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Mechanism of ventricular extrasystoles with fixed coupling
Mechanism of VentricularExtrasystoles With Fixed Coupling A Theoretical Model Derived From the Concept of Longitudinal Dissociation in the Reentrant Pathway of Extrasystoles
Shinji Kinoshita, MD, Go Konishi, PharmB, and York0 Kinoshita, PharmM
Abstract: An electrocardiogram taken from a 29-year-old man with old myocardial infarction is presented as an exemplary case of ventricular extrasystoles with fured 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 fued coupling. Pan 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. Key words: ventricular extrasystole, fured coupling, longitudinal dissociation. reentry, concealed extrasystole.
It is known that in ventricular extrasystoles, the range of coupling intervals to the preceding sinus QRS complexes is usually narrow, namely, coupling intervals are almost fixed. In cases of ventricular concealed bigeminy, with short and somewhat variable coupling intervals, it has been suggested that when coupling intervals of extrasystoles gradually shorten, extrasystoles disappear because coupling intervals
become shorter than the effective refractory period of ordinary ventricular myocardium. ‘f2 On the other hand, there are many cases of intermittent ventricular bigeminy in which coupling intervals of extrasystoles are aImost fixed and much longer than QT intervals of the preceding sinus QRS compiexes, In such cases, disappearance of extrasystoles carmot be explained by gradual shortening of coupling intervals. In this article, we present an exemplary case of inte~ittent ventricular bigeminy in which coupling intervals are usually fixed and much longer than QT
From the Health Administration Center, Hokkaido University, Sapand the Hokkaido Institute of ~ha~ace~ticai Sciences, &am.
pore,
Reprintrequests; Shinji Kinoshita, MD, Health Ad~nistration Center. Hokkaido University, Sapporo 060, Japan.
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of Electrocardiology
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intervals of the preceding sinus QRS complexes. In a previous paper,3 a theoretical model for reentrant extrasystoles was derived from the concepts of “longitudinal dissociation” and “electrotonically mediated conduction.” In this article, to explain the mechanism of ventricular extrasystoles with fixed coupling, a theoretical model similar to Kinoshita’s is derived from the concept of longitudinal dissociation in the reentrant pathway of extrasystoles.
Case Report Electrocardiograms were taken from a 29-year-old man with old inferior myocardial infarction. During the recording, he was not receiving antiarrhythmic therapy. Figure 1 shows parts of a long continuous recording in which ventricular extrasystoles are frequently seen. The first three strips are continuous and the last two strips are continuous. The sinus rate during the recording was usually slower than 8 1 beats/mm. The first three strips show that in such a sinus rate, coupling intervals of the extrasystoles are fixed to 0.53 set, which is much longer than the sinus QT interval. When the sinus rate ranges between 66 and 81 beats/min, a sinus QRS complex is always followed by an extrasystole with a fixed coupling of 0.5 3 set, namely, ventricular
bigeminy continues, as seen in the top strip. In the second strip, when the sinus rate gradually decreases below 66 beats/min, a sinus QRS complex, Slo, abruptly fails to be followed by an extrasystole, without gradual shortening of coupling intervals of the preceding extrasystoles. In the latter half of the second strip, temporary sinus arrest is seen, which was caused by vagal stimulation due to pressure on the eyeball. This indicates the absence of parasystole. The sinus rate in this case sometimes increased beyond 81 beats/mm. The last two strips show that in such a sinus rate, coupling intervals of extrasystoles progressively lengthen beyond 0.53 set until a sinus QRS complex fails to be followed by an extrasystole. This suggests that Wenckebach block occurs in the pathway of extrasystolic impulses, though Wenckebach periodicity is somewhat atypical.4 In such a rapid sinus rate, the interectopic interval during ventricular bigeminy, XSX, is always 1.48 (or 1.49) set, which is the shortest XSX interval in Figure 1.
