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Ann Thorac Surg 2000;70:1931-1934
© 2000 The Society of Thoracic Surgeons

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Original article: cardiovascular

DDD pacing mode survival in children with a dual-chamber pacemaker

^a Division of Cardiology, University Children’s Hospital, Zurich, Switzerland
^b Department of Cardiovascular Surgery, University Hospital, Zurich, Switzerland

Accepted for publication May 13, 2000.

Address reprint requests to Dr Bauersfeld, Division of Cardiology, University Children’s Hospital, Steinwiesstr 75, CH-8032 Zurich, Switzerland
e-mail: bauersfe{at}kispi.unizh.ch

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. The persistence of DDD pacing is well documented in adults, however, in children survival of the DDD pacing mode is less clear.

Methods. We studied the survival of dual-chamber (DDD) pacing in 36 children aged 1 week to 16 years who underwent implantation of a dual-chamber pacing system between January 1986 and October 1998. The children were divided in the following two groups: 26 had epicardial pacing systems and 10 had endocardial pacing systems.

Results. During long-term follow-up 11 patients lost the DDD pacing mode. The DDD pacing survival rate at 3 months and 1, 2, and 5 years was 80%, 77%, 73%, and 69%, respectively. Age, weight, congenital heart disease, and epicardial pacing leads were not found to be risk factors for loss of DDD pacing mode. However, P-wave values of less than 2.5 mV at implantation of epicardial leads were associated with loss of the DDD pacing mode.

Conclusions. The majority of children remain in the DDD pacing mode during long-term follow-up. A P-wave value of less than 2.5 mV at implantation of epicardial leads is a risk factor for loss of the DDD pacing mode.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
The main indication for permanent cardiac pacing in children is congenital or postoperative heart block [1]. Although the implantation and follow-up of dual-chamber pacing systems are more complex, atrioventricular synchronization by DDD stimulation in children with heart block can improve hemodynamics when compared to single-chamber ventricular (VVI(R)) pacing [2]. The long-term outcome in some patients with congenital heart disease and atrioventricular block may also be superior with DDD pacing [3]. Furthermore, symptoms related to pacemaker syndrome can be widely abolished by use of a DDD pacing mode [4]. As has occurred in adults, advances in lead and pacemaker technologies over the last decade have resulted in an increasing rate of implantation of dual-chamber pacemakers in children. Although these advances also facilitated the implantation of transvenous pacing systems in small children, cardiovascular anatomy or concern about venous obstruction by transvenous leads still necessitates the implantation of epicardial pacing systems in children, as well as in some adults with congenital heart disease [5–7]. Promising experiences with new bipolar epicardial pacing leads also favored the implantation of epicardial DDD pacing systems in pediatric patients and in adults who were not ideal candidates for transvenous pacing systems [8, 9]. However, studies of adult patients with DDD pacing systems revealed a reprogramming rate of up to 20% during long-term follow-up, mainly because of the occurrence of atrial arrhythmias, especially atrial fibrillation [10–12]. Although atrial fibrillation is uncommon in pediatric patients, factors such as small patient size, continuous growth, and cardiovascular anatomy may jeopardize lead implantation, and implanted pacing systems may eventually lose the DDD pacing mode. Furthermore, previous reports have described a high pacemaker system failure rate in children, citing a pacemaker related reoperation rate of up to 50% at the fourth year of follow-up [13, 14]. Thus, the purpose of this study was to define the survival rate of DDD pacing in a series of pediatric patients with endocardial or epicardial dual-chamber pacing systems and to define potential risk factors for loss of the DDD pacing mode.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Between January 1986 and October 1998, 36 consecutive children underwent implantation of a dual-chamber pacing system at our institution. Patient demographics, clinical characteristics, and indications for pacing are described in Table 1. For detailed analyses patients were assigned to one of two groups, depending on whether they had an endocardial or epicardial pacing system. In 13 of 26 children with an epicardial pacing system, the implantation was performed in conjunction with cardiac surgery or in the postoperative period after cardiac surgery. No endocardial pacing system was implanted at the time of cardiac surgery or in the postoperative period after cardiac surgery. The main indications for implantation of an epicardial pacing system were cardiovascular anatomy precluding endocardial systems (n = 16) and small patient size (n =10).

