Concealed rhythms by double ventricular parasystole

rhyfhms

by double ventrkular

Electrocardiograms taken from 11 patients in sinus rhythm with ventricuiar ectopic rhythms from two dtfferent foci were analyzed to flnd the number of slnur beats, S, between the ectopic rhythms (S values). Three out of 11 patients had the S values typical for conceakd eotopic rhythms. One of them had concealed bigeminy of Pn-1 form that occaahmatly to 2n form. Following the shift, S values of 2n-1 form were always achieved by the ocOurrenoe of doubie ventricular ectopic rhythms in succession. Concealed trigeminy of 3n and 3n-2 form was seen in the other two patients. Double ventricular ectopic rhythms had btxarre abnormal 8618 corngtexes of two different morphoiogies and were inscribed in opgoslte directions. Eetegk rhythms in each case had perasystolic characteristics. These observations suggest blfocd automatietty as a mechanism for bidirectional ventricular tachycardia. (AM HEART J lSQ1;122:469.)

Vijay Kishore Singh, MBBS. Delhi, India

Apparently random ventricular ectopic events in sinus rhythm may sometimes reveal remarkable order on careful examination. The number of sinus beats between ectopic events (S values) may sometimes be always odd, i.e., 1,3,5,7, etc.l or always even, i.e., 2, 4,6, etc.2 The arrhythmia is called concealed bigeminy and is expressed by equations S = 2n-1 (odd form) and 2n (even form) where n = any integer. Similarly, other equations have been recognized such as S = 3n-1,3n-2, and 3n for concealed trigeminy.lp 3 Although several investigators4 describe variants of such concealed rhythms as unifocal ventricular ectopic rhythms, no study has been undertaken to demonstrate the maintenance of such concealed rhythms by ventricular ectopics from two different foci except a single case by Schamrothl (case No. 64). The present study demonstrates concealed bigeminy and trigeminy maintained by double ventricular ectopic rhythms. METHODS

Eleven casesof double ventricular ectopic rhythms in sinus rhythm were selected. Ectopic rhythms were of two types, i.e., XA and XB. As shown in Figs. 1 to 3, XA ectopits are reflected by an rS pattern in standard lead II, e.g.,

From DST Centre for Visceral Mechanisms, V.P. Chest Institute, University of Delhi; and Asthma, Bronchitis, and Cancer Lung Foundation of India, Gautam Nagar, New Delhi. Received

for publication

July

3, 1990; accepted

Jan.

‘7, 1991.

Reprint requests: Dr. V. K. Singh, DST Centre for Visceral Mechanisms, V.P. Chest Institute, University of Delhi, P.O. Box 2101, Delhi-110007, India. 4/l/29563

the second QRS complex in the upper strip of Fig. 1. XB ectopic rhythms, on the other hand, have an upright QRS complex in standard lead II, e.g., the second QRS complex in the upper strip (Figs. 2 and 3). First of all, S values between ventricular ectopic rhythms irrespective of XA or XB were determined for any of the known expressions for concealed ventricular rhythms.4 After that both the ventricular ectopic rhythms were analyzed to find whether they represent “regular” or “irregular” parasystole from the variation index described by Oreto et al5 Variation index was calculated from the ratio of two parameters: (1) the difference between the longest and the shortest manifest or calculated parasystolic cycle (XA-XA) (XBXB) and (2) the global mean ectopic cycle leng&h of (XA-XA) and (XBXB) intervals.5 The casesof irregular parasystole were then analyzed to determine whether the irregularity was casual or due to influence of sinus rhythm (modulation) or resetting (intermittent parasystole). Msasurements of the interectopic intervals and related calculations trverelimited to a 4-minute continuous strip of the resting electrocardiogram (EGG) to avoid changes due to autonomic tone or spontaneous fluctuations of the ectopic cycle length.5 RESULTS

Three out of 11 cases exhibited the features of concealed ectopic rhythms. In all the cases three types of QRS complexes were evident, as shown in Figs. 1 to 3: (1) Sinus QRS cornpl~~s ventricular ectopics of rS pattern ventricular ectopics with up&$& beled XB. In addition, there were several fusion beats. Exemplary

pati6nts

Case No. 1. Fig. 1 shows parts of a long recording in lead II. The sinus R-R intervals varied from 0.60 469

470

Singh

Amorlcan

4

XA

August 1991 Heart Journal

XB

1. All strips are not continuous. First and second strips showing S values of 1,3, and 7 are continuous. The fourth and third strips are also continuous but are separate from the first, second, or fifth strips. S, Sinus beat; XA, ectopic rhythm of rS pattern; XB, ectopic rhythm with upright QRS; FA, fusion due to XA and S; FB, fusion due to XB and S. Numbers above strips reflect S values. Numbers within strips reflect time intervals such as coupling (S-XA or S-XB) or interectopic (X-X). All time intervals are expressed in hundredths of a second. All recordings were made in lead II.

