Pediatr Cardiol 13:44-47, 1992
Pediatric Cardiology 9 Springer-Verlag New York inc. 1992
Sick S i n u s S y n d r o m e a n d D i f f u s e I m p a i r m e n t o f t h e C o n d u c t i o n S y s t e m in a Child: S u c c e s s f u l P a c i n g w i t h a S t e r o i d E l u t i n g E n d o c a r d i a l P a c i n g L e a d Alessandro Capucci,l Giuseppe Boriani,J Roberto Galli,2 Fernando Maria Picchio, Angelo Pierangeli, 2 and Bruno Magnani l tIstituto di Malattie dell'Apparato Cardiovascolare, Universit5~ degli Studi di Bologna; and 2Cattedra di Chirurgia del Cuore e dei Grossi Vasi, Universitfi degli Studi di Bologna, Bologna, Italy
SUMMARY. A 9-year-old patient who had had a syncope was found to have atrial flutter in a resting electrocardiogram (ECG). Brief phases of sinus arrest had previously occurred after drug conversion to sinus rhythm. Structural heart disease was excluded by cardiac catheterization and angiography. Electrophysiologic study revealed a sick sinus syndrome, associated with diffuse impairment of the conduction system (supra-, infra-, and intrahisian block). Epimyocardial and an endocardial pacemaker implantation failed because of high stimulation threshold, after 3 years and 2 weeks, respectively. At the third implantation a steroid-eluting endocardial pacing lead was used and satisfactory pacing was still present 2 years later. KEY WORDS: Atrial flutter - Atrioventricular block - - Pacemaker - - Sick sinus syndrome
Permanent pacemaker implantation in children with atrioventricular block and sinus node disorders is now an accepted form of treatment. Previous reports [2, 4, 5, 9, l l] have emphasized the specific etiology of the rhythm disturbances in this subset of patients, related technical problems, and the natural history of those arrhythmias, which require permanent pacing. Few data have to our knowledge been published on the concomitant presence in the same patient of a sick sinus syndrome, atrioventricular and intraventricular conduction disturbances, and atrial flutter a,s possibly masking an underlying diffuse impairment of conduction. We herein report the case of a 9-year-old patient who'came under our observation after a syncopal attack. He had had atrial flutter in the first electrocardiogram (ECG) and was found to have a diffuse disease of the entire conduction system with a very high stimulation threshold, which required "dedicated" pacemaker implantation. Case Report A 9-year-old boy came to our observation because he had had a syncopal episode at rest. A 12-lead ECG showed atrial flutter Address offprint requests to: Dr. Alessandro Capucci, Istituto di Malanie dell'Apparato Cardiovascolare, Via Massarenti 9, 40138 Bologna, Italy.
with a mean ventricular rate of 100 beats/rain (Fig. 1). Clinical examination, chest x-ray, and two-dimensional echocardiography excluded the presence of cardiac abnormalities; this finding was further confirmed by a hemodynamic and angiographic study. No family history of bradyarrhythmias or tachyarrhythmias was elicited. Digoxin intravenously failed to restore the sinus rhythm, while amiodarone (5 mg/kg as intravenous bolus and then 15 mg/kg/24 h by intravenous infusion) was successful. Subsequently, when sinus rhythm was restored, brief phases of sinus arrest with a junctional escape rhythm (rate 22 beats/min) occurred; amiodarone infusion was stopped and no further therapy was administered. After 20 days, to allow for a wash out of all antiarrhythmic drugs, a Holter recording and an electrophysiologic study were undertaken. The 24-h Holter recording showed sinus rhythm during the entire recording period with phases of sinus bradycardia (55 beats/rain) and frequent monomorphic ventricular premature beats (1748/24 h). Electrophysiologic study in a basal condition (cycle length, 1100 ms) showed PA and AH intervals within normal limits, but revealed an infrahisian conduction delay (HV = 65 ms) (Fig. 2). The corrected sinus node recovery time was above normal limits (1300 ms) at 450 ms cycle length. During programmed electrical stimulation either a suprahisian conduction delay (Wenckebach point at 105 beats/rain with AH interval of 320 ms at 600 ms cycle length) or an intrahisian conduction delay was demonstrated (during pacing at 780 ms cycle length, splitting of HH' of 100 ms after an atrial extrastimulus coupled at 280 ms). After intravenous administration of ajmaline (1 mg/kg) the HV interval increased to 145 ms and subsequently a high-degree atrioventricular block occurred, combined with a significant increase in ventricular stimulation threshold (no response to stimuli at 10 V amplitude and 5 ms length) (Fig. 3), but this was overcome by isoproterenol infusion.