Implantation procedure
Standard implant techniques were used. Surgical access for epicardial lead implantation was accomplished with a left lateral thoracotomy in 20 children and a sternotomy in 6 children; generators were placed in a submuscular rectus sheath. Although the subxyphoid approach may be favorable for the implantation of unipolar atrial leads, we avoided this implant technique for bipolar leads because of concerns of atrial sensing dysfunctions. With a subxyphoid approach atrial lead tips are potentially closer to the atrioventricular groove, with a chance of sensing ventricular potentials and possibly low P waves, because that position is more likely to be perpendicular to atrial activation. All endocardial leads were introduced through a subclavian vein and the generator placed in a subpectoral pocket. Lead impedances, A and R waves, and pacing thresholds were determined intraoperatively as usual and used for later data analyses. A Holter recording and pacemaker follow-up including telemetry data, A-wave and R-wave measurements, and pacing thresholds were done before hospital discharge.

Follow-up data collection
Pacemaker telemetry data, A and R waves, and pacing thresholds were obtained 6 weeks, 3 months, and 6 months after implantation, and thereafter at 6-month intervals. In case of reprogramming out of the DDD pacing mode, the reasons for reprogramming, time to reprogramming, and need for secondary surgical intervention were recorded. The occurrence of arrhythmias as indicated by ECG, Holter monitoring, or exercise testing was registered when observed

Statistical analyses
Continuous variables are presented as mean values ± standard deviations. Comparative data were analyzed by using a -square or two-tailed t test. Cumulative survival curves for DDD pacing and freedom of reintervention were calculated by the Kaplan-Meier method. Differences between survival curves for risk factor analyses were calculated using the Mantel-Haenszel test. Age and body weight at implantation, congenital heart disease, lead type, and differences of implant data were analyzed as possible risk factors for reprogramming out of the DDD pacing mode. Statistical significance is indicated by the calculated p values.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Pacemaker survival in the DDD mode
During long-term follow-up loss of the DDD pacing mode occurred in 11 of 36 patients (30%). The DDD mode survival rate at 3 months and 1, 2, and 5 years was 80%, 77%, 73%, and 69%, respectively (Figure 1). There was no statistically significant difference in survival rates of epicardial or endocardial pacing systems.

View larger version (15K): [in this window] [in a new window]   Fig 1. Kaplan-Meier time to loss of the DDD pacing mode (n = 36). Separate curves indicate survival for epicardial (n = 26), endocardial (n = 10), and total pacing systems.

Freedom from intervention
Freedom from reintervention for pacing system failure at 3 months, 1 year, and 5 years was 94%, 91%, and 91%, respectively. Reinterventions consisted of repositioning atrial leads in 2, new lead and pacemaker implant after lead fracture in 1 patient and after pacing system infection in 1 patient. In the remaining 7 patients loss of DDD pacing resulted in reprogramming to VVI(R) pacing mode in 6 patients and to single-chamber atrial-inhibited pacing with rate modulation (AAIR pacing mode) in 1 patient.

Risk factors for loss of DDD pacing mode
Implant data revealed significant P-wave differences between reprogrammed epicardial DDD pacing systems and persisting epicardial DDD systems (Table 3). Applying a cut-off point of 2.5 mV P waves in patients with epicardial leads, the likelihood of DDD pacing survival was significantly lower (p = 0.0045) in patients with P-wave values less than 2.5 mV than in those with values of 2.5 mV or higher at the time of lead implantation.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
Several studies have addressed the benefit of synchronized pacing in children [2, 3]. The advancement in lead and pacemaker technology made it feasible to implant dual-chamber pacing systems even in neonates [5]. However, the higher complexity of dual-chamber pacing systems at implantation and follow-up may result in a higher failure rate compared with that of VVI(R) pacing systems. Studies in adult patients have indicated a substantial reprogramming rate during follow-up, with atrial fibrillation being the most common cause [10–12]. Atrial fibrillation is very uncommon in children, and the implemented multiprogrammability in modern pacemakers and mode-switch algorithms in case of atrial flutter should preclude arrhythmias as a reason for reprogramming DDD pacemakers in children. Loss of the DDD pacing mode in children is therefore more likely to be related to young age and low weight at implantation, congenital heart disease, and lead malfunctions.

