For the coupling interval 350 ms, the 95% confidence intervals for the difference between means was 52 to 78 ms (preceding sinus complex) and 56 to 82 ms (following sinus complex) (p less than 0.00001). There was no correlation between the coupling interval and the magnitude of the "adjusted" QT dispersion. CONCLUSION--These results accord fully with expected differences in ventricular recovery time dispersion and offer further support for the hypothesis that QT dispersion reflects regional variation in ventricular recovery. If substantiated by invasive studies, these findings have wide implications for both the usefulness and the method of QT measurement.     

QT dispersion in sinus beats and ventricular extrasystoles in normal hearts.

OBJECTIVE--Recent studies have suggested that QT interlead variability (dispersion) on the surface electrocardiogram may have potential as a measure of recovery time dispersion. To test this hypothesis further QT dispersion occurring in sinus beats was compared with that in ventricular extrasystoles. DESIGN--Simultaneous electrocardiograms were recorded at 50 mm/s during sinus rhythm in a drug free state while ventricular extrastimuli were introduced by programmed right ventricular stimulation at different coupling intervals. QT dispersion, defined as the difference between the maximum and minimum QT, was calculated separately for the extrasystoles and preceding and following sinus complexes. To correct for the influence of the number of measurable leads on QT dispersion, an "adjusted" QT dispersion calculated as QT dispersion/square root of the number of measurable leads, was used to compare sinus complexes and extrasystoles. PATIENTS--Nine patients were studied who were undergoing electrophysiological study for investigation of palpitation and were found to have electrically normal ventricles. RESULTS--At all coupling intervals tested "adjusted" QT dispersion was significantly greater in the ventricular extrasystoles than in either the preceding or following sinus complexes. For the coupling interval 350 ms, the 95% confidence intervals for the difference between means was 52 to 78 ms (preceding sinus complex) and 56 to 82 ms (following sinus complex) (p less than 0.00001). There was no correlation between the coupling interval and the magnitude of the "adjusted" QT dispersion. CONCLUSION--These results accord fully with expected differences in ventricular recovery time dispersion and offer further support for the hypothesis that QT dispersion reflects regional variation in ventricular recovery. If substantiated by invasive studies, these findings have wide implications for both the usefulness and the method of QT measurement.     

Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms

Objective—A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms.Mathematical model—The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism.Clinical observation—To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (>1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability <200 ms) over a wide range of RR intervals (>700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39·3%) in whom coupling interval/RR diagrams were not definitive.Conclusion—These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms.     

Reappraisal of the coupling interval of ventricular extrasystoles as an index of ectopic mechanisms

Objective—A mathematical model of modulated ventricular parasystole based on the relation between the coupling interval and the preceding RR interval was developed in an attempt to distinguish between parasystolic automaticity and other mechanisms.

Mathematical model—The relation between the coupling interval and the preceding RR interval was examined by plotting the coupling interval of each extrasystole against the preceding RR interval (coupling interval/RR diagram). The coupling interval/RR diagrams obtained from simulations with various modulation modes suggested that the parasystolic mechanism was likely when the dots representing extrasystoles appeared as discrete clusters. In contrast, a linear horizontal accumulation of dots indicated a non-parasystolic mechanism.

Clinical observation—To verify the validity of the simulations, 24 hour electrocardiographic recordings from 60 patients with frequent ventricular extrasystoles (>1000/day) were analysed to determine whether the extrasystoles showed intrinsic periodicity. Intrinsic periodicity indicative of a parasystolic mechanism was seen in 14 (93%) of 15 patients in whom the coupling interval/RR diagram was characteristic of a parasystolic mechanism. When the coupling interval did not change (variability <200 ms) over a wide range of RR intervals (>700 ms) intrinsic periodicity was never identified (0/17). Parasystolic automaticity was the likely mechanism in 11 of the remaining 28 patients (39·3%) in whom coupling interval/RR diagrams were not definitive.

Conclusion—These data indicate that definite patterns of coupling interval/RR diagrams can be used to distinguish between parasystolic and non-parasystolic mechanisms.