Figure 2 summarizes the relationship of XS intervals to the occurrence of the subsequent extrasystoles. XS represents the interval between an extrasystole and the following sinus QRS complex. When an XS interval is shorter than 0.84 set (the first three strips of Fig. 2), the sinus QRS complex, S, fails to be followed by an extrasystole, probably
: 164= 16+148 j
Fig. 1. Intermittent ventricular bigeminy. The first three strips are continuous and the last two strips are continuous. In this and Figure 2, time intervals are expressed in hundredths of a second. In the strips, numerals without parentheses represent coupling intervals of extrasystoles to the preceding sinus QRS complexes, and numerals in parentheses represent intervals between an extrasystole and the following sinus QRS complex. When manifest bigeminy discontinues, alternating Wenckebach periodicity’0-12 may occur in the dual pathways. S, sinus QRS complex; X, manifest ventricular extrasystole; (X) , concealed ventricular extrasystole.
Extrasystoles With Fixed Coupling
Pig. 2. Relationship
of XS intervals to the occurrence of the subsequent extrasystoles. S, sinus QRS complex; X, manifest ventricular extrasystole; (X) concealed ventricular extrasystole.
the following extrasystolic impulse is blocked in the pathway of extrasystolic impulses. When an XS interval is 0.84-0.95 set (the fourth to sixth strips), the sinus complex, S, is followed by an extrasystole with a variable coupling of 0.53-0.64 set, whereas the XSX interval is a constant value of 1.48 sec. When an XS interval is 0.95-1.28 set (the seventh to ninth strips), the sinus compIex, S, is followed by an extrasystole with a fixed coupbng of 0.53 sec. When an XS interval is longer than 1.28 set (the last three strips), the sinus complex, S, fails to be followed by a manifest extrasystole. In other words, when XS intervals gradually lengthen, a sinus QRS because
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complex abruptly fails to be followed by a manifest extrasystole wi~out gradual shortening of coupling intervals of the preceding extrasystoles. This suggests that such a sinus QRS complex is also followed by an extrasystole (eg, a concealed extrasystole, (X1,), in the second strip of Fig. 1) though its coupling interval is shorter than the sinus QT interval and the extrasystole fails to become manifest. In the third strip of Figure 1, the first sinus QRS complex, S 1I, appears to be followed by a concealed extrasystole, (X, 1), in the same way as in S to of the second strip. The S 1lXla interval is 1.64 set, which exceeds the shortest XSX interval of 1.48 set by only 0.16 sec. This suggests that the coupling interval of the concealed extrasystole, (X1,), is much shorter than the fixed coupling (0.53 set) of manifest extrasystoles. Thus it appears that, in the second strip of Figure 1, the last sinus QRS complex, So, abruptIy faiIs to be followed by a manifest extrasystole because of sudden and marked shortening of the coupling interval of the following extrasystole, (X,,). The above relationship of XS intervals to the disappearance or reappearance of the subsequent manifest extrasystoles was also seen in electrocardiograms taken on other days. In the electrocardiograms, bradycardia-dependent disappearance of manifest extrasystoles was seen without vagal stimulation. In one, the even-numbered variant of concealed bigeminy was seen, which is the same form as in a previous case reported by Kinoshita. ’ The above findings strongly suggest the possibility that sudden and marked sho~e~ng of the conduction time occurs in the reentrant pathway of extrasystoIes. As was suggested in cases of periodic variation in atrioventricular (AV) conduction time,4-6 such sudden shortening or lengthening appears to be caused by longitudinal dissociation in the pathway.
The Theoretical Model Figure 3 shows the theoretical model derived from the concept of longitudinal dissociation in the reentrant pathway of ventricular extrasystoles. These diagrams represent impulse conduction in the reentrant pathway. In the pathway, excitability is much depressed and the degree of depression is inhomogeneous in both the transverse and longitudinal directions. In C and D, functional longitudinal dissociation divides the pathway into dual pathways F and S. Sinus impulses coming from above cannot enter the pathway, because of unidirectional block. On the
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Fig. 3. The mechanism
of extrasystoles but become concealed extrasystoles because of insu~cient conduction delay in the pathway. Figure 3A shows that one of such alternate sinus impulses passes through both of dual pathways F and S and that summation or interference of impulses traveling along pathways F and S hastens the impulse conduction in the pathways. Thus, conduction delay in the pathway is not enough for the sinus impulse to exit through the site of unidirectional block, and it becomes a concealed extrasystole. Figure 3B shows that the next sinus impulse is blocked in both pathways F and S after invading some portions of the pathways because the longest effective refractory periods in pathways F and S are both longer than one sinus cycle during the concealed bigeminal rhythm.2
of ventricular extrasystoles with fured coupling. Functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. Slow conduction is represented by zigzag lines. other hand, sinus impulses coming from below can enter the pathway, though the effective refractory periods for the impulses are abnormally prolonged, because impulses are electrotonically propagated across inexcitable gaps, as in Kinoshita’s mode1.3 The longest refractory period in pathway F is considerably longer than that in pathway S.
