If the battery of a pacemaker becomes depleted or the device malfunctions, the conventional practice has been to replace the pacemaker or pacemaker lead without questioning the need for continued cardiac pacing. However, the clinician occasionally encounters patients referred for pacemaker replacement in whom the original indication for cardiac pacing is unclear or the pathologic process that resulted in the need for a pacemaker seems to have resolved. Moreover, pacemakers are sometimes implanted in patients who do not meet class I or class II specifications.

Pacemaker replacement has the potential to cause illness. In particular, reported infection rates have ranged from 1% to 7% in patients receiving pacemakers (although rates are currently toward the lower end of this range) and are higher with reoperation [6-8]. Young patients who receive a permanent pacemaker have to undergo pacemaker replacement and lead revisions several times during their lifetime. Such patients are exposed to cumulative health risks and a substantial financial burden. Therefore, it may be appropriate to consider that some patients may not need lifelong cardiac pacing.

Methods

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In an effort to characterize clinical scenarios in which the discontinuation of cardiac pacing might be reasonable, we retrospectively examined medical records at the University of Minnesota Hospital and attempted to identify patients in whom permanent cardiac pacing had been terminated. Five such patients were identified. These patients had been selected from approximately 80 patients who had been referred for pacemaker replacement or lead revision between 1992 and 1995. It was determined that pacemaker replacement was not necessary because of young age, presence of sinus rhythm with a narrow QRS complex on the electrocardiogram at admission, and improvement or reversal of the rhythm disturbance that led to the original implantation of the device.

Results

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Table 1 summarizes the demographic and clinical characteristics of the five patients who were identified. These patients had a mean age of 43 years and had had cardiac pacing for a mean of 10 years (range, 9 months to 18 years).

During removal of the pacemaker, extraction of the leads