Capucci et al.: Sick Sinus Syndrome Pacing
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The final diagnosis was sick sinus syndrome and supra-, infra-, and intrahisian block. The arrhyt:hmia which presumably had caused the syncopal attack was not definitively identified. However, sinus dysfunction and diffuse impairment of the conduction system were shown to be present and, since the patient had symptoms, pacemaker implantation was indicated, the syncope having been due to either sinus arrest or sinus node suppression after atrial flutter (brady-tachycardia syndrome) or to a transient atrioventricular block9 The epimyocardial technique of pacemaker implantation was preferred because of the relatively young age of the patient. An epimyocardial sutureless screw-in lead (Medtronic 6917) was positioned on the right ventricular wall via a subxiphoidal approach and a generator (Medtronic 8423) was placed in the left hypochondrium. The stimulation threshold at implantation was 1.9 V, 4.3 mA at 0.5 ms. The initial pacemaker settings were:
I
VVI mode, rate 55 beats/min, sensitivity 2.5 mV. One month later an acute pericarditis occurred with moderate pericardial effusion, revealed by two-dimensional echocardiography. A slight increase in the stimulation threshold and a partial sensing defect were also found and corrected by reprogramming the generator (sensitivity 1.25 mV). The pericardial effusion resolved after oral prednisone administration, and no clinical problems were noted during the following 3 years. At the age of 13 years, the boy had another syncopal episode with an exit block in the surface ECG (stimulation threshold > 2 ms at 5 V). A transvenous pacemaker implantation was subsequently performed with a Medtronic 4012 target tip bipolar lead and a Medtronic 8400 VVI generator. The stimulation threshold was normal at implantation (0.5 V, 1.3 mA at 0.5 ms), but then increased significantly after 2 weeks, when a new exit block occurred (stimulation threshold > 2 ms at 5 V), requiring
46
Pediatric Cardiology Vol. 13, No. 1, 1992
A
V
A
V
PA = 25ms AH = 85ms HV = 65ms,
HB
~ Fig. 3, High-stimulation threshold during electrophysiologic tests after intravenous administration of ajmaline (1 mg/kg): the extra stimuli delivered in the right ventricle at 10 V amplitude and 5 ms duration failed to elicit a myocardial response.
LA
.vL
V 100 ms
yet another pacemaker implantation. By that time a steroid-eluting endocardial pacing lead (Medtronic CapSure 4003) was inserted together with a rate responsive pacemaker (Medtronic Activitrax 8403). The stimulation threshold was 0.7 V, 1.8 mA at 0.5 ms at the time of implantation and subsequently (Table 1) remained within normal values. The pacemaker settings were: VVI mode, rate 85 beats/min, with a sensitivity of 5 inV. During follow-up at 2 years no clinical problems due to pacemaker malfunction had occurred and serial pacemaker evaluations have documented a continuing stimulation threshold of 0.05 ms at 5 V amplitude.