Mechanism of Ventricular Extrasystoles With Fixed Coupling Figure 3 demonstrates the mechanism ular extrasystoles with fixed coupling.
of ventric-
Concealed Extrasystoles In concealed bigeminal rhythm,2 when manifest extrasystoles are not found for a long time, alternate sinus impulses pass through the reentrant pathway
Figure 3C shows that when the sinus impulse next to that in Figure 3A occurs somewhat later than that in Figure 3B, this impulse falls after the longest refractory period in pathway S though the impulse falls in the Iongest refractory period in pathway F. Thus, functional longitudinal dissociation occurs and the impulse travels very slowly only through pathway S without summation or interference of impulses. As a result, the impulse passes through pathway S with enough conduction delay to exit through the site of unidirectional block and becomes a manifest extrasystole (eg, extrasystole Xl2 in the third strip). Part of the impulse passing through pathway S enters pathway F retrogradely. In a comparatively slow sinus rate, the sinus impulse conducted to the ventricles next to that in Figure 3C falls after the longest refractory period in pathway S and passes through pathway S again because of the presence of a compensator pause. On the other hand, this sinus impulse is blocked in pathway F again because it fails in the effective refractory period following the retrograde impulse conduction in Figure 3C. Thus, in such a sinus rate, once a manifest extrasystole appears, manifest bigeminy continues for some time. Though conduction times for impulses to pass through pathway S are considerably long in such a slow sinus rate, they are invariable because the sinus impulses fall considerably after the longest effective refractory period in pathway S. Such a sudden transition from a period of short conduction times to a period of long invariable conduction times is similar to that in cases of periodic variation in AV conduc-
Extrasystoles With Fixed Coupling
tion time probably caused by longitudinal AV dissociation.6 This suggests that longitudinal dissociation occurs in the reentrant pathway of ventricular bigeminal extrasystoles with fixed, long couplings (eg, the bigeminy in the first strip of Fig. 1). Bradycardia-dependent Disappearance of Manifest Extrasystoles When the sinus rate becomes even slower than that during the bigeminy with fixed coupling, the sinus impulse next to that in Figure 3C falls after both of the longest effective refractory periods in pathways F and S. Thus the impulse passes through both of the dual pathways and becomes a concealed extrasystole, as shown in Figure 3A (eg, extrasystole (X,,) in the second strip of Fig. 1). Such a sudden change from a period of long conduction times to a period of short conduction times is also similar to that in cases of periodic variation in AV conduction time.6 Wenckbach Block in the Reentrant Pathway When, on the other hand, the sinus rate increases beyond a certain critical value, conduction times in pathway S in Figure 3C progressively lengthen until a sinus impulse is blocked in pathway S, as shown in Figure 3B; namely, Wenckebach block occurs in pathway S (eg, in the last two strips of Fig. 1). The Wenckeba~h periodicity here is somewhat atypical; namely, interectopic intervaIs during the bigeminy (XSX intervals) are invariable. In typical AV Wenckebach periodicity, the first RR interval is longest in a period between two blocked P waves, in which the AV refractory period following the first conducted impulse is the longest because the preceding interval between conducted impulses is much longer than the others. On the contrary, the findings in previous cases of tachycardia-dependent bundIe branch block have suggested that the length of the abnormally long refractory period in a pathway of the ventricular conduction system is independent of changes in the preceding interval between conducted impulses. ‘*’ This may explain the occurrence of invariable XSX intervah in the Wenckebach pe~odicity here. Initiation of Ventricular Tachycardia Figure 3C shows that in usual cases, the impulse retrogradely traveling along pathway F fails to reen-
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ter pathway S because the refractory period of pathway S is abno~ally long. Figure 3D shows that in some cases, when the retrogradely conducted impulse falls in the supernormal period of pathway S, it reenters pathway S and initiates a ventricular couplet or tachycardia, as in Kinoshita’s model.’ (In the case reported in this study, ventricular couplets or tachycardia was not found).
