| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1997;95:650-654.)
© 1997 American Heart Association, Inc.
Articles |
Incidence of Induced Atrial Fibrillation/Flutter in Complete Atrioventricular Block
A Concept of `Atrial-Malfunctioning' Atrio-Hisian Block
the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo (Japan).
Correspondence to Takeshi Yamashita, MD, The Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background Atrial fibrillation/flutter (Af) has been considered to occur coincidentally with atrioventricular (AV) block. However, a case with complete AV block was reported to histologically show fibrotic changes solely in the atrial muscles but neither in the AV node nor in the His bundle, indicating a possible relation between AV block and atrial tachyarrhythmias. To test a hypothesis that AV block and Af are causally interrelated, we investigated the incidence and electrophysiological characteristics of Af in complete AV block.
Methods and Results Forty-two patients with persistent complete AV block underwent the electrophysiological study. Patients with spontaneous/electrically induced Af were compared with the other patients with respect to their electrophysiological variables. Of the 42 patients, Af was transiently induced by electrical stimulation in 5 patients (11.9%), while persistent Af was observed in 2 patients (4.8%, AH and HV block). AV block in the 5 patients with induced Af was invariably due to AH block. AH block complicated by persistent/induced Af was marked by relatively short RR intervals, significantly short junctional recovery time, and impaired intra-atrial conduction.
Conclusions Electrically induced Af in complete AV block was associated frequently with complete AH block. These patients were characterized differently from the commonly recognized AV block and therefore may stand as a unique subgroup of AH block.
Key Words: atrial flutter • fibrillation • conduction • atrioventricular node • heart block
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Atrial fibrillation occurs at times concomitantly with complete atrioventricular (AV) block.1 2 3 4 5 6 A characteristic ECG finding, regular RR intervals in atrial fibrillation, suggests the existence of complete AV block and indicates the need for the further treatment.1 2 The concomitant existence of atrial fibrillation and complete AV block has been thought to be incidental in previous case reports.3 4 5 6
However, of the many clinical reports correlating electrophysiological and histological findings in complete AV block,5 7 8 9 10 11 12 13 14 15 16 a previous one5 from Japan attributed complete AV block to pathological lesions in the atrial muscles including the internodal tracts. This histological observation, AV block due to atrial lesions, might indicate a possible association between AV block and atrial tachyarrhythmias.
In the present study, to examine the possible association between AV block and atrial tachyarrhythmias, we surveyed the incidence of spontaneous and electrically induced atrial fibrillation/flutter (Af) in complete AV block and studied the electrophysiological characteristics and clinical outcome of these patients with complete AV block complicated by spontaneous/induced Af.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Patients
The study group comprised 42 patients, in whom ambulatory 24-hour ECG recordings showed persistent complete AV block throughout the day, referred for evaluation of persistent complete AV block at the Second Department of Internal Medicine, Tokyo University Hospital, between January 1980 and August 1995. In the present study, to exclude the participation of the functional block in the AV node, we did not enroll patients with second-degree or advanced AV block. There were 18 men and 24 women, 64±13 years of age (range, 43 to 87). In the surface 12-lead ECG, 21 patients had AV junctional rhythm with narrow QRS complexes (<0.12 second), and the remaining 21 patients with wide QRS complexes (
0.12 second). One patient with narrow QRS complexes and 1 patient with wide QRS complexes showed persistent Af. Thirty-eight patients had no apparent structural heart disease: 2 patients had idiopathic dilated cardiomyopathy and 2 patients had sarcoidosis with pulmonary infiltration. Six patients had essential hypertension and 2 patients had diabetes mellitus. All the patients had experienced episodes of syncope, dizziness, and/or shortness of breath.
