- Email: [email protected]
Apparent bradycardia-dependent right bundle branch block associated with atypical atrioventricular wenckebach periodicity as a possible mechanism
Journal of Electrocardiology Vol. 36 No. 4 2003
Case Report
Apparent Bradycardia-dependent Right Bundle Branch Block Associated With Atypical Atrioventricular Wenckebach Periodicity as a Possible Mechanism Shinji Kinoshita, MD, Takakazu Katoh, MD, Yoshinori Tsujimura, MD, and Yoshihiko Sasaki, MT
Abstract: The Holter monitor electrocardiogram was taken from a 15-year-old male athlete. Intermittent right bundle branch block frequently occurred at rest. When sinus cycles gradually lengthened, sinus impulses were conducted to the ventricles with right bundle branch block (RBBB) in succession. When, thereafter, sinus cycles gradually shortened, sinus impulses were conducted without RBBB. However, it seems that these findings do not show true bradycardia-dependent RBBB. Atypical atrioventricular Wenckebach periodicity was occasionally found in which sudden shift from the period of comparatively short PR intervals to the period of long PR intervals occurred. In the Wenckebach periodicity, when a QRS complex occurs after a much longer pause, RBBB was not found, while when it occurs after a much shorter period, RBBB was found. This suggests that this case may be apparent bradycardia-dependent RBBB, namely, a form of tachycardiadependent RBBB. This is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles, as a possible mechanism. Key words: Apparent bradycardia-dependent block, atypical Wenckebach periodicity, right bundle branch block, tachycardiadependent block, atrioventricular block.
In our previous reports on tachycardia-dependent bundle branch block (1– 4), it was shown that when sinus cycles gradually shortened below a
critical period, a sinus impulse fell in the abnormally long effective refractory period of a bundle branch, and was blocked in the bundle branch. On the other hand, we reported that apparent bradycardia-dependent block occurred in some cases of atypical atrioventricular (AV) Wenckebach periodicity associated with longitudinal AV dissociation (5,6). In those cases, when sinus cycles gradually lengthened, the effective refractory period of the fast AV pathway was markedly prolonged beyond the sinus cycle length. As a result, a sinus
From the Hokkaido Women’s University, Ebetsu, Hokkaido; Katoh Cardiovascular Clinic, Ohtsu; Division of Cardiology and Division of Hemodialysis, Ohtsu Municipal Hospital, Ohtsu; Japan. Reprint requests: Shinji Kinoshita, MD, School of Human Services, Hokkaido Women’s University, Bunkyodai 23, Ebetsu, Hokkaido 069-8511, Japan. © 2003 Elsevier Inc. All rights reserved. 0022-0736/03/3604-0011$30.00/0 doi:10.1054/S0022-0736(03)00081-5
355
356 Journal of Electrocardiology Vol. 36 No. 4 October 2003 impulse fell in the refractory period of the fast pathway, and was blocked in the fast pathway. It was suggested that respiratory changes in vagal tone affected conductivity in the AV junction to a greater degree than automaticity in the sinus node. These findings show that such “apparent bradycardia-dependent block” associated with gradual lengthening of sinus cycles is not true bradycardiadependent block but a form of tachycardia-dependent block. In our previously reported cases, it was also shown that such apparent bradycardia-dependent block associated with gradual lengthening of sinus cycles occurred in the sinoatrial junction (7,8) and in the accessory pathway (9). In cases of intermittent bundle branch block, however, such block in a bundle branch has never been reported before. In the present paper, a 15-year-old athlete is reported in whom apparent bradycardia-dependent right bundle branch block (RBBB) associated with gradual lengthening of sinus cycles was suggested as a possible mechanism.