Fig.

s

x6

1

XB

XA

1 XA

XA

2. All the strips (lead II) are continuous, showing S values of 1,31,10, and 1, consistent with the 3n-2 form of concealed trigeminy. Abbreviations as in Fig. 1.

Fig.

to 0.80 second. The number of sinus beats between ventricular ectopic rhythms irrespective of type XA or XB is 1,3, and 7, suggesting the 2n-1 form of concealed bigeminy, as shown in the upper two strips. Sometimes the S values were only 4 and 8, suggesting the 2n form of concealed bigeminy. From these even values of S, a 2n-1 rhythm was achieved only by the occurrence of double ventricular ectopics in succession-ectopic QRS complexes inscribed in opposite directions, as shown in the lower three strips. The coupling interval of type XB ectopic rhythm to the preceding dominant beat varied from 0.48 to 0.68 second. The interectopic intervals (XB-XB) are irregular, as expressed by a variation index of 14.7. The irregularity was not due to modulation or resetting (intermittent parasystole). The short XB-XB intervals

varied from 1.48 to 1.72 seconds. The long

XB-XB intervals were a multiple of 1.58 to 1.70 seconds. Thus both the short and long interectopic intervals are variable but are mathematically related. All the values of S-i.e., 1, 3, 5, 7, and g-could be seen at the same ectopic rhythm to first sinus beat (XB-Sl) intervals. Furthermore, the short XB-XB intervals (S = 1) at times were associated with short XB-Sl intervals, whereas long XB-XB intervals (S = 3, 5, 7, and 9) had long XB-Sl intervals. A phase-response curve could therefore not be drawn. XB ectopics, however, can be diagnosed as regular parasystole for two reasons. (1) The shortest XB-XB intervals varied up to 0.24 second. It has been reported that the shortest interectopic interval in regular parasystole can vary up to 0.27 second.5 (2) S values other than the odd numbers in this case were only 4 and 8. Odd numbers in this case were 1, 3, 5,

Volume 122 Number 2

s XB

9

9

XB

XA

3

XA

24

Fia. 3. Both strios (lead II) are continuous, showing S values of 9,9,3, and 24, consistent with the 3n form ofconcealed trigiminy. Abbreviations as in Fig. 1. -

7, and 9, and each of them could succeeditself, in contrast to the evennumbers.Either 4 or 8 could not succeeditself. These features somehow appear to obey someof the new rules of pure parasystole.6The rules derived from the pure parasystoledynamics are (1) for any ratio of sinus and ectopic pacemakerperiod, there are at most three different valuesof S; (2) one and only one of these three different values is odd; (3)if there arethree possiblevaluesof S, the sum of the two smaller values is one less than the larger value; (4) in any sequenceof S in which three values are possible, only one of these can succeed itself. These rules have been derived for two competing pacemakersand here the S values in Fig. 1 are the result of three competing pacemakers(onesinus and two ventricular ectopic pacemakers, i.e., XB and XA). Nevertheless,the most common odd S values was 3, which succeededitself more frequently than the other odd numbers.The triplets of 3,4, and 8 are characteristics of the dynamics of pure parasystole. S-XB intervals were also variable with fusions. The coupling interval of XA ectopics to the precedingdominant beetvaried from 0.40to 0.52second, and the interectopic (XA-XA) intervals were mathemetically related. The variation index of XA-XA intervals was 3.42,suggestinga regular parasystole.5 CaseNo. 2. In Fig. 2, the coupling interval of XA ectopics to the preceding sinus QRS complexesare fixed (0.48 second) and the interectopic intervals (XA-XA) had a variation index of 3.8. The coupling intervals of XB ectopics to the precedingsinus beat arealsofixed (0.44set), and the XB-XB intervals had a variation index of 2.2. The values of S between ventricular ectopic rhythms irrespective of type XA or XB satisfied the criteria for the 3n-2 form of concealedtrigeminy, i.e.,S = 1,4,7,10 . . . 31, and so on.3 The sinus R-R intervals varied from 0.88to 1 second. A low variation index 55 suggestsregular parasystole which, however,doesnot rule out a weak modulating influenceof sinus rhythm on the parasystolic focus5 Such a weakmodulation can be clinically sus-