Discussion For ventricular extrasystoles with fixed coupling to originate in the reentrant pathway, the conduction times in the pathway must be invariable and markedly long beyond the effective refractory period of ordinary ventricular myocardium. In previous cases of periodic variation in AV conduction time,” it was demonstrated that sudden changes occurred between a period of short conduction times and a period of markedly long and almost invariable conduction times. It appeared that such sudden changes were caused by Iongitudinal dissociation in the AV node. The findings in these previous cases and the case reported here strongly suggest the possibility that sudden and marked changes in conduction time occur in the reentrant pathway of ventricular extrasystoles with fixed coupling because of longitudinal dissociation in the pathway. It seems that in the reentrant pathway of such extrasystoles, not only the conduction time but also the refractory period is markedly long. The longest effective refractory period in the pathway is usually longer than one sinus cycle2; namely, it is abnormally prolonged much beyond the action potential duration of ordinary ventricular myocardium. It is suggested that such markedly depressed refractoriness and conductivity in the reentrant pathway are caused by electrotonically mediated impulse propagation across much depressed regions in the pathway, as in a biological model of Jalife and h4oe.9 In the reentrant pathway of ventricular extrasystoles, the degree of depression in excitability is inhomogeneous. Thus, multilevel block2,‘o-‘2 and longitudinal dissociation”,i4 in the pathway are caused by inhomogeneous excitability. Part of the impulse passing through one of the dual pathways (pathway S) enters the other pathway (pathway F) retrogradely, but thereafter it usually fails to reenter pathway S because of markedly long refractoriness in the pathway. For ventricular couplets or tachycardia to be initiated by reentry in the dual pathways, the retrogradely conducted impulse must fall in the supernormal period of pathway S.3,‘4 In a case of tachy-
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cardia-dependent bundle branch block, Kinoshita” showed that the supernormal period was found in the abnormally long effective refractory period of a bundle branch. It seems that the theoretical model in this study satisfactorily explains the mechanism of ventricular extrasystoles with fixed coupling _ _ and the initiation of ventricular tachycardia.
References 1. Kinoshita S: Concealed ventricular extrasystoles due to interference and due to exit block. Circulation 52:230, 1975 2. Kinoshita S, Takahashi K, Nakagawa K et al: Mechanism of concealed ventricular bigeminy: the concept of concealed conduction in the reentrant pathway. J Electrocardiol 19:67, 1986 3. Kinoshita S: Mechanisms of ventricular arrhythmias: a theoretical model derived from the concepts of “electrotonic interaction” and “longitudinal dissociation.” Am J Cardiol 52:1350, 1983 4. Kinoshita S, Konishi G: Atrioventricular Wenckebach periodicity in athletes: influence of increased vagal tone on the occurrence of atypical periods. J Electrocardiol 20:272, 1987 5. Schamroth L, Perlman MM: Periodic variation in AV conduction time: the “supernormal” phase of A-V conduction: a study in differential dual A-V pathway conductivity and refractoriness. J Electrocardiol6:8 1, 1973 6. Kinoshita S, Kawasaki T, Fujiwara S, Okimori K: Pe-
7.
8.
9.
10.
11.
12.
13. 14.