Case Report A 15-year-old male athlete of Rugby football was recommended for further examination because firstdegree AV block was found in his 12-lead electrocardiogram. At the first examination, the 12-lead electrocardiogram showed phasic sinus arrhythmia caused by respiration and first-degree AV block (the PR interval of 0.26 s) without any abnormalities in the QRS complex. His physical examinations and echocardiogram showed no abnormalities. He did not experience any symptoms associated with the arrhythmia. The Holter monitor electrocardiogram was taken from this athlete, in which intermittent RBBB was frequently found at rest. Occasionally, atypical AV Wenckebach periodicity was found in which the period of comparatively short PR intervals shifted suddenly to the period of markedly long PR intervals (5,6). Electrophysiologic studies and other invasive studies were not performed. Figure 1 shows parts of the Holter monitor recording at rest. Time intervals are expressed in hundredths of a second. Numerals within the strips indicate PR intervals. Leads (V1) and (V5) correspond to leads V1 and V5, respectively, in the 12-lead electrocardiogram. The upper strip shows that the first 3 sinus impulses (S1, S2, and S3) are conducted to the ventricles without RBBB. When the sinus cycle gradually lengthens from 0.82 to 0.96 s, the sinus impulse (S4) is conducted with
RBBB. The subsequent 3 sinus impulses (S5, S6, and S7) are also conducted with RBBB in which sinus cycles are comparatively long. The lower strip in Figure 1 shows that the first 3 sinus impulses (S1, S2, and S3) are conducted to the ventricles with RBBB. When the sinus cycle shortens to 0.98 s, the sinus impulse (S4) is conducted without RBBB. The subsequent 3 sinus impulses (S5, S6, and S7) are also conducted without RBBB in which sinus cycles are comparatively short. Figure 2 shows other parts of the Holter monitor recording. The strips also show that the occurrence of RBBB is bradycardia-dependent and the disappearance of RBBB is tachycardia-dependent. However, it seems that these findings do not indicate true bradycardia-dependent RBBB as shown in Figure 3. The first strip in Figure 3 shows that the first 4 sinus impulses (S1 to S4) are conducted to the ventricles with RBBB, in which PR intervals range from 0.28 to 0.32 s. When the sinus cycle (S4-S5) shortens to 0.79 s, the sinus impulse (S5) is conducted with a markedly long PR interval of 0.69 s. As a result, the RR interval is also markedly prolonged to 1.17 s. Sinus impulse S5, however, is conducted without RBBB. This suggests that this case may be not true bradycardia-dependent RBBB but a form of tachycardia-dependent RBBB. Namely, it is possible that this case may be apparent bradycardia-dependent RBBB. The diagram below the strip shows that as a result of longitudinal dissociation in the AV junction, atypical AV Wenckebach periodicity termed variant III by us (6) occurs; namely, that the period of comparatively short PR intervals shifts suddenly to the period of markedly prolonged PR intervals. Thus, sinus impulse S5 falls after the effective refractory period of the right bundle branch (RBB). In the diagram, conduction of sinus impulses through the slow AV pathway and conduction through the left bundle branch (LBB) is represented by dashed lines. The second strip in Figure 3 shows that in atypical AV Wenckebach periodicity of variant III, the period of markedly long PR intervals without RBBB shifts suddenly to the period of comparatively short PR intervals with RBBB. The last impulse (S3) in the period of longer PR intervals passes through the RBB. Shortly (0.47 s) after that, the ensuing impulse (S4) with a shorter PR interval reaches the RBB and is blocked in the RBB. These findings also suggest that this case may be apparent bradycardiadependent RBBB, namely, a form of tachycardiadependent RBBB. The diagram below the strip shows that impulse S4 falls in the supernormal
Apparent Bradycardia-dependent RBBB •
Kinoshita et al. 357
Fig. 1. Apparent bradycardia-dependent RBBB. Time intervals are expressed in hundredths of a second. Numerals within the strips indicate PR intervals. Shaded horizontal bars indicate the effective refractory period of the RBB. Conduction of impulses through the LBB is shown by dashed lines. (V1) and (V5), leads corresponding to V1 and V5, respectively; S, sinus impulse; A, atria; AV, atrioventricular junction; RBB, right bundle branch; V, ventricles.
period of the fast AV pathway. The abnormally long effective refractory periods in the fast AV pathway and in the RBB are represented by shaded horizontal bars. The bottom strip in Figure 3 was recorded during
exercise by going up and down the stairs. The strip shows that when the sinus rate is increased during exercise, RBBB is not found. These findings also suggest that this case may be apparent bradycardiadependent RBBB.
358 Journal of Electrocardiology Vol. 36 No. 4 October 2003
Fig. 2. Apparent bradycardia-dependent RBBB. Time intervals are expressed in hundredths of a second.
Figure 4 shows the 12-lead electrocardiograms during normal conduction and during RBBB. During RBBB, an initial slow conduction is slightly seen in leads V1 and V5, although it does not seem that this suggests the presence of preexcitation because the PR and PJ intervals are considerably longer than those during normal conduction.
Discussion Various mechanisms have been postulated to explain the etiology of apparent paradox of bradycardia-dependent block (10,11). These include: the phenomenon of supernormality; the Wedensky phenomenon; vagotonia (12); the phenomenon of concealed conduction; stretching of the conducting tissues resulting from over-filling during the long diastolic intervals; hypoxia; and more pronounced depolarization as a result of a longer phase 4 depolarization of pacemaking cells (13). In our recent reports (14,15), apparent bradycardia-dependent block caused by concealed electrotonic conduction (16) was suggested in the AV junction. In the present case, although electophysiologic studies and other invasive studies were not performed, the electrocardiographic findings suggest that apparent bradycardia-dependent block associated with gradual lengthening of sinus cycles occurred in the RBB, as a possible mechanism. It seems that this is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles.