Electrophysiological Study
After informed consent, the standard electrophysiological study was performed under the use of local anesthesia in the fasting state.17 Quadripolar electrode catheters (6F) with an interelectrode distance of 10 mm were introduced percutaneously from the right femoral vein and positioned in the high right atrium, right ventricular apex, and His bundle region. In some patients, the catheters were positioned in the coronary sinus from the left subclavian vein. The distal pair of electrodes were used for electrical stimulation and the proximal pair for recording. Stimulation was performed with 2-ms rectangular pulses at twice the late diastolic threshold with the use of a digital programmable stimulator (BC02, Fukuda Denshi). Intracardiac electrograms filtered at 50 to 500 Hz, and ECG leads I, aVF, and V1 were recorded simultaneously at paper speeds of 50 to 100 mm/s on an ink-jet recorder (Mingo 7, Siemens-Elema) and on FM tape with a cassette tape recorder (MR-40, TEAC) for later analysis. Pacing protocols were high right atrial (HRA) overdrive pacing for 30 seconds and right ventricular apical (RV) overdrive pacing for 20 seconds at rates of 100, 120, 140, 160, 180, and 200 bpm and HRA and RV extrastimulus during the sinus rhythm and at a basic cycle length of 600 ms. The coupling intervals of extrastimuli were shortened in 10-ms decrements. In all the patients without persistent Af, the P-wave duration in lead II, intra-atrial activation time from the atrial electrogram in HRA to that in the His bundle region during sinus rhythm, and the effective refractory period of HRA were measured to assess the atrial electrophysiological properties. The junctional recovery time was defined as the longest RR interval after RV pacing for 20 seconds.18
Clinical Follow-up
All patients received pacemaker implants after the electrophysiological study (DDD/DDDR, 31 patients; VVI/VVIR, 11 patients). Each patient was followed up once or twice every year to check the function of the implanted pacemaker. During the follow-up period, pacemaker generators were replaced twice in 4 patients and once in 10 patients. The development of Af and maintenance of the junctional escape rhythm >30 bpm were examined at each stage of the clinical follow-up.
Statistical Analysis
Data are expressed as mean±SD. Comparisons were performed by means of a 
2 test, ANOVA, or an unpaired t test where appropriate. Statistical significance was set at a value of P<.05.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Electrophysiological Block Site
In 21 patients with narrow QRS complexes, 14 patients showed complete AH block and 7 patients showed complete HH' block. In the remaining 21 patients with wide QRS complexes, most of the patients had complete HV block except 2 patients with HH' block.
Incidence of Persistent and Electrically Induced Af
Persistent Af was observed in 2 patients (4.8%): 1 patient with AH block and 1 patient with HV block. Of 40 patients without persistent Af, Af was induced transiently in 5 patients (12.5%) by electrical pacing (both atrial flutter and fibrillation in 2 patients and atrial fibrillation in 3 patients). Notably, complete AV block in these 5 patients was invariably due to AH block. Atrial pacing failed to induce Af in any subjects with HH' and HV block. Consequently, persistent/induced Af was more frequently observed in patients with AH block than in those with HH' and HV block (AH block, 6 of 14; HH' block, 0 of 9; HV block, 1 of 19; P<.01; Fig 1
).
|
Electrophysiological Characteristics of Complete AV Block With Induced Af
To obtain an insight into the electrophysiological background of the coexistence of complete AH block and Af, we divided the patients into four groups: AH block with persistent/induced Af, AH block without Af, HH' block, and HV block. The patient profiles in each group are summarized in the Table.
|
The RR interval, which may represent the intrinsic automaticity of the escape rhythm, was not significantly different in the four groups. Sinus node recovery time (SNRT) also showed no significant differences, although 1 patient with AH block complicated by induced Af revealed an increased SNRT, suggesting a complication of sick sinus syndrome. Characteristically in AH block with Af, the escape focus showed almost no overdrive suppression by ventricular pacing in all the patients (Fig 2). In contrast, junctional recovery time was significantly more increased in the other groups (P<.05 by ANOVA; Fig 3).
|
|
Patients with complete AH block complicated by induced Af also showed remarkable atrial conduction disturbances compared with the other groups. In the surface ECG recordings, the P-wave duration determined in lead II was prolonged and, characteristically, the P wave showed bizarre morphology particularly in leads II and V4 through V6 in AH block with induced Af (Fig 3
). In contrast, the other groups showed almost normal P-wave morphology and duration (P<.01 by ANOVA; Fig 3). Similarly, the intra-atrial activation time from the high to the low right atrium at the His bundle region was more prolonged in AH block with induced Af compared with the other types of AV block (P<.01 by ANOVA; Fig 3). While the P-wave duration and the intra-atrial activation time were significantly different in the four groups, the effective refractory period of the high right atrium at a basic cycle length of 600 ms showed no intergroup differences.