Table 1. Stimulation thresholds with the steroid-eluting endocardial pacing lead Time after implantation
3 days 7 days 21 days 2 months 6 months 12 months 24 months
Stimulus characteristics 2.5 V (ms)
5 V (ms)
0.1 0.2 0.1 0. l Not performed Not performed Not performed
0.05 0.1 0.1 0.05 0.05 0.05 0.05
Discussion
Sick sinus syndrome has been reported less often in children, with either unoperated congenital heart disease or structurally normal hearts, than in adults [2, 12]. In these few cases atrial flutter was rare, Beder et al. [2] reporting only one case among 11 with nonsurgical sick sinus syndrome. Sinus node dysfunction in children or apparently healthy males has been reported as being associated with sudden death [3, 7); postmortem examination in one case [7] showing hemorragic and fibrotic foci within the sinus node and narrowing of the sinus node artery. It is, however, striking to note how in that relatively large series of cases none presented initially with supraventricular tachycardia (flutter in our case) masking the underlying sinus node disease and probable evidence of widespread atrial disease, at least in terms of conduction properties. There is also a lack of informations in the literature about the possible association in children with sick sinus syndrome with other specific abnormalities of the conduction system. Alboni et al. [1] described a case in 1977 with contemporaneous involvement of sinus node, atrioventricular node, and intraventricular conduction. In that case, as in ours, there was no familial incidence. It has been de-
scribed [6] that there is a common embryologic origin of sinus node, atrioventricular node, and the proximal His bundle from the primitive sinus venosus, while the distal part of the conduction system is coming from the intraventricular septum, the two structures linking together around the second fetal month. This would explain how atrioventricular node involvement may be found in some patients with primary sinus node dysfunction [2]. In our case there was diffuse involvement of the conduction system as the only clinical manifestation of the disease, this being localized not only within the nodes but also within the His bundle and below, as evidence by the long HV interval and the high stimulation threshold in the right ventricle. The finding is even more striking because there was no specific familial history. The major complication of the pacing system in children concerns the development of high thresholds with epicardial leads [4, 5]. We nonetheless chose this approach because of our patient's small body surface and our intention to avoid future growth problems related to the electrode. This was certainly a mistake in retrospect. It is noteworthy that a high threshold was found even on endocardiaI
Capucci et al.: Sick Sinus Syndrome Pacing
implantation later on. Even in the reviews of the threshold problems in children [4, 5, 9, 1I] it is very rare to find mention of the need for a high output by employing endocardial stimulation. In our case only a low threshold profile and a desametazone-eluting tip electrode finally solved the problem, previously reported by King et ai. [8]. Our observation confirms how this type of electrode, already found very useful for chronic stimulation in adults [10], can in some cases be mandatory for the proper and continuing pacing in children.
References 1. Alboni P, Maiacarne C, Baggioni GF, Antonioli GE (1977) "Sick sinus syndrome" idiopatica con turbe della conduzione A-V ed intraventricolare in un bambino. Primo rapporto in eta' pediatrica. G ltal Cardiol 7:514-520 2. Beder SD, Gillette PC, Garson A, Jr, Porter C J, McNamara DG (1983) Symptomatic sick sinus syndrome in children and adolescents as the only manifestation of cardiac abnormality or associated with unoperated congenital heart disease. Am J Cardio151:1133-1136
47
3. Bharati S, Nordenberg A, Bauernfiend R, Varghese JP, Carvatho AG, Rosen K, Lev M (1980) The anatomic substrate for the sick sinus syndrome in adolescence. A m J Cardiol 46:163-172
4. Ennker J, Stegmann Th, Luhmer I, Oetert H (1985) Risks and benefits of cardiac pacing in children. Int J Cardiol 8:125-134 5. Gillette PC, Shannon C, Blair H, Garson A, Jr, Porter CJ, McNamara DG (1983) Transvenous pacing in pediatric patients. A m Heart J 105:843-847 6. James TN (1970) Cardiac conduction system: Fetal and postnatal development. A m J Cardiol 25:213-226 7. James TN, Frogatt P, Marshall TK (1967) Sudden death in young athletes. Ann Intern M e d 67:1013-1021 8. King DH, Gillette PC, Shannon C, Cuddy TE (1983) Steroid eluting endocardial pacing lead for treatment of exit block. Am Heart H 106:1438-1440