Mechanism of Apparent Bradycardiadependent RBBB Attempts will be made to explain apparent bradycardia-dependent RBBB in the present case, in a way similar to those in our previous reports on apparent bradycardia-dependent block associated with gradual lengthening of sinus cycles (5–9) as a possible mechanism. Such gradual lengthening of sinus cycles seems to be caused by increased vagal tone. In the present case, it is thought that increased vagal tone might depress conductivity in the RBB to a greater degree than automaticity in the sinus node. In usual cases, changes in vagal tone hardly affect automaticity or conductivity in the ventricular conducting system. However, it is possible that in some cases such as athletes with compensatory increase in vagal tone, changes in vagal tone may considerably affect automaticity and conductivity in the ventricles (17–19). The diagrams below the strips in Figure 1 explain bradycardia-dependent RBBB in the present case, as a possible mechanism. The effective refractory period of the RBB is represented by shaded horizontal bars which are abnormally prolonged. In the upper strip, sinus impulses S1, S2, and S3 fall after the effective refractory period, and are conducted to the ventricles without RBBB. Sinus cycles gradually lengthen from 0.82 to 0.96 s. The effective refractory period lengthens to a greater degree than the sinus cycle. It is thought that increased vagal tone during expiration may depress conduction in the RBB to a greater degree than automaticity in the sinus node. As a
Apparent Bradycardia-dependent RBBB •
Kinoshita et al. 359
Fig. 3. Atypical AV Wenckebach periodicity of variant III. In the AV junction, shaded horizontal bars show the abnormally long effective refractory period of the fast pathway which is interrupted by the supernormal period (s). Conduction of impulses in the slow pathway is represented by dashed lines. The bottom strip was taken during exercise. R, QRS complex. The other abbreviations are the same as in Figure 1.
result, impulse S4 falls in the effective refractory period of the RBB, and was blocked in the RBB. Impulse S4 is conducted to the ventricles through the LBB. Thereafter, the impulse is conducted retrogradely through the RBB and reaches the site of block in the RBB. Thus, once a sinus impulse is blocked in the RBB, some of the subsequent sinus impulses are blocked in the RBB in succession. Conduction of sinus impulses through the LBB is represented by dashed lines. It seems that such marked lengthening of the refractory period is caused by compensatory increase in vagal tone at rest in the same way as in atypical AV Wenckebach periodicity in athletes (6).
The diagram below the lower strip in Figure 1 shows that impulses S1, S2, and S3 fall in the effective refractory period of the RBB, and are blocked in the RBB. When the sinus cycle shortens to 0.98 s, impulse S4 falls after the effective refractory period, and is conducted to the ventricles without RBBB. It is thought that decreased vagal tone during inspiration may increase conductivity in the RBB to a greater degree than automaticity in the sinus node. The subsequent impulses S5, S6, S7 also fall after the effective refractory period of the RBB in succession.
360 Journal of Electrocardiology Vol. 36 No. 4 October 2003
Fig. 4. 12-lead electrocardiograms (A) during normal conduction and (B) during RBBB.
Sudden Shift to the Period of Short PR Intervals in Atypical AV Wenckebach Periodicity In our previous reports (5,6), it was suggested that in atypical AV Wenckebach periodicity (which was termed variant III by us), sudden shift from the period of comparatively short PR intervals to the period of markedly long PR intervals was caused by longitudinal dissociation in the AV junction, as shown in the diagram below the first strip in Figure 3. In our previous reports, however, it was sug-
gested that the period of markedly long PR intervals shifted suddenly to the period of comparatively short PR intervals because the effective refractory period of the fast AV pathway was shortened. As shown in the diagram below the second strip in Figure 3, it is suggested that in the present case, R4 occurs immediately after R3 because impulse S4 falls in the supernormal period of the fast AV pathway. This is the first report on sudden shift to the period of comparatively short PR intervals associated with supernormal AV conduction in atypical AV Wenckebach periodicity of variant III.
Apparent Bradycardia-dependent RBBB •
The Site of Apparent Bradycardiadependent RBBB 7.