This study describes the survival of epicardial and endocardial DDD pacing systems in children; the mean follow-up time was 2 to 4 years. Although most children had complex cardiac defects necessitating cardiac surgery with numerous difficult pacemaker implantations at the time of cardiac surgery or in the postoperative period, the observed survival rate of the DDD pacing mode of 77% at 1-year and 69% at 5-year follow-up is only slightly lower than reported in adult studies. The DDD mode survival rates are also very favorable in view of previous reports indicating high pacemaker and lead failure rates in children [13]. Most of the DDD mode loss in this study occurred during the first few weeks after implantation, with sensing dysfunction of epicardial leads and dislodgment of endocardial atrial leads being the most common causes of reprogramming. Atrial arrhythmias were observed but did not necessitate reprogramming. Freedom from reoperation for pacing system failure was still 91% at 5-year follow-up. However, in some patients this was at the expense of using a hemodynamically less advantageous VVI(R) pacing mode, which was felt to be acceptable at least until the next generator replacement. But even with later reprogramming, DDD mode pacing may have improved early postoperative hemodynamics in the occasional patient with cardiac surgery and postoperative heart block.

A comparison of implant data identified a P-wave sensing of less than 2.5 mV as risk factor for loss of DDD pacing with epicardial leads. The significance of this finding is not completely clear, as the sensing characteristics of epicardial steroid-eluting electrodes are expected to be stable over time [8]. As most of these epicardial leads were implanted at the time of cardiac surgery or in the postoperative period, P-wave measurements could have been jeopardized by hemodynamic compromises, drugs, and atrial rhythm instead of sinus rhythm. Furthermore, sensing characteristics may have deteriorated because of scarring related to cardiac surgery rather than because of the lead implantation itself.

Even though the implantation of DDD pacing systems is expected to be more difficult in younger children and in children with congenital heart defects, we found that age, weight, and congenital heart disease were not risk factors for DDD pacing failure. Beaufort-Krol and colleagues have already shown that in pediatric patients, the performance of steroid-eluting epicardial leads is comparable to that of endocardial leads [8]. However, this study demonstrates that DDD mode survival with steroid-eluting bipolar epicardial leads is not statistically significantly different from survival with modern endocardial leads. This is remarkable, as the implant conditions for most epicardial leads were more difficult in younger and smaller children in the postoperative period after cardiac surgery.

Despite the encouraging results with epicardial leads, more efficient and cost-saving implant processes seem to be possible in some patients. Often the epicardial ventricular lead is positioned first and a DDD generator implanted even in case of unsatisfactory atrial thresholds. We suggest that the epicardial atrial lead should be implanted first, which allows use of the lead on the ventricle and implantation of a VVI(R) device in case of high atrial pacing thresholds or inadequate atrial sensing (< 2.5 mV). The implantation of newer epicardial leads may now become more attractive even when the patient is an older child; that may help to preserve venous access for endocardial pacing systems later on. However, whether atrial sensing dysfunctions of epicardial leads still favor implantation of endocardial pacing systems has to be evaluated in further studies.

In conclusion, the majority of children with DDD pacing systems remain in DDD pacing mode during long-term follow-up. Loss of the DDD pacing mode, which is only slightly more common than in adults, is mainly related to sensing failure and lead dislodgment. Reinterventions for DDD pacing failure are rare in children. Current epicardial DDD pacing systems have a performance comparable with that of endocardial systems. Adequate atrial sensing may be assured with a P wave exceeding 2.5 mV at implantation of epicardial leads.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

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