Clinical Course of Patients With Complete AV Block With Induced Af
During the mean follow-up period of 93±60 months, 2 patients died as the result of congestive heart failure caused by dilated cardiomyopathy and sarcoidosis and 1 patient died as the result of a traffic accident (all with HV block). Two patients with AH block complicated by induced Af (6 months after DDD pacing and 33 months after VVI pacing) and 1 patient with HV block (56 months after VVI pacing) developed persistent Af after pacemaker implantation. The risk of developing Af after pacemaker implantation was significantly higher in patients with AH block complicated by induced Af than in the other types of complete AV block (AH block with induced Af, 2 of 5; AH block without induced Af, 0 of 8; HH' block, 0 of 9; HV block, 1 of 18; P<.05). The escape rhythm >30 bpm could not be observed in 12 patients during the follow-up period (8 patients with HV block, 2 patients with HH' block, and 2 patients with AH block without spontaneous/induced Af). All the patients with AH block complicated by spontaneous/induced Af maintained an escape rhythm >30 bpm throughout the follow-up period of 84±55 months. The risk of developing escape rhythm slower than 30 bpm was 0 of 6 in AH block with spontaneous/induced Af, 2 of 8 in AH block without Af, 2 of 9 in HH' block and 8 of 19 in HV block (NS).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Major Findings
The major findings of the present study were as follows. (1) Electrically induced Af was frequently interrelated with AH block in complete AV block. (2) Patients with AH block complicated by induced Af had particular electrophysiological characteristics compared with patients with AH block not complicated by Af: (a) stable escape rhythm reflected by a short junctional recovery time and (b) atrial conduction disturbances as suggested by a prolonged P-wave duration, increased intra-atrial activation time, and the bizarre P-wave morphology. (3) Af was frequently observed in these patients during the follow-up after pacemaker implantation.
Association Between AH Block and Af
Although Af complicated by complete AV block has been well appreciated by clinical electrophysiologists with its characteristic ECG finding, regular RR intervals during Af, the coexistence of Af, and complete AV block have been attributed to mere coincidence.1 2 3 4 5 6 Correspondingly, in our 42 cases, only 2 (4.8%) had persistent Af. In contrast, Af was electrically induced in no small numbers (5 patients, 11.9%). This figure may be suggestive of the incidence of paroxysmal Af in complete AV block, considering that Af is more readily induced by electrical pacing in patients with a history of paroxysmal Af. However, the natural incidence of paroxysmal Af in complete AV block is unknown, partly because paroxysmal Af rarely causes serious symptoms in a condition of complete AV block without a dual-chamber pacemaker.
More noteworthy in the present study is that Af was induced only in patients with complete AH block. This disproportional prevalence of induced Af suggested some relations between Af and AH type of AV block. Actually, cases with complete AV block complicated by Af exhibiting narrow QRS complexes were found in the literature.1 2 4 5 6 A familial case with AV block complicated by atrial flutter was shown to exhibit AH block at the electrophysiological study.4 On the basis that most of AV blocks with narrow QRS complexes are due to AH block,19 these previous cases may support our view.
What Is the Main Lesion in AH Block?