     

Modes of onset ("initiating events") for paroxysmal atrial tachycardia in infants and children

Observations of spontaneous onset of paroxysmal atrial tachycardia (PAT) in infants and children have been infrequently reported. This study reports on modes of spontaneous onset of PAT in 22 infants and 8 children in whom onset of PAT was recorded during continuous electrocardiographic recording. During PAT, all 30 patients used the normal specialized atrioventricular conduction system for ventricular activation, with atrial activation occurring through an accessory atrioventricular connection (orthodromic reciprocating tachycardia). Wolff-Parkinson-White syndrome was present in 7 patients. Analysis of the mode of onset of PAT revealed that infants initiated PAT with atrial extrasystoles or sinus acceleration (a gradual shortening of the P-P interval). In 10 infants more than 10 PAT onsets were recorded, and in these infants the mode of onset was sinus acceleration. In 7 infants, both atrial extrasystole and sinus acceleration were observed to initiate PAT. In the older children, onset of PAT followed atrial extrasystole (3 patients), ventricular extrasystole (2 patients), and sinus pause with junctional escape (3 patients). It has been previously recognized that the natural history of these "initiating events" varies with patient age. Variations in frequency of spontaneous episodes of PAT may relate to chronologic variations in frequency and type of initiating events.     

Three variants of concealed bigeminy.

Long electrocardiographic strips were analyzed from five patients who exhibited periods of typical "concealed bigeminy," i. e., recurrent unifocal extrasystoles which were separated from one another by odd numbers of normally conducted sinus beats. However, in each of these patients, there were periods in which one of three different variants of concealed bigeminy was observed. Three patients displayed an "even number" variant; i. e., there were large numbers of consecutive extrasystoles which were separated exclusively or preponderantly by even rather than by odd numbers of sinus beats. One other patient exhibited an "interpolated extrasystole" variant: those interectopic intervals which were initiated by an interpolated extrasystole contained an even number of sinus beats, whereas all other interectopic intervals contained an odd number. In the fifth patient, the distribution of the numbers of sinus beats separating extrasystoles was such as to suggest a periodic fluctuation between the classical forms of concealed bigeminy and concealed trigeminy; i. e., a "combined bigeminy and trigeminy" variant.     

Initiation of ventricular fibrillation by supraventricular beats in patients with acute myocardial infarction

The role of supraventricular extrasystoles in the initiation of ventricular arrhythmia was studied in 72 consecutive patients who developed primary ventricular fibrillation during the acute phase of myocardial infarction. In six patients (8%), a total of 12 episodes of ventricular fibrillation and 16 episodes of ventricular tachycardia were initiated by supraventricular extrasystoles. Ventricular fibrillation and tachycardia were initiated by single supraventricular extrasystoles in 16 and by salvos greater than or equal to two beats in 12 episodes. The RR coupling interval of the supraventricular impulse immediately preceding ventricular tachycardia ranged from 240 to 420 ms (mean 356 (62)) and was characteristic of R-on-T (prematurity index less than 1) in 63% of episodes. Average peak serum creatine kinase activity in the six patients in whom ventricular tachycardia was initiated by a supraventricular extrasystole was 1275 units compared with 720 units in the remaining 66 patients. Five of these six patients later showed evidence of pump failure. Lignocaine or procainamide or both suppressed the ventricular arrhythmia in five of the six patients. The initiation of ventricular fibrillation or tachycardia by supraventricular extrasystoles in acute myocardial infarction is not uncommon and may reflect the increased vulnerability of the heart after a large infarct. These arrhythmias may respond to drugs that suppress ventricular irritability.     

Initiation of ventricular fibrillation by supraventricular beats in patients with acute myocardial infarction.

The role of supraventricular extrasystoles in the initiation of ventricular arrhythmia was studied in 72 consecutive patients who developed primary ventricular fibrillation during the acute phase of myocardial infarction. In six patients (8%), a total of 12 episodes of ventricular fibrillation and 16 episodes of ventricular tachycardia were initiated by supraventricular extrasystoles. Ventricular fibrillation and tachycardia were initiated by single supraventricular extrasystoles in 16 and by salvos greater than or equal to two beats in 12 episodes. The RR coupling interval of the supraventricular impulse immediately preceding ventricular tachycardia ranged from 240 to 420 ms (mean 356 (62)) and was characteristic of R-on-T (prematurity index less than 1) in 63% of episodes. Average peak serum creatine kinase activity in the six patients in whom ventricular tachycardia was initiated by a supraventricular extrasystole was 1275 units compared with 720 units in the remaining 66 patients. Five of these six patients later showed evidence of pump failure. Lignocaine or procainamide or both suppressed the ventricular arrhythmia in five of the six patients. The initiation of ventricular fibrillation or tachycardia by supraventricular extrasystoles in acute myocardial infarction is not uncommon and may reflect the increased vulnerability of the heart after a large infarct. These arrhythmias may respond to drugs that suppress ventricular irritability.     