petted when the ectopic rhythm shows an entreinment pattern, es will be discussedsubsequently. CaseNo. 3. In Fig. 3, the coupling interval of XA ectopics to the preceding sinus QRS complexesare fixed (0.40 second) and the interectopic intervals (XA-XA) had a variation index of 4.1, The coupling intervals of XB ectopiceare alaofixed (0.32second) and the interectopic intervals (XB-XB) had a variation index of 3.2. The valuesof S betweenventricular ectopic rhythms exclusiveof type XA or XB satisfied the criteria for the 3n form of csncealed trigeminy, i.e., S = 3,6, 9, 12 . . . 24, end so on3 The sinus R-R intervals varied from 0.52 to 0.80 second. The P wave configuration is variable, suggesting atrial ectopicsthat did not disturb the 3n sequence. The link betweenatrial and ventricular extrasystoles hasbeendescribedasanexpressionofmoduletedparasystole.7 DISCIJSSION

Concealedpatterned ventricular ectopic beating has been attributed both to the reentry213*8 and pacemaking mechanisms.l~4yg evidence now suggeststhat distribution of sinus beatsbetween ventricular ectopic rhythms is determined by complex electrotonic10-12and nonlinear interactionsf3 betweenthe sinus and ectopic ventricular pacemakers. Modulated parasystoleas a mechanism for concealedbigeminy has beeneloquently domonstreted.g Here the concealedrhythms arethe e%pressionof interaction betweenthree areasof a&omaticity-i.e., one sinus and two ventricular ectopic pacemakers. Double ventricular parasystole is a rare arrhythmiai4, l5 in which both parasyatolic foci have been shown to be deeply affected by extraneous impulses-one focussubjectto electrotonic modulation and the other to resetting by dominant rhythm, suggestingintermittent parasy&.ole.16 The precisemathematical distribution of sinus beats betweendouble ventricular ectopic rhythme in the casesdescribed here shows that the genesis of both the ectopic

472

Singh

impulses (XA and XB) is regular. S values described in all the cases can occur only in the presence of a defined parasystolic/sinus cycle length ratio and a definite phase-response curve of the ectopic pacemaker, characterized by critical variations of the parasystolic cycle in response to sinus impulses.g However, as described earlier, a phase-response curve could not be drawn. Concealed bigeminy as shown in Fig. 1 is maintained by double ventricular regular parasystole. This has therefore been explained by the dynamics of “pure parasystole” developed by Glass et a1.6 The shift from the 2n to the 2n-1 form of bigeminy always occurred due to double ventricular ectopic rhythms in succession. This is in keeping with the regularly discharging nature of double ventricular parasystole. Alternatively, the change alternating from the 2n to the 2n-1 forms might be explained by a change in the block in a reentrant 10op.~ According to the reentry model, three regions of block exist in the reentry loop to produce the 2n-1 rhythm by unifocal ventricular ectopics. To account for a shift to the 2n form, the existence of an additional site of block (phase 4 type) has been postulated. Such a complex electrophysiologic situation involving multiple blocks in the reentrant loop of both the ectopic ventricular foci governing the concealed bigeminy appears unlikely, however. The 3n-2 and 3n forms of concealed trigeminy in two other cases (Figs. 2 and 3) can only be explained by the nonlinear dynamics of the modulated parasystole developed by Courtemanche et alI3 The fixed coupling of ectopic rhythms XA and XB to the preceding dominant beats reflects a weak level of modulation that is taking place between the three pacemakers. This results in fixed coupling of both the XA and XB ectopics to the dominant beats. The interectopic intervals (XA-XA and XB-XB) in these cases had a very low variation index.5 It appears that weak interaction is not able to produce a significant change in the ectopic pacemaker period but is sufficient to give rise to an entrainment pattern that gives the S values of the 3n and 3n-2 forms of concealed trigeminy. These features reflect quasiperiodic dynamics,13 which is not fully consistent with the theoretic prediction because of complexities caused by triple pacemakers. In case No. 3 (Fig. 3), both the sinus and ectopic atrial beats could maintain the concealed trigeminy by double ventricular ectopics. Oreto et a17’ have described the link between atrial and ventricular ectopic activity. They were able to derive a biphasic phase-response curve in this respect, thus suggesting modulated parasystole. Observations in the present study support the automatic and bifocal origin of bidirectional ventricu-