Histologically, the lesions of AH block are controversial, different from those of HH' and HV block.5 10 11 16 While HH' and HV block were due to fibrosis of the corresponding regions of the conduction system, ie, the His bundle and the bilateral bundle branches,5 7 8 9 10 11 12 13 14 15 16 AH block could be caused by fibrotic changes either in the approaches to the AV node, the AV node itself, the upper part of the His bundle, or the branching portion of the His bundle.10 11 16 We found it surprising that complete AH block sometimes lacked lesions in the conduction system of the heart.5 These electrophysiological and histological correlations might indicate the diversity of AH block. Our cases with AH block complicated by spontaneous/induced Af resembled a previous case5 in which paroxysmal Af and prolonged P-wave duration with complete AH block were manifested. In this case, histologically, the main lesions were observed neither in the AV node nor in the His bundle but in the atrial muscles including the internodal tracts.5
Electrophysiological characteristics of our patients with persistent complete AH block complicated by induced Af were (1) reliable junctional escape focus and (2) intra-atrial conduction disturbances. Since the escape focus should exist right below the block site in the conduction system, the relatively short RR intervals and short junctional recovery time in these subjects suggested that the blockage occurred at higher levels than in AH block without spontaneous/induced Af. Impaired intra-atrial conduction seems to indicate some damage to the internodal tracts located above the AV node,20 which has been known clinically and experimentally to be related to the genesis of atrial tachyarrhythmias.21 22 23 24 25 26 When we interpret these points all at once, these electrophysiological findings suggest that AH block with spontaneous/induced Af in the present study might result from (a) a lesion in the upper part of the AV node or AV nodal approaches, expanding to the atrial muscles including the internodal tracts that gather into the AV node, or (b) a lesion that exists solely in the atrial muscles including the internodal tracts, while, in contrast, AH block without Af might be attributed to a lesion in the lower part of the AV node or the upper part of the His bundle. Possibility (b) has been histologically demonstrated in the previous case,5 in which complete AH block with paroxysmal atrial fibrillation was manifested. In both possibilities (a) and (b), impulses by the ventricular overdrive pacing would not be able to enter the escape focus readily because of the intervening AV node and His-Purkinje system and therefore would minimally affect the escape focus. In contrast, when the lesion exists below the AV node or in the lower part of the AV node, the junctional escape focus would be protected from the ventricular pacing solely by the His-Purkinje system but not by the AV node, thereby facilitating the suppression of the junctional escape focus.
Clinical Implications
Complete AV block is an indication for a permanent cardiac pacemaker,27 which was applied in all our cases. The selection of the pacing mode and the clinical follow-up including the pacemaker check is mandatory for the therapy. Commonly, the DDD/R mode is suitable for AV block without Af, while the VVI/R mode is more suitable for AV block with persistent Af.27 In our characteristic cases for which AV block was complicated by induced Af and not by persistent Af, it may be suitable to implant a mode-switching device. However, on the sole basis of the present study, we as yet are unable to offer any clinical recommendations because we could not deny that the development of Af in our subjects was related more or less to VVI/R pacing applied in the earlier days.
Study Limitations
There are some limitations in the present study. First is the relatively small number of patients, so the concept of "atrial-malfunctioning" atrio-Hisian block is hypothetical. This should be elucidated in larger prospective studies as well as clinicopathological studies in the future. Second, we could not rule out the possibility of induced Af being a totally coincidental complication of complete AH block in some patients. Though limited for these reasons, the present study is the first to raise the possibility that AH block and Af may be causally interrelated and could thus provide an enhanced understanding of the clinical electrophysiological basis for persistent complete AH block.
Received June 10, 1996; revision received September 5, 1996; accepted September 30, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Watanabe Y, Dreifus LS. Atrioventricular block: basic concepts. In: Mandel WJ, ed. Cardiac Arrhythmias. Their Mechanisms, Diagnosis and Management. 2nd ed. Philadelphia, Pa: JB Lippincott; 1987:297-320.
2. Chou TC. Atrioventricular junctional rhythms. In: Chou TC, ed. Electrocardiography in Clinical Practice. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1991:347-365.
3.
Reid DS, Jachuck SJ, Henderson CB. Cardiac pacing in incomplete atrioventricular block with atrial fibrillation. Br Heart J. 1973;35:1154-1160.
4.
Amat-y-Leon F, Racki AJ, Denes P, Ten-Eick RE, Singer DH, Bharati S, Lev M, Rosen KM. Familial atrial dysrhythmia with A-V block. Circulation. 1974;50:1097-1104.
5.
Ohkawa S, Sugiura M, Itoh Y, Kitano K, Hiraoka K, Ueda K, Murakami M. Electrophysiologic and histologic correlations in chronic complete atrioventricular block. Circulation.. 1981;64:215-231.
6. Kumar RK, Saxena A, Talwar KK. Lone atrial fibrillation with complete heart block in a child. Int J Cardiol.. 1992;30:349-351.
7. Lev M, Paul MH, Cassels DE. Complete atrioventricular block associated with atrial septal defect of the fossa ovalis (secondum) type: a histopathologic study of the conduction systems. Am J Cardiol.. 1967;19:266-274.[Medline] [Order article via Infotrieve]
8.
Rosen KM, Rahimtoola SH, Gunnar RM, Lev M. Transient and persistent atrial standstill with His bundle lesions: electrophysiologic and pathologic correlations. Circulation.. 1971;44:220-236.