15.
riodic variation in atrioventricular conduction time: mechanisms of initiation, maintenance and termination of periods of long PR intervals. Am J Cardiol 53:1288, 1984 Denes P, Wu D, Dhingra RC et al: Electrophysiological observations in patients with rate dependent bundle branch block. Circulation 5 1:244, 1975 Kinoshita S: Variations in the critical cycle length inducing rate dependent bundle branch block. Am Heart J 96:54, 1978 Jalife J, Moe GK: Excitation, conduction, and reflection of impulses in isolated bovine and canine cardiac Purkinje fibers. Circ Res 49:233, 1981 Kinoshita S, Fujita K, Kawaguchi H et al: Concealed (proximal) Wenckebach phenomenon with distal 2 : 1 exit block in the ectopic-ventricular junction. Chest 73: 198, 1978 Kinoshita S, Kurokawa S, Ohnishi S, Oyama Y: Type A alternating Wenckebach periodicity in the re-enn-ant path of ventricular extrasystoles. J Electrocardiol 13:285, 1980 Kinoshita S, Konishi G, Kawasaki T: Type A alternating Wenckebach periodicity in the reentrant pathway of interpolated ventricular extrasystoles. Cardiology 75440, 1988 Kinoshita S, Fujita K, Kanda K et al: A cause of paired ventricular extrasystoles. Circulation 60: 1395, 1979 Kinoshita S, Kato Y, Kawasaki T, Okimori K: Ventricular tachycardia initiated by late-coupled ventricular extrasystoles: the concept of longitudinal dissociation in the microreentry pathway. Am Heart J 103: 1090, 1982 Kinoshita S: Mechanism of tachycardia-dependent bundle branch block. Am J Cardiol 53: 1456, 1984
Shinji Kinoshita, MD, Go Konishi, PharmB, and York0 Kinoshita, PharmM
Abstract: An electrocardiogram taken from a 29-year-old man with old myocardial infarction is presented as an exemplary case of ventricular extrasystoles with fured 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 fued coupling. Pan 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. Key words: ventricular extrasystole, fured coupling, longitudinal dissociation. reentry, concealed extrasystole.
It is known that in ventricular extrasystoles, the range of coupling intervals to the preceding sinus QRS complexes is usually narrow, namely, coupling intervals are almost fixed. In cases of ventricular concealed bigeminy, with short and somewhat variable coupling intervals, it has been suggested that when coupling intervals of extrasystoles gradually shorten, extrasystoles disappear because coupling intervals
become shorter than the effective refractory period of ordinary ventricular myocardium. ‘f2 On the other hand, there are many cases of intermittent ventricular bigeminy in which coupling intervals of extrasystoles are aImost fixed and much longer than QT intervals of the preceding sinus QRS compiexes, In such cases, disappearance of extrasystoles carmot be explained by gradual shortening of coupling intervals. In this article, we present an exemplary case of inte~ittent ventricular bigeminy in which coupling intervals are usually fixed and much longer than QT
From the Health Administration Center, Hokkaido University, Sapand the Hokkaido Institute of ~ha~ace~ticai Sciences, &am.
pore,
Reprintrequests; Shinji Kinoshita, MD, Health Ad~nistration Center. Hokkaido University, Sapporo 060, Japan.
249
250
Journal
of Electrocardiology
Vol. 23 No. 3 July 1990
intervals of the preceding sinus QRS complexes. In a previous paper,3 a theoretical model for reentrant extrasystoles was derived from the concepts of “longitudinal dissociation” and “electrotonically mediated conduction.” In this article, to explain the mechanism of ventricular extrasystoles with fixed coupling, a theoretical model similar to Kinoshita’s is derived from the concept of longitudinal dissociation in the reentrant pathway of extrasystoles.