9. Kugler JD, Danford DA (1989) Pacemakers in children: An update. A m Heart J 117:665-679 10. Mond H, Stokes K, Helland J, Grigg L, Kertes P, Pate B, Hunt D (1988) The porous titanium steroid eluting electrode: A double blind study assessing the stimulation threshold effects of steroid. PACE I1:214-219 11. Simon AB, Dick M II, Stern AM, Behrendt DM, Sloan H (1982) Ventricular pacing in children. PACE 5:836-844 12. Yabek SM, Swensson RE, Jarmakani JM (1977) Electrocardiographic recognition of sinus node dysfunction in children and young adults. Circulation 56:235-239
Pediatric Cardiology 9 Springer-Verlag New York inc. 1992
Sick S i n u s S y n d r o m e a n d D i f f u s e I m p a i r m e n t o f t h e C o n d u c t i o n S y s t e m in a Child: S u c c e s s f u l P a c i n g w i t h a S t e r o i d E l u t i n g E n d o c a r d i a l P a c i n g L e a d Alessandro Capucci,l Giuseppe Boriani,J Roberto Galli,2 Fernando Maria Picchio, Angelo Pierangeli, 2 and Bruno Magnani l tIstituto di Malattie dell'Apparato Cardiovascolare, Universit5~ degli Studi di Bologna; and 2Cattedra di Chirurgia del Cuore e dei Grossi Vasi, Universitfi degli Studi di Bologna, Bologna, Italy
SUMMARY. A 9-year-old patient who had had a syncope was found to have atrial flutter in a resting electrocardiogram (ECG). Brief phases of sinus arrest had previously occurred after drug conversion to sinus rhythm. Structural heart disease was excluded by cardiac catheterization and angiography. Electrophysiologic study revealed a sick sinus syndrome, associated with diffuse impairment of the conduction system (supra-, infra-, and intrahisian block). Epimyocardial and an endocardial pacemaker implantation failed because of high stimulation threshold, after 3 years and 2 weeks, respectively. At the third implantation a steroid-eluting endocardial pacing lead was used and satisfactory pacing was still present 2 years later. KEY WORDS: Atrial flutter - Atrioventricular block - - Pacemaker - - Sick sinus syndrome
Permanent pacemaker implantation in children with atrioventricular block and sinus node disorders is now an accepted form of treatment. Previous reports [2, 4, 5, 9, l l] have emphasized the specific etiology of the rhythm disturbances in this subset of patients, related technical problems, and the natural history of those arrhythmias, which require permanent pacing. Few data have to our knowledge been published on the concomitant presence in the same patient of a sick sinus syndrome, atrioventricular and intraventricular conduction disturbances, and atrial flutter a,s possibly masking an underlying diffuse impairment of conduction. We herein report the case of a 9-year-old patient who'came under our observation after a syncopal attack. He had had atrial flutter in the first electrocardiogram (ECG) and was found to have a diffuse disease of the entire conduction system with a very high stimulation threshold, which required "dedicated" pacemaker implantation. Case Report A 9-year-old boy came to our observation because he had had a syncopal episode at rest. A 12-lead ECG showed atrial flutter Address offprint requests to: Dr. Alessandro Capucci, Istituto di Malanie dell'Apparato Cardiovascolare, Via Massarenti 9, 40138 Bologna, Italy.
with a mean ventricular rate of 100 beats/rain (Fig. 1). Clinical examination, chest x-ray, and two-dimensional echocardiography excluded the presence of cardiac abnormalities; this finding was further confirmed by a hemodynamic and angiographic study. No family history of bradyarrhythmias or tachyarrhythmias was elicited. Digoxin intravenously failed to restore the sinus rhythm, while amiodarone (5 mg/kg as intravenous bolus and then 15 mg/kg/24 h by intravenous infusion) was successful. Subsequently, when sinus rhythm was restored, brief phases of sinus arrest with a junctional escape rhythm (rate 22 beats/min) occurred; amiodarone infusion was stopped and no further therapy was administered. After 20 days, to allow for a wash out of all antiarrhythmic drugs, a Holter recording and an electrophysiologic study were undertaken. The 24-h Holter recording showed sinus rhythm during the entire recording period with phases of sinus bradycardia (55 beats/rain) and frequent monomorphic ventricular premature beats (1748/24 h). Electrophysiologic study in a basal condition (cycle length, 1100 ms) showed PA and AH intervals within normal limits, but revealed an infrahisian conduction delay (HV = 65 ms) (Fig. 2). The corrected sinus node recovery time was above normal limits (1300 ms) at 450 ms cycle length. During programmed electrical stimulation either a suprahisian conduction delay (Wenckebach point at 105 beats/rain with AH interval of 320 ms at 600 ms cycle length) or an intrahisian conduction delay was demonstrated (during pacing at 780 ms cycle length, splitting of HH' of 100 ms after an atrial extrastimulus coupled at 280 ms). After intravenous administration of ajmaline (1 mg/kg) the HV interval increased to 145 ms and subsequently a high-degree atrioventricular block occurred, combined with a significant increase in ventricular stimulation threshold (no response to stimuli at 10 V amplitude and 5 ms length) (Fig. 3), but this was overcome by isoproterenol infusion.