American

August 1991 Heart Journal

lar tachycardia.l The postulated mechanisms for this arrhythmia have been summarized by Schamrothl as follows. Levy and Lewis in 1911 postulated that there are two ectopic ventricular foci discharging alternatively-the two QRS morphologies corresponding to two ventricular foci of impulse formation. This concept was supported by Schwensen in 1922 and by Felberbaum in 1923. Luten (1925) was, however, sceptical as to whether two ventricular foci could discharge with such regularity. Scherf and Kisch in 1939 likewise argued against this mechanism, since it would require the presence of a parasystolic protective block of both foci. Ventricular ectopics in most of the cases had extrasystolic and not parasystolic characteristics. These controversies were obviously due to the concept of parasystole as conceived by Kaufman and Rothberger.17 The concept of modulated parasystole lo-l2 has, however, revised the definition of both the parasystolic and extrasystolic rhythms. Studies have shown that both the rhythms are more or less linked to sinus rhythm. Further investigations have shown complex dynamics occurring with modulated parasystole due to nonlinear interaction between the sinus node and the ectopic ventricular focus.13 Recent studies6 have shown that even pure parasystole possesses dynamic subtleties. These investigations 5l 6 lo-l3 have provided invaluable clues for exploring the complex interactions between sinus and ectopic ventricular pacemakers. Concealed bigeminy and trigeminy by double ventricular ectopics suggest the need to extend the theoretical models of pure6 and modu.lated13 parasystole to characterize more complex interactions among the multiple pacemakers. Concealed ectopic ventricular rhythms, although described some 30 years ag~,~~plg still have several properties that remain elusive.lp 2o I thank Mr. H. K. Vatsa for technical assistance, Mr. S. Mazumdar for the photography, and Mr. C. L. Dhar for the artistic work.

REFERENCES

Schamroth L. The disorders of cardiac rhythm. 2nd ed. Oxford: Blackwell Scientific Publications Ltd, 1980. Levy MN, Adler DS, Levy JR. Three variants of concealed bigeminy. Circulation 1975;51:646-55. Levy MN, Mori I, Kerin N. Two variants of concealed trigeminy. AM HEART J 1977;93:183-8. Schamroth L, Martin DH, Pachter M. The extrasystolic mechanism as the entrainment of an oscillator. AM HEART J 1988;115:1363-8. 5. Oreto G, Satullo G, Luzza F, Donate A, Sacca CM, Arrigo F, Consolo F, Schamroth L. “Irregular” ventricular parasystole: the influence of sinus rhythm on a parasystolic focus. AM HEART

J 1988;115:121-33.

Glass L, Goldberger AL, Belair J. Dynamics of pure parasystole. Am J Physiol 1986;251:H841-7. 7. Oreto G, Satullo G, Luzza F. Concealed ventricular quad6.

Volume 122 Number 2

8.

9. 10. 11. 12.

13.

rigeminy linked to atria1 quadrigeminy: a manifestation of modulated parasystole. J Electrocardiol 1987;20:176-87. Kinoshita S, Takahashi K, Nakagawa K, Sagawa A, Tanabe Y, Kawasaki T. Mechanisms of concealed ventricular bigeminy: the concept of concealed conduction in the reentrant pathway. J Electrocardiol 1986;19:67-76. Oreto G. Luzza F. Satullo G. Schamroth L. Modulated ventricular parasystole as a mechanism for concealed bigeminy. Am J Cardiol 1986;58:954-8. Jalife J, Moe GK. Effects of electrotonic potentials on pacemaker activity of canine Purkinje fibers in relation to parasystole. Circ Res 1976;39:801-8. Moe GK, Jalife J, Mueller WJ, Moe B. A mathematical model of parasystole and its application to clinical arrhythmias. Circulation 1977;56:968-79. Antzelevitch C, Bernstein MJ, Feldman HN, Moe GK. Parasystole, reentry, and tachycardia: a canine preparation of cardiac arrhythmias occurring across inexcitable segments of tissues. Circulation 1983;68:1101-15. Courtemanche M, Glass L, Rosengarten MD, Goldberger AL. Beyond pure parasystole: promises and problems in modeling complex arrhythmias. Am J Physiol 1989;257:H693-706.