Case Report Electrocardiograms were taken from a 29-year-old man with old inferior myocardial infarction. During the recording, he was not receiving antiarrhythmic therapy. Figure 1 shows parts of a long continuous recording in which ventricular extrasystoles are frequently seen. The first three strips are continuous and the last two strips are continuous. The sinus rate during the recording was usually slower than 8 1 beats/mm. The first three strips show that in such a sinus rate, coupling intervals of the extrasystoles are fixed to 0.53 set, which is much longer than the sinus QT interval. When the sinus rate ranges between 66 and 81 beats/min, a sinus QRS complex is always followed by an extrasystole with a fixed coupling of 0.5 3 set, namely, ventricular
bigeminy continues, as seen in the top strip. In the second strip, when the sinus rate gradually decreases below 66 beats/min, a sinus QRS complex, Slo, abruptly fails to be followed by an extrasystole, without gradual shortening of coupling intervals of the preceding extrasystoles. In the latter half of the second strip, temporary sinus arrest is seen, which was caused by vagal stimulation due to pressure on the eyeball. This indicates the absence of parasystole. The sinus rate in this case sometimes increased beyond 81 beats/mm. The last two strips show that in such a sinus rate, coupling intervals of extrasystoles progressively lengthen beyond 0.53 set until a sinus QRS complex fails to be followed by an extrasystole. This suggests that Wenckebach block occurs in the pathway of extrasystolic impulses, though Wenckebach periodicity is somewhat atypical.4 In such a rapid sinus rate, the interectopic interval during ventricular bigeminy, XSX, is always 1.48 (or 1.49) set, which is the shortest XSX interval in Figure 1.
Figure 2 summarizes the relationship of XS intervals to the occurrence of the subsequent extrasystoles. XS represents the interval between an extrasystole and the following sinus QRS complex. When an XS interval is shorter than 0.84 set (the first three strips of Fig. 2), the sinus QRS complex, S, fails to be followed by an extrasystole, probably
: 164= 16+148 j
Fig. 1. Intermittent ventricular bigeminy. The first three strips are continuous and the last two strips are continuous. In this and Figure 2, time intervals are expressed in hundredths of a second. In the strips, numerals without parentheses represent coupling intervals of extrasystoles to the preceding sinus QRS complexes, and numerals in parentheses represent intervals between an extrasystole and the following sinus QRS complex. When manifest bigeminy discontinues, alternating Wenckebach periodicity’0-12 may occur in the dual pathways. S, sinus QRS complex; X, manifest ventricular extrasystole; (X) , concealed ventricular extrasystole.
Extrasystoles With Fixed Coupling
Pig. 2. Relationship
of XS intervals to the occurrence of the subsequent extrasystoles. S, sinus QRS complex; X, manifest ventricular extrasystole; (X) concealed ventricular extrasystole.
the following extrasystolic impulse is blocked in the pathway of extrasystolic impulses. When an XS interval is 0.84-0.95 set (the fourth to sixth strips), the sinus complex, S, is followed by an extrasystole with a variable coupling of 0.53-0.64 set, whereas the XSX interval is a constant value of 1.48 sec. When an XS interval is 0.95-1.28 set (the seventh to ninth strips), the sinus compIex, S, is followed by an extrasystole with a fixed coupbng of 0.53 sec. When an XS interval is longer than 1.28 set (the last three strips), the sinus complex, S, fails to be followed by a manifest extrasystole. In other words, when XS intervals gradually lengthen, a sinus QRS because
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complex abruptly fails to be followed by a manifest extrasystole wi~out gradual shortening of coupling intervals of the preceding extrasystoles. This suggests that such a sinus QRS complex is also followed by an extrasystole (eg, a concealed extrasystole, (X1,), in the second strip of Fig. 1) though its coupling interval is shorter than the sinus QT interval and the extrasystole fails to become manifest. In the third strip of Figure 1, the first sinus QRS complex, S 1I, appears to be followed by a concealed extrasystole, (X, 1), in the same way as in S to of the second strip. The S 1lXla interval is 1.64 set, which exceeds the shortest XSX interval of 1.48 set by only 0.16 sec. This suggests that the coupling interval of the concealed extrasystole, (X1,), is much shorter than the fixed coupling (0.53 set) of manifest extrasystoles. Thus it appears that, in the second strip of Figure 1, the last sinus QRS complex, So, abruptIy faiIs to be followed by a manifest extrasystole because of sudden and marked shortening of the coupling interval of the following extrasystole, (X,,). The above relationship of XS intervals to the disappearance or reappearance of the subsequent manifest extrasystoles was also seen in electrocardiograms taken on other days. In the electrocardiograms, bradycardia-dependent disappearance of manifest extrasystoles was seen without vagal stimulation. In one, the even-numbered variant of concealed bigeminy was seen, which is the same form as in a previous case reported by Kinoshita. ’ The above findings strongly suggest the possibility that sudden and marked sho~e~ng of the conduction time occurs in the reentrant pathway of extrasystoIes. As was suggested in cases of periodic variation in atrioventricular (AV) conduction time,4-6 such sudden shortening or lengthening appears to be caused by longitudinal dissociation in the pathway.