Assessment of heart rhythm in patients with dilated cardiomyopathy based on daily ECG monitoring data

The quantitative and qualitative characteristics of arrhythmias were examined, using continuous 24-hour ECG monitoring, in 25 patients with dilatation cardiomyopathy. Supraventricular extrasystole was found in 100% of patients with the sinus rhythm, and ventricular extrasystoles, in 94% of patients, being most commonly associated with poor prognosis (polytopic extrasystoles in 84%, paired extrasystoles in 60%, and paroxysmal ventricular tachycardia in 40%). Disorders of atrio-ventricular conductivity were recorded in 47.6% of patients with the sinus rhythm, 23.8% of those showing a permanent 1st-degree block, and the rest, a transient block of the 1st--3d degree. It was demonstrated that arrhythmias could serve as a permanent sign of dilatation cardiomyopathy, being most commonly of a complex nature and associated with poor prognosis.     

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.     

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.     

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.     

Determining factors of the repetitive bursts in ventricular tachycardia

24-h ECG recordings were studied in 60 patients suffering from salvos of repetitive ventricular tachycardia (VT), in order to determine the parameters affecting the repetitive response in ventricular arrhythmias. The tracings were analysed with the use of ATREC II system allowing the systematic study of 15 RR intervals and the heart rate in the 3 min preceding each type of event. The mean number of events taken into account per patient and per 24h of recording amounted to 673 +/- 521 for isolated ventricular extrasystoles, to 568 +/- 461 for paired ventricular extrasystoles and 435 +/- 810 for bursts of VT. The whole group was divided into two groups according to the absence (A) or presence (B) of associated cardiopathy. Group A included 30 patients with a mean age of 42 +/- 17 years, group B included 30 patients with a mean age of 42 +/- 17 years, group B included 30 patients with a mean age of 57.4 +/- 12 years. Three major factors responsible for the repetitive activity could be disclosed: The heart rate preceding isolated ventricular extrasystoles was lower than that preceding the salvos of VT (p less than 0.01) the duration of which increased in a linear way with the sinus rate; Duration of the cycle preceding the last sinus beat before the bursts (long duration in 77% in group A and in 57% in group B). In 60% of cases in group A and 40% in group B the coupling interval was all the more long as the response was repetitive.(ABSTRACT TRUNCATED AT 250 WORDS)     

Phase 2 reentry in man.

BACKGROUND: Ventricular extrasystoles are characterized by a fixed coupling interval to the last QRST complex preceding it. OBJECTIVES: We hypothesized that this QRST complex differed from QRST complexes of other sinus beats not followed by ventricular extrasystoles. Further, we investigated whether phase 2 reentry, demonstrated in animal experiments to initiate ventricular extrasystoles, ventricular tachycardia, and ventricular fibrillation, also plays a role in humans. METHODS: We examined 18 patients with ventricular extrasystoles and/or ventricular tachycardia by signal averaging of the ECG (group A) or by single-beat analysis of intracardiac electrograms (group B). Group A consisted of six patients without structural heart disease and one patient with the Brugada syndrome. Six of the seven patients had right ventricular outflow tract ventricular extrasystoles. Group B consisted of 11 patients undergoing radiofrequency ablation. Eight of the 11 patients had right ventricular outflow tract extrasystoles. RESULTS: In six of the seven patients in group A, we demonstrated significant ST-elevation and/or T-wave changes in the sinus beat preceding ventricular extrasystoles compared with the second last sinus beat in one or more of the three orthogonal leads X, Y, and Z. In 9 of the 11 patients in group B, single-beat analysis of unipolar and bipolar electrograms recorded close to successful ablation sites demonstrated similar changes, that is, ST-elevation (median peak voltage gradient 150 muV, range 0-1,700) and T-wave changes in the sinus beat prior to ventricular ectopy. In addition, J-point elevation was demonstrated in several cases. In total, significant changes were demonstrated in 15 of the 18 patients studied (83%). CONCLUSION: J-point elevation, ST-elevation, and T-wave changes documented in the last sinus beat prior to ventricular extrasystoles are in agreement with phase 2 reentry, suggesting that this may be the responsible mechanism for ventricular extrasystoles and ventricular tachycardia/fibrillation. The phenomenon has been demonstrated in only animal experiments to date.