It has been suggested that apparent bradycardiadependent block associated with gradual lengthening of sinus cycles occurs because increased vagal tone depresses conductivity to a greater degree than automaticity in the sinus node. It seems that such influence of increased vagal tone may occur usually in the supraventricular conducting system such as in the sinoatrial junction (7,8) and in the AV junction (5,6), and not in the ventricular conducting system. It is possible that in the present case of apparent bradycardia-dependent RBBB, the site of block may not be located in the RBB. Namely, it is possible that longitudinal dissociation may occur in the His bundle (20 –22), and that the RBB may connect to one pathway of the dual pathways in the His bundle. Thus, in the present case of apparent bradycardia-dependent RBBB, block might occur at a site above the RBB as a possible mechanism although it was not disclosed because invasive electrophysiologic studies were not performed in the present case. As shown in Figures 1 and 4, the initial portion of the QRS complexes during RBBB is somewhat different in configuration from that during normal conduction. It is possible that such a difference in configuration might be caused also by intrahisian conduction disturbance with longitudinal dissociation, although the exact mechanism cannot be disclosed because invasive electrophysiologic studies were not performed.
References 1. Kinoshita S: Variations in the critical cycle length inducing rate dependent bundle branch block. Am Heart J 96:54, 1978 2. Kinoshita S: Mechanism of tachycardia-dependent bundle branch block. Am J Cardiol 53:1456, 1984 3. Katoh T, Kinoshita S, Sasaki Y, et al: Intermittent right bundle branch block with supernormal conduction showing various QRS complexes (in Japanese). Respir Circ 47:841, 1999 4. Katoh T, Kinoshita S, Tsujimura Y, et al: Tachycardiadependent right bundle branch block with supernormal conduction. Clin Cardiol 22:59, 2000 5. Kinoshita S, Kawasaki T, Fujiwara S, et al: Periodic variation in atrioventricular conduction time: Mechanisms of initiation, maintenance and termination of periods of long PR intervals. Am J Cardiol 53:1288, 1984 6. Kinoshita S, Konishi G: Atriovetricular Wenckebach periodicity in athletes: Influence of increased vagal
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
Kinoshita et al. 361
tone on the occurrence of atypical periods. J Electrocardiol 20:272, 1987 Katoh T, Kinoshita S: Mechanism of atrial escapecapture bigeminy: Second degree sinoatrial exit and entrance block. J Electrocardiol 31:145, 1998 Katoh T, Kinoshita S, Tsujimura Y, et al: Apparent bradycardia-dependent sinoatrial block associated with respiration. J Electrocardiol 33:375, 2000 Kinoshita S, Katoh T: Apparent bradycardia-dependent block in the accessory pathway in intermittent Wolff-Parkinson-White syndrome. J Electrocardiol 31:151, 1998 Rosenbaum MB, Elizari MV, La´zzari JO, et al: The physiologic basis of intermittent bundle branch block, in Dreifus LS, Likoff W (eds): Cardiac Arrhythmias. New York, NY, Grune & Stratton, 1973, p 349 Schamroth L: Bradycardia-dependent block, in Schamroth L (ed): The Disorders of Cardiac Rhythm (ed 2). Oxford, Blackwell Scientific, 1979, p 345 Nishimura M, Habuchi Y, Hiromasa S, et al: Ionic basis of depressed automaticity and conduction by acetylcholine in rabbit AV node. Am J Physiol 255: H7, 1988 Watanabe Y, Nishimura M: Terminology and electrophysiologic concepts in cardiac arrhythmias: IV: phase 3 block and phase 4 block. PACE 2:624, 1979 Kinoshita S, Katoh T, Tsujimura Y, et al: Apparent bradycardia-dependent right bundle branch block associated with atrial fibrillation: Concealed electrotonic conduction as a possible mechanism. J Electrocardiol 34:81, 2001 Katoh T, Kinoshita S, Ueji I, et al: Apparent bradycardia-dependent advanced second-degree atrioventricular block. J Electrocardiol 35:153, 2002 Antzelevitch C. , Moe GK. Electrotonic inhibition and summation of impulse conduction in mammalian Purkinje fibers. Am J Physiol 245:H42, 1983 Kinoshita S, Mashimo K: Effect of vagal stimulation on ventricular impulse formation in a case of ventricular parasystole (in Japanese). Shinzo 1:1185, 1969 Kinoshita S: Wenckebach phenomenon of entrance block in intermittent ventricular parasystole. Chest 