The Theoretical Model Figure 3 shows the theoretical model derived from the concept of longitudinal dissociation in the reentrant pathway of ventricular extrasystoles. These diagrams represent impulse conduction in the reentrant pathway. In the pathway, excitability is much depressed and the degree of depression is inhomogeneous in both the transverse and longitudinal directions. In C and D, functional longitudinal dissociation divides the pathway into dual pathways F and S. Sinus impulses coming from above cannot enter the pathway, because of unidirectional block. On the
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B
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v D
C
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Manifest Extrasystoles With Fixed Coupling
I
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Fig. 3. The mechanism
of extrasystoles but become concealed extrasystoles because of insu~cient conduction delay in the pathway. Figure 3A shows that one of such alternate sinus impulses passes through both of dual pathways F and S and that summation or interference of impulses traveling along pathways F and S hastens the impulse conduction in the pathways. Thus, conduction delay in the pathway is not enough for the sinus impulse to exit through the site of unidirectional block, and it becomes a concealed extrasystole. Figure 3B shows that the next sinus impulse is blocked in both pathways F and S after invading some portions of the pathways because the longest effective refractory periods in pathways F and S are both longer than one sinus cycle during the concealed bigeminal rhythm.2
of ventricular extrasystoles with fured coupling. Functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. Slow conduction is represented by zigzag lines. other hand, sinus impulses coming from below can enter the pathway, though the effective refractory periods for the impulses are abnormally prolonged, because impulses are electrotonically propagated across inexcitable gaps, as in Kinoshita’s mode1.3 The longest refractory period in pathway F is considerably longer than that in pathway S.
Mechanism of Ventricular Extrasystoles With Fixed Coupling Figure 3 demonstrates the mechanism ular extrasystoles with fixed coupling.
of ventric-
Concealed Extrasystoles In concealed bigeminal rhythm,2 when manifest extrasystoles are not found for a long time, alternate sinus impulses pass through the reentrant pathway
Figure 3C shows that when the sinus impulse next to that in Figure 3A occurs somewhat later than that in Figure 3B, this impulse falls after the longest refractory period in pathway S though the impulse falls in the Iongest refractory period in pathway F. Thus, functional longitudinal dissociation occurs and the impulse travels very slowly only through pathway S without summation or interference of impulses. As a result, the impulse passes through pathway S with enough conduction delay to exit through the site of unidirectional block and becomes a manifest extrasystole (eg, extrasystole Xl2 in the third strip). Part of the impulse passing through pathway S enters pathway F retrogradely. In a comparatively slow sinus rate, the sinus impulse conducted to the ventricles next to that in Figure 3C falls after the longest refractory period in pathway S and passes through pathway S again because of the presence of a compensator pause. On the other hand, this sinus impulse is blocked in pathway F again because it fails in the effective refractory period following the retrograde impulse conduction in Figure 3C. Thus, in such a sinus rate, once a manifest extrasystole appears, manifest bigeminy continues for some time. Though conduction times for impulses to pass through pathway S are considerably long in such a slow sinus rate, they are invariable because the sinus impulses fall considerably after the longest effective refractory period in pathway S. Such a sudden transition from a period of short conduction times to a period of long invariable conduction times is similar to that in cases of periodic variation in AV conduc-
Extrasystoles With Fixed Coupling