Capucci et al.: Sick Sinus Syndrome Pacing
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45
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It ~"~/I
AFTER
~St [-
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The final diagnosis was sick sinus syndrome and supra-, infra-, and intrahisian block. The arrhyt:hmia which presumably had caused the syncopal attack was not definitively identified. However, sinus dysfunction and diffuse impairment of the conduction system were shown to be present and, since the patient had symptoms, pacemaker implantation was indicated, the syncope having been due to either sinus arrest or sinus node suppression after atrial flutter (brady-tachycardia syndrome) or to a transient atrioventricular block9 The epimyocardial technique of pacemaker implantation was preferred because of the relatively young age of the patient. An epimyocardial sutureless screw-in lead (Medtronic 6917) was positioned on the right ventricular wall via a subxiphoidal approach and a generator (Medtronic 8423) was placed in the left hypochondrium. The stimulation threshold at implantation was 1.9 V, 4.3 mA at 0.5 ms. The initial pacemaker settings were:
I
VVI mode, rate 55 beats/min, sensitivity 2.5 mV. One month later an acute pericarditis occurred with moderate pericardial effusion, revealed by two-dimensional echocardiography. A slight increase in the stimulation threshold and a partial sensing defect were also found and corrected by reprogramming the generator (sensitivity 1.25 mV). The pericardial effusion resolved after oral prednisone administration, and no clinical problems were noted during the following 3 years. At the age of 13 years, the boy had another syncopal episode with an exit block in the surface ECG (stimulation threshold > 2 ms at 5 V). A transvenous pacemaker implantation was subsequently performed with a Medtronic 4012 target tip bipolar lead and a Medtronic 8400 VVI generator. The stimulation threshold was normal at implantation (0.5 V, 1.3 mA at 0.5 ms), but then increased significantly after 2 weeks, when a new exit block occurred (stimulation threshold > 2 ms at 5 V), requiring
46
Pediatric Cardiology Vol. 13, No. 1, 1992
A
V
A
V
PA = 25ms AH = 85ms HV = 65ms,
HB
~ Fig. 3, High-stimulation threshold during electrophysiologic tests after intravenous administration of ajmaline (1 mg/kg): the extra stimuli delivered in the right ventricle at 10 V amplitude and 5 ms duration failed to elicit a myocardial response.
LA
.vL
V 100 ms
yet another pacemaker implantation. By that time a steroid-eluting endocardial pacing lead (Medtronic CapSure 4003) was inserted together with a rate responsive pacemaker (Medtronic Activitrax 8403). The stimulation threshold was 0.7 V, 1.8 mA at 0.5 ms at the time of implantation and subsequently (Table 1) remained within normal values. The pacemaker settings were: VVI mode, rate 85 beats/min, with a sensitivity of 5 inV. During follow-up at 2 years no clinical problems due to pacemaker malfunction had occurred and serial pacemaker evaluations have documented a continuing stimulation threshold of 0.05 ms at 5 V amplitude.