66:530, 1974 Kinoshita S, Mitsuoka T: Effect of standing on ventricular parasystole: Shortening of the parasystolic cycle length. Heart 77:133, 1997 Katoh T, Nishimura M, Tsuji Y, et al: Double His deflections caused by intrahisian conduction disturbance with longitudinal dissociation. Am J Cardiol 53:368, 1984 Katoh T, Kinoshita S, Tsujimura Y, et al: Double ventricular response caused by longitudinal dissociation in the His bundle. J Electrocardiol 35:69, 2002 Katoh T, Kinoshita S, Tsujimura Y, Sasaki Y: Atypical atrioventricular Wenckebach periodicity caused by conduction through triple atrioventricular junctional pathways as a probable mechanism. J Electrocardiol 36:73, 2003
Case Report
Apparent Bradycardia-dependent Right Bundle Branch Block Associated With Atypical Atrioventricular Wenckebach Periodicity as a Possible Mechanism Shinji Kinoshita, MD, Takakazu Katoh, MD, Yoshinori Tsujimura, MD, and Yoshihiko Sasaki, MT
Abstract: The Holter monitor electrocardiogram was taken from a 15-year-old male athlete. Intermittent right bundle branch block frequently occurred at rest. When sinus cycles gradually lengthened, sinus impulses were conducted to the ventricles with right bundle branch block (RBBB) in succession. When, thereafter, sinus cycles gradually shortened, sinus impulses were conducted without RBBB. However, it seems that these findings do not show true bradycardia-dependent RBBB. Atypical atrioventricular Wenckebach periodicity was occasionally found in which sudden shift from the period of comparatively short PR intervals to the period of long PR intervals occurred. In the Wenckebach periodicity, when a QRS complex occurs after a much longer pause, RBBB was not found, while when it occurs after a much shorter period, RBBB was found. This suggests that this case may be apparent bradycardia-dependent RBBB, namely, a form of tachycardiadependent RBBB. This is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles, as a possible mechanism. Key words: Apparent bradycardia-dependent block, atypical Wenckebach periodicity, right bundle branch block, tachycardiadependent block, atrioventricular block.
In our previous reports on tachycardia-dependent bundle branch block (1– 4), it was shown that when sinus cycles gradually shortened below a
critical period, a sinus impulse fell in the abnormally long effective refractory period of a bundle branch, and was blocked in the bundle branch. On the other hand, we reported that apparent bradycardia-dependent block occurred in some cases of atypical atrioventricular (AV) Wenckebach periodicity associated with longitudinal AV dissociation (5,6). In those cases, when sinus cycles gradually lengthened, the effective refractory period of the fast AV pathway was markedly prolonged beyond the sinus cycle length. As a result, a sinus
From the Hokkaido Women’s University, Ebetsu, Hokkaido; Katoh Cardiovascular Clinic, Ohtsu; Division of Cardiology and Division of Hemodialysis, Ohtsu Municipal Hospital, Ohtsu; Japan. Reprint requests: Shinji Kinoshita, MD, School of Human Services, Hokkaido Women’s University, Bunkyodai 23, Ebetsu, Hokkaido 069-8511, Japan. © 2003 Elsevier Inc. All rights reserved. 0022-0736/03/3604-0011$30.00/0 doi:10.1054/S0022-0736(03)00081-5
355
356 Journal of Electrocardiology Vol. 36 No. 4 October 2003 impulse fell in the refractory period of the fast pathway, and was blocked in the fast pathway. It was suggested that respiratory changes in vagal tone affected conductivity in the AV junction to a greater degree than automaticity in the sinus node. These findings show that such “apparent bradycardia-dependent block” associated with gradual lengthening of sinus cycles is not true bradycardiadependent block but a form of tachycardia-dependent block. In our previously reported cases, it was also shown that such apparent bradycardia-dependent block associated with gradual lengthening of sinus cycles occurred in the sinoatrial junction (7,8) and in the accessory pathway (9). In cases of intermittent bundle branch block, however, such block in a bundle branch has never been reported before. In the present paper, a 15-year-old athlete is reported in whom apparent bradycardia-dependent right bundle branch block (RBBB) associated with gradual lengthening of sinus cycles was suggested as a possible mechanism.