tion time probably caused by longitudinal AV dissociation.6 This suggests that longitudinal dissociation occurs in the reentrant pathway of ventricular bigeminal extrasystoles with fixed, long couplings (eg, the bigeminy in the first strip of Fig. 1). Bradycardia-dependent Disappearance of Manifest Extrasystoles When the sinus rate becomes even slower than that during the bigeminy with fixed coupling, the sinus impulse next to that in Figure 3C falls after both of the longest effective refractory periods in pathways F and S. Thus the impulse passes through both of the dual pathways and becomes a concealed extrasystole, as shown in Figure 3A (eg, extrasystole (X,,) in the second strip of Fig. 1). Such a sudden change from a period of long conduction times to a period of short conduction times is also similar to that in cases of periodic variation in AV conduction time.6 Wenckbach Block in the Reentrant Pathway When, on the other hand, the sinus rate increases beyond a certain critical value, conduction times in pathway S in Figure 3C progressively lengthen until a sinus impulse is blocked in pathway S, as shown in Figure 3B; namely, Wenckebach block occurs in pathway S (eg, in the last two strips of Fig. 1). The Wenckeba~h periodicity here is somewhat atypical; namely, interectopic intervaIs during the bigeminy (XSX intervals) are invariable. In typical AV Wenckebach periodicity, the first RR interval is longest in a period between two blocked P waves, in which the AV refractory period following the first conducted impulse is the longest because the preceding interval between conducted impulses is much longer than the others. On the contrary, the findings in previous cases of tachycardia-dependent bundIe branch block have suggested that the length of the abnormally long refractory period in a pathway of the ventricular conduction system is independent of changes in the preceding interval between conducted impulses. ‘*’ This may explain the occurrence of invariable XSX intervah in the Wenckebach pe~odicity here. Initiation of Ventricular Tachycardia Figure 3C shows that in usual cases, the impulse retrogradely traveling along pathway F fails to reen-
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ter pathway S because the refractory period of pathway S is abno~ally long. Figure 3D shows that in some cases, when the retrogradely conducted impulse falls in the supernormal period of pathway S, it reenters pathway S and initiates a ventricular couplet or tachycardia, as in Kinoshita’s model.’ (In the case reported in this study, ventricular couplets or tachycardia was not found).
Discussion For ventricular extrasystoles with fixed coupling to originate in the reentrant pathway, the conduction times in the pathway must be invariable and markedly long beyond the effective refractory period of ordinary ventricular myocardium. In previous cases of periodic variation in AV conduction time,” it was demonstrated that sudden changes occurred between a period of short conduction times and a period of markedly long and almost invariable conduction times. It appeared that such sudden changes were caused by Iongitudinal dissociation in the AV node. The findings in these previous cases and the case reported here strongly suggest the possibility that sudden and marked changes in conduction time occur in the reentrant pathway of ventricular extrasystoles with fixed coupling because of longitudinal dissociation in the pathway. It seems that in the reentrant pathway of such extrasystoles, not only the conduction time but also the refractory period is markedly long. The longest effective refractory period in the pathway is usually longer than one sinus cycle2; namely, it is abnormally prolonged much beyond the action potential duration of ordinary ventricular myocardium. It is suggested that such markedly depressed refractoriness and conductivity in the reentrant pathway are caused by electrotonically mediated impulse propagation across much depressed regions in the pathway, as in a biological model of Jalife and h4oe.9 In the reentrant pathway of ventricular extrasystoles, the degree of depression in excitability is inhomogeneous. Thus, multilevel block2,‘o-‘2 and longitudinal dissociation”,i4 in the pathway are caused by inhomogeneous excitability. Part of the impulse passing through one of the dual pathways (pathway S) enters the other pathway (pathway F) retrogradely, but thereafter it usually fails to reenter pathway S because of markedly long refractoriness in the pathway. For ventricular couplets or tachycardia to be initiated by reentry in the dual pathways, the retrogradely conducted impulse must fall in the supernormal period of pathway S.3,‘4 In a case of tachy-
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Vol. 23 No. 3 July 1990
cardia-dependent bundle branch block, Kinoshita” showed that the supernormal period was found in the abnormally long effective refractory period of a bundle branch. It seems that the theoretical model in this study satisfactorily explains the mechanism of ventricular extrasystoles with fixed coupling _ _ and the initiation of ventricular tachycardia.
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