Table 1. Stimulation thresholds with the steroid-eluting endocardial pacing lead Time after implantation
3 days 7 days 21 days 2 months 6 months 12 months 24 months
Stimulus characteristics 2.5 V (ms)
5 V (ms)
0.1 0.2 0.1 0. l Not performed Not performed Not performed
0.05 0.1 0.1 0.05 0.05 0.05 0.05
Discussion
Sick sinus syndrome has been reported less often in children, with either unoperated congenital heart disease or structurally normal hearts, than in adults [2, 12]. In these few cases atrial flutter was rare, Beder et al. [2] reporting only one case among 11 with nonsurgical sick sinus syndrome. Sinus node dysfunction in children or apparently healthy males has been reported as being associated with sudden death [3, 7); postmortem examination in one case [7] showing hemorragic and fibrotic foci within the sinus node and narrowing of the sinus node artery. It is, however, striking to note how in that relatively large series of cases none presented initially with supraventricular tachycardia (flutter in our case) masking the underlying sinus node disease and probable evidence of widespread atrial disease, at least in terms of conduction properties. There is also a lack of informations in the literature about the possible association in children with sick sinus syndrome with other specific abnormalities of the conduction system. Alboni et al. [1] described a case in 1977 with contemporaneous involvement of sinus node, atrioventricular node, and intraventricular conduction. In that case, as in ours, there was no familial incidence. It has been de-
scribed [6] that there is a common embryologic origin of sinus node, atrioventricular node, and the proximal His bundle from the primitive sinus venosus, while the distal part of the conduction system is coming from the intraventricular septum, the two structures linking together around the second fetal month. This would explain how atrioventricular node involvement may be found in some patients with primary sinus node dysfunction [2]. In our case there was diffuse involvement of the conduction system as the only clinical manifestation of the disease, this being localized not only within the nodes but also within the His bundle and below, as evidence by the long HV interval and the high stimulation threshold in the right ventricle. The finding is even more striking because there was no specific familial history. The major complication of the pacing system in children concerns the development of high thresholds with epicardial leads [4, 5]. We nonetheless chose this approach because of our patient's small body surface and our intention to avoid future growth problems related to the electrode. This was certainly a mistake in retrospect. It is noteworthy that a high threshold was found even on endocardiaI
Capucci et al.: Sick Sinus Syndrome Pacing
implantation later on. Even in the reviews of the threshold problems in children [4, 5, 9, 1I] it is very rare to find mention of the need for a high output by employing endocardial stimulation. In our case only a low threshold profile and a desametazone-eluting tip electrode finally solved the problem, previously reported by King et ai. [8]. Our observation confirms how this type of electrode, already found very useful for chronic stimulation in adults [10], can in some cases be mandatory for the proper and continuing pacing in children.
References 1. Alboni P, Maiacarne C, Baggioni GF, Antonioli GE (1977) "Sick sinus syndrome" idiopatica con turbe della conduzione A-V ed intraventricolare in un bambino. Primo rapporto in eta' pediatrica. G ltal Cardiol 7:514-520 2. Beder SD, Gillette PC, Garson A, Jr, Porter C J, McNamara DG (1983) Symptomatic sick sinus syndrome in children and adolescents as the only manifestation of cardiac abnormality or associated with unoperated congenital heart disease. Am J Cardio151:1133-1136
47
3. Bharati S, Nordenberg A, Bauernfiend R, Varghese JP, Carvatho AG, Rosen K, Lev M (1980) The anatomic substrate for the sick sinus syndrome in adolescence. A m J Cardiol 46:163-172
4. Ennker J, Stegmann Th, Luhmer I, Oetert H (1985) Risks and benefits of cardiac pacing in children. Int J Cardiol 8:125-134 5. Gillette PC, Shannon C, Blair H, Garson A, Jr, Porter CJ, McNamara DG (1983) Transvenous pacing in pediatric patients. A m Heart J 105:843-847 6. James TN (1970) Cardiac conduction system: Fetal and postnatal development. A m J Cardiol 25:213-226 7. James TN, Frogatt P, Marshall TK (1967) Sudden death in young athletes. Ann Intern M e d 67:1013-1021 8. King DH, Gillette PC, Shannon C, Cuddy TE (1983) Steroid eluting endocardial pacing lead for treatment of exit block. Am Heart H 106:1438-1440
9. Kugler JD, Danford DA (1989) Pacemakers in children: An update. A m Heart J 117:665-679 10. Mond H, Stokes K, Helland J, Grigg L, Kertes P, Pate B, Hunt D (1988) The porous titanium steroid eluting electrode: A double blind study assessing the stimulation threshold effects of steroid. PACE I1:214-219 11. Simon AB, Dick M II, Stern AM, Behrendt DM, Sloan H (1982) Ventricular pacing in children. PACE 5:836-844 12. Yabek SM, Swensson RE, Jarmakani JM (1977) Electrocardiographic recognition of sinus node dysfunction in children and young adults. Circulation 56:235-239