Case Report A 15-year-old male athlete of Rugby football was recommended for further examination because firstdegree AV block was found in his 12-lead electrocardiogram. At the first examination, the 12-lead electrocardiogram showed phasic sinus arrhythmia caused by respiration and first-degree AV block (the PR interval of 0.26 s) without any abnormalities in the QRS complex. His physical examinations and echocardiogram showed no abnormalities. He did not experience any symptoms associated with the arrhythmia. The Holter monitor electrocardiogram was taken from this athlete, in which intermittent RBBB was frequently found at rest. Occasionally, atypical AV Wenckebach periodicity was found in which the period of comparatively short PR intervals shifted suddenly to the period of markedly long PR intervals (5,6). Electrophysiologic studies and other invasive studies were not performed. Figure 1 shows parts of the Holter monitor recording at rest. Time intervals are expressed in hundredths of a second. Numerals within the strips indicate PR intervals. Leads (V1) and (V5) correspond to leads V1 and V5, respectively, in the 12-lead electrocardiogram. The upper strip shows that the first 3 sinus impulses (S1, S2, and S3) are conducted to the ventricles without RBBB. When the sinus cycle gradually lengthens from 0.82 to 0.96 s, the sinus impulse (S4) is conducted with
RBBB. The subsequent 3 sinus impulses (S5, S6, and S7) are also conducted with RBBB in which sinus cycles are comparatively long. The lower strip in Figure 1 shows that the first 3 sinus impulses (S1, S2, and S3) are conducted to the ventricles with RBBB. When the sinus cycle shortens to 0.98 s, the sinus impulse (S4) is conducted without RBBB. The subsequent 3 sinus impulses (S5, S6, and S7) are also conducted without RBBB in which sinus cycles are comparatively short. Figure 2 shows other parts of the Holter monitor recording. The strips also show that the occurrence of RBBB is bradycardia-dependent and the disappearance of RBBB is tachycardia-dependent. However, it seems that these findings do not indicate true bradycardia-dependent RBBB as shown in Figure 3. The first strip in Figure 3 shows that the first 4 sinus impulses (S1 to S4) are conducted to the ventricles with RBBB, in which PR intervals range from 0.28 to 0.32 s. When the sinus cycle (S4-S5) shortens to 0.79 s, the sinus impulse (S5) is conducted with a markedly long PR interval of 0.69 s. As a result, the RR interval is also markedly prolonged to 1.17 s. Sinus impulse S5, however, is conducted without RBBB. This suggests that this case may be not true bradycardia-dependent RBBB but a form of tachycardia-dependent RBBB. Namely, it is possible that this case may be apparent bradycardia-dependent RBBB. The diagram below the strip shows that as a result of longitudinal dissociation in the AV junction, atypical AV Wenckebach periodicity termed variant III by us (6) occurs; namely, that the period of comparatively short PR intervals shifts suddenly to the period of markedly prolonged PR intervals. Thus, sinus impulse S5 falls after the effective refractory period of the right bundle branch (RBB). In the diagram, conduction of sinus impulses through the slow AV pathway and conduction through the left bundle branch (LBB) is represented by dashed lines. The second strip in Figure 3 shows that in atypical AV Wenckebach periodicity of variant III, the period of markedly long PR intervals without RBBB shifts suddenly to the period of comparatively short PR intervals with RBBB. The last impulse (S3) in the period of longer PR intervals passes through the RBB. Shortly (0.47 s) after that, the ensuing impulse (S4) with a shorter PR interval reaches the RBB and is blocked in the RBB. These findings also suggest that this case may be apparent bradycardiadependent RBBB, namely, a form of tachycardiadependent RBBB. The diagram below the strip shows that impulse S4 falls in the supernormal
Apparent Bradycardia-dependent RBBB •
Kinoshita et al. 357
Fig. 1. Apparent bradycardia-dependent RBBB. Time intervals are expressed in hundredths of a second. Numerals within the strips indicate PR intervals. Shaded horizontal bars indicate the effective refractory period of the RBB. Conduction of impulses through the LBB is shown by dashed lines. (V1) and (V5), leads corresponding to V1 and V5, respectively; S, sinus impulse; A, atria; AV, atrioventricular junction; RBB, right bundle branch; V, ventricles.
period of the fast AV pathway. The abnormally long effective refractory periods in the fast AV pathway and in the RBB are represented by shaded horizontal bars. The bottom strip in Figure 3 was recorded during
exercise by going up and down the stairs. The strip shows that when the sinus rate is increased during exercise, RBBB is not found. These findings also suggest that this case may be apparent bradycardiadependent RBBB.
358 Journal of Electrocardiology Vol. 36 No. 4 October 2003
Fig. 2. Apparent bradycardia-dependent RBBB. Time intervals are expressed in hundredths of a second.
Figure 4 shows the 12-lead electrocardiograms during normal conduction and during RBBB. During RBBB, an initial slow conduction is slightly seen in leads V1 and V5, although it does not seem that this suggests the presence of preexcitation because the PR and PJ intervals are considerably longer than those during normal conduction.
Discussion Various mechanisms have been postulated to explain the etiology of apparent paradox of bradycardia-dependent block (10,11). These include: the phenomenon of supernormality; the Wedensky phenomenon; vagotonia (12); the phenomenon of concealed conduction; stretching of the conducting tissues resulting from over-filling during the long diastolic intervals; hypoxia; and more pronounced depolarization as a result of a longer phase 4 depolarization of pacemaking cells (13). In our recent reports (14,15), apparent bradycardia-dependent block caused by concealed electrotonic conduction (16) was suggested in the AV junction. In the present case, although electophysiologic studies and other invasive studies were not performed, the electrocardiographic findings suggest that apparent bradycardia-dependent block associated with gradual lengthening of sinus cycles occurred in the RBB, as a possible mechanism. It seems that this is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles.