9.
Rosen KM, Rahimtoola SH, Gunnar RM, Lev M. Site of heart block as defined by His bundle recording: pathologic correlations in three cases. Circulation.. 1972;45:965-987.
10. Lev M. The pathology of atrioventricular block. Cardiovasc Clin.. 1972;4:159-186.[Medline] [Order article via Infotrieve]
11.
Hunt D, Lie JT, Vohra J, Sloman G. Histopathology of heart block complicating acute myocardial infarction: correlation with the His bundle electrogram. Circulation.. 1973;48:1252-1261.
12. Rosen KM, Rahimtoola SH, Bharati S, Lev M. Bundle branch block with intact atrioventricular conduction: electrophysiologic and pathologic correlations in three cases. Am J Cardiol.. 1973;32:783-793.[Medline] [Order article via Infotrieve]
13.
Bharati S, Lev M, Wu D, Denes P, Dhingra R, Rosen KM. Pathophysiologic correlations in two cases of split His bundle potentials. Circulation.. 1974;49:615-623.
14. Bharati S, Lev M, Dhingra R, Wu D, Aruguete J, Mir J, Rosen KM. Pathologic correlations in three cases of bilateral bundle branch disease with unusual electrophysiologic manifestations in two cases. Am J Cardiol.. 1976;38:508-518.[Medline] [Order article via Infotrieve]
15. Ohkawa S, Matsushita S, Ueda K, Matsuo H, Sugiura M. Electrophysiological and histological correlations in two cases of complete heart block. Jpn Heart J.. 1977;18:287-297.[Medline] [Order article via Infotrieve]
16. Bharati S, Lev M. Pathology of atrioventricular block. Cardiol Clin.. 1984;2:741-751.[Medline] [Order article via Infotrieve]
17. Yamashita T, Inoue H, Nozaki A, Kuo T-T, Usui M, Saihara S, Sugimoto T. A new method for estimating preexcitation index without extrastimulus technique and its usefulness in determining the mechanism of supraventricular tachycardia. Am J Cardiol.. 1991;67:830-834.[Medline] [Order article via Infotrieve]
18.
Narula OS, Narula JT. Junctional pacemakers in man: response to overdrive suppression with and without parasympathetic blockade. Circulation.. 1978;57:880-889.
19. Narula OS, Scerlag BJ, Samet P, Javier RP. Atrioventricular block: localization and classification by His bundle recordings. Am J Med.. 1971;50:146-165.[Medline] [Order article via Infotrieve]
20.
Sano T, Yamagishi S. Spread of excitation from the sinus node. Circ Res.. 1965;16:423-430.
21.
Leier CV, Meacham JA, Schaal SF. Prolonged atrial conduction time: a major predisposing factor for the development of atrial flutter. Circulation.. 1978;57:213-216.
22.
Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter: activation and entrainment mapping guided by intracardiac echocardiography. Circulation.. 1995;92:1839-1848.
23. Yamashita T, Inoue H, Nozaki A, Sugimoto T. Role of anatomical architecture in atrial reentry and double potentials. Am Heart J.. 1992;124:938-946.[Medline] [Order article via Infotrieve]
24. Yamashita T, Oikawa N, Inoue H, Murakawa Y, Nakajima T, Usui M, Ajiki K, Ohkawa S, Sugimoto T. Slow abnormal conduction in the low right atrium: its anatomical basis and relevance to atrial reentry. Am Heart J.. 1994;127:353-359.[Medline] [Order article via Infotrieve]
25. Yamashita T, Inoue H, Nozaki A, Usui M, Kuo T-T, Sugimoto T. Role of anisotropy in determining the selective action of antiarrhythmics in atrial flutter in the dog. Cardiovasc Res.. 1992;124:938-946.
26.
Yamashita T, Nakajima T, Hamada E, Hazama H, Murakawa Y, Omata M. Regional differences in the transient outward current density and repolarization inhomogeneities in the rabbit right atrium. Circulation.. 1995;92:3061-3069.
27.
Ray SG, Griffith MJ, Jamieson S, Bexton RS, Gold RG. Impact of the recommendations of the British Pacing and Electrophysiology Group on pacemaker prescription and on the immediate costs of pacing in the northern region. Br Heart J.. 1992;68:531-534.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||