14. Chung EK. Douhlr

ventricular

parasystole.

Ah{ HEAK”I’

,J

1964;67:162-5. 15.

16. 17. 18.

19. 20.

Tenczer J, Littman L. Double irregular ventricular parasystole: rate-dependent entrance block and “Lupernormal” exit conduction. Circulation 1978;58:723-31. Oreto G. Donato A. Satullo G. Schamroth 1,. Double ventricular parasystole with modulation and intermittenry. Am .J Cardiol 1988;62:655-7. Kaufman R, Rothberger CJ. Beitrage zur Kenntnis der Entstehungsweise extrasystolischer allorhythmien. % Ges Exp Med 1917;5:349-70. Satoh T, Kinoshita S, Tanabe Y, Kawasaki T. Katou K, Oda M, Yamamoto K, Kamada H, Yoshida T. Impulse conduct.ivity in the region surrounding the extrasystolic focus: Wenckebath phenomenon of the coupling intervals and the “rule of multiples” (in Japanese). Saishin-Igaku 1960;15:1865-70. Schamroth L, Marriot HJL. Intermittent ventricular parasystole with observations on its relationship to ent rasystolic bigeminy. Am J Cardiol 1961;7:79!3-809. Singh VK. Progressively decreasing ectoplc to second sinus beat intervals in concealed trigeminy. .I F:lectrocardiol 1987;20:284-6.

are unaltered by vemtridar e reduction in heart f Exacerbatton of heart faiture may increase susceptibility to arrhythmias. Therefore tests to assess the rkk of arrhythmia, performed after hemodynamic improvement, may be of limited vdue. To determine whether hemodynamic improvement alters ventricuiar late potenthais detected by signabaveraged ECG, we studkd 27 consecutive patient8 wtth dilated heart failure (left verttricukr eJection fraction 0.20 + 0.06, 15 with coronary aftery dkease) before and 3 rt 2 days aftor tailored vasoditator and diuretic therapy reduced ventricular f#fting pressures. GRS d~ation, terRllnal G#?S amplitude (root mean square [RMS)), and low-amptitude (<40 PV) signal (LAS) duration were determined by an automated algorithm from the vector magnitude of the GRS ht@+paes ftttared at 25 HE and at 40 Hz. Despite marked decreases in pulmonary capillary wedge (27 + 7 to 10 2 5 mm Hg, p < 0.001) and right atrial (13 k 7 to 7 I 4 mm Hg, p < 0.001) pressures and a 20% increase in cardiac output, there was not a significant change in QRS or LAS. Before and after therapy late potentials, defined 88 abnormal GRS duration, dwration iWS,‘or LAS, were present in 14 (52%) patients with fifteflng at 25 Hz and in 22 (81%) patter@ wrth ffltering at 40 Hx. The slgnal-averaged EC0 after hemodynamic Improvement predtcted the reeutts during exacerbation of heart failure in all pattents. Thus in patients with advanced heert falkrre the signal-averaged ECG obtained after hemodynamic improvement reflects the findings during exacerbation of heart failure. (AM HEART J lgg1;122:473.)

William G. Stevenson, MD, Mary A. Woo, MN, RN, Debra K. Moser, MN, RN, and Lynne W. Stevenson, MD. Los Angeles, Calif.

From the Department

of Medicine,

Division

of Cardiology,

UCLA

School of

Medicine. Received

for publication

Sept. 18, 1990; accepted

Feb. 15, 1991.

Reprint requests: William G. Stevenson, MD, 10833 Le Conte Ave., Division of Cardioloev.-” IJCLA. CHS 47.123. Los An&es. CA 90024-1679. 4/1/298i32

Patients with advanced heart failure are at high risk for ventricular arrhythmias and sudden death.l, 2 One of the substrates for reentrant ventricular arrhythm& is slow conduction in the myocardial scar. Areas of slow conduction can be detected noninva473