Mechanism of Apparent Bradycardiadependent RBBB Attempts will be made to explain apparent bradycardia-dependent RBBB in the present case, in a way similar to those in our previous reports on apparent bradycardia-dependent block associated with gradual lengthening of sinus cycles (5–9) as a possible mechanism. Such gradual lengthening of sinus cycles seems to be caused by increased vagal tone. In the present case, it is thought that increased vagal tone might depress conductivity in the RBB to a greater degree than automaticity in the sinus node. In usual cases, changes in vagal tone hardly affect automaticity or conductivity in the ventricular conducting system. However, it is possible that in some cases such as athletes with compensatory increase in vagal tone, changes in vagal tone may considerably affect automaticity and conductivity in the ventricles (17–19). The diagrams below the strips in Figure 1 explain bradycardia-dependent RBBB in the present case, as a possible mechanism. The effective refractory period of the RBB is represented by shaded horizontal bars which are abnormally prolonged. In the upper strip, sinus impulses S1, S2, and S3 fall after the effective refractory period, and are conducted to the ventricles without RBBB. Sinus cycles gradually lengthen from 0.82 to 0.96 s. The effective refractory period lengthens to a greater degree than the sinus cycle. It is thought that increased vagal tone during expiration may depress conduction in the RBB to a greater degree than automaticity in the sinus node. As a
Apparent Bradycardia-dependent RBBB •
Kinoshita et al. 359
Fig. 3. Atypical AV Wenckebach periodicity of variant III. In the AV junction, shaded horizontal bars show the abnormally long effective refractory period of the fast pathway which is interrupted by the supernormal period (s). Conduction of impulses in the slow pathway is represented by dashed lines. The bottom strip was taken during exercise. R, QRS complex. The other abbreviations are the same as in Figure 1.
result, impulse S4 falls in the effective refractory period of the RBB, and was blocked in the RBB. Impulse S4 is conducted to the ventricles through the LBB. Thereafter, the impulse is conducted retrogradely through the RBB and reaches the site of block in the RBB. Thus, once a sinus impulse is blocked in the RBB, some of the subsequent sinus impulses are blocked in the RBB in succession. Conduction of sinus impulses through the LBB is represented by dashed lines. It seems that such marked lengthening of the refractory period is caused by compensatory increase in vagal tone at rest in the same way as in atypical AV Wenckebach periodicity in athletes (6).
The diagram below the lower strip in Figure 1 shows that impulses S1, S2, and S3 fall in the effective refractory period of the RBB, and are blocked in the RBB. When the sinus cycle shortens to 0.98 s, impulse S4 falls after the effective refractory period, and is conducted to the ventricles without RBBB. It is thought that decreased vagal tone during inspiration may increase conductivity in the RBB to a greater degree than automaticity in the sinus node. The subsequent impulses S5, S6, S7 also fall after the effective refractory period of the RBB in succession.
360 Journal of Electrocardiology Vol. 36 No. 4 October 2003
Fig. 4. 12-lead electrocardiograms (A) during normal conduction and (B) during RBBB.
Sudden Shift to the Period of Short PR Intervals in Atypical AV Wenckebach Periodicity In our previous reports (5,6), it was suggested that in atypical AV Wenckebach periodicity (which was termed variant III by us), sudden shift from the period of comparatively short PR intervals to the period of markedly long PR intervals was caused by longitudinal dissociation in the AV junction, as shown in the diagram below the first strip in Figure 3. In our previous reports, however, it was sug-
gested that the period of markedly long PR intervals shifted suddenly to the period of comparatively short PR intervals because the effective refractory period of the fast AV pathway was shortened. As shown in the diagram below the second strip in Figure 3, it is suggested that in the present case, R4 occurs immediately after R3 because impulse S4 falls in the supernormal period of the fast AV pathway. This is the first report on sudden shift to the period of comparatively short PR intervals associated with supernormal AV conduction in atypical AV Wenckebach periodicity of variant III.
Apparent Bradycardia-dependent RBBB •
The Site of Apparent Bradycardiadependent RBBB 7.
It has been suggested that apparent bradycardiadependent block associated with gradual lengthening of sinus cycles occurs because increased vagal tone depresses conductivity to a greater degree than automaticity in the sinus node. It seems that such influence of increased vagal tone may occur usually in the supraventricular conducting system such as in the sinoatrial junction (7,8) and in the AV junction (5,6), and not in the ventricular conducting system. It is possible that in the present case of apparent bradycardia-dependent RBBB, the site of block may not be located in the RBB. Namely, it is possible that longitudinal dissociation may occur in the His bundle (20 –22), and that the RBB may connect to one pathway of the dual pathways in the His bundle. Thus, in the present case of apparent bradycardia-dependent RBBB, block might occur at a site above the RBB as a possible mechanism although it was not disclosed because invasive electrophysiologic studies were not performed in the present case. As shown in Figures 1 and 4, the initial portion of the QRS complexes during RBBB is somewhat different in configuration from that during normal conduction. It is possible that such a difference in configuration might be caused also by intrahisian conduction disturbance with longitudinal dissociation, although the exact mechanism cannot be disclosed because invasive electrophysiologic studies were not performed.
References 1. Kinoshita S: Variations in the critical cycle length inducing rate dependent bundle branch block. Am Heart J 96:54, 1978 2. Kinoshita S: Mechanism of tachycardia-dependent bundle branch block. Am J Cardiol 53:1456, 1984 3. Katoh T, Kinoshita S, Sasaki Y, et al: Intermittent right bundle branch block with supernormal conduction showing various QRS complexes (in Japanese). Respir Circ 47:841, 1999 4. Katoh T, Kinoshita S, Tsujimura Y, et al: Tachycardiadependent right bundle branch block with supernormal conduction. Clin Cardiol 22:59, 2000 5. Kinoshita S, Kawasaki T, Fujiwara S, et al: Periodic variation in atrioventricular conduction time: Mechanisms of initiation, maintenance and termination of periods of long PR intervals. Am J Cardiol 53:1288, 1984 6. Kinoshita S, Konishi G: Atriovetricular Wenckebach periodicity in athletes: Influence of increased vagal
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
Kinoshita et al. 361
tone on the occurrence of atypical periods. J Electrocardiol 20:272, 1987 Katoh T, Kinoshita S: Mechanism of atrial escapecapture bigeminy: Second degree sinoatrial exit and entrance block. J Electrocardiol 31:145, 1998 Katoh T, Kinoshita S, Tsujimura Y, et al: Apparent bradycardia-dependent sinoatrial block associated with respiration. J Electrocardiol 33:375, 2000 Kinoshita S, Katoh T: Apparent bradycardia-dependent block in the accessory pathway in intermittent Wolff-Parkinson-White syndrome. J Electrocardiol 31:151, 1998 Rosenbaum MB, Elizari MV, La´zzari JO, et al: The physiologic basis of intermittent bundle branch block, in Dreifus LS, Likoff W (eds): Cardiac Arrhythmias. New York, NY, Grune & Stratton, 1973, p 349 Schamroth L: Bradycardia-dependent block, in Schamroth L (ed): The Disorders of Cardiac Rhythm (ed 2). Oxford, Blackwell Scientific, 1979, p 345 Nishimura M, Habuchi Y, Hiromasa S, et al: Ionic basis of depressed automaticity and conduction by acetylcholine in rabbit AV node. Am J Physiol 255: H7, 1988 Watanabe Y, Nishimura M: Terminology and electrophysiologic concepts in cardiac arrhythmias: IV: phase 3 block and phase 4 block. PACE 2:624, 1979 Kinoshita S, Katoh T, Tsujimura Y, et al: Apparent bradycardia-dependent right bundle branch block associated with atrial fibrillation: Concealed electrotonic conduction as a possible mechanism. J Electrocardiol 34:81, 2001 Katoh T, Kinoshita S, Ueji I, et al: Apparent bradycardia-dependent advanced second-degree atrioventricular block. J Electrocardiol 35:153, 2002 Antzelevitch C. , Moe GK. Electrotonic inhibition and summation of impulse conduction in mammalian Purkinje fibers. Am J Physiol 245:H42, 1983 Kinoshita S, Mashimo K: Effect of vagal stimulation on ventricular impulse formation in a case of ventricular parasystole (in Japanese). Shinzo 1:1185, 1969 Kinoshita S: Wenckebach phenomenon of entrance block in intermittent ventricular parasystole. Chest 66:530, 1974 Kinoshita S, Mitsuoka T: Effect of standing on ventricular parasystole: Shortening of the parasystolic cycle length. Heart 77:133, 1997 Katoh T, Nishimura M, Tsuji Y, et al: Double His deflections caused by intrahisian conduction disturbance with longitudinal dissociation. Am J Cardiol 53:368, 1984 Katoh T, Kinoshita S, Tsujimura Y, et al: Double ventricular response caused by longitudinal dissociation in the His bundle. J Electrocardiol 35:69, 2002 Katoh T, Kinoshita S, Tsujimura Y, Sasaki Y: Atypical atrioventricular Wenckebach periodicity caused by conduction through triple atrioventricular junctional pathways as a probable mechanism. J Electrocardiol 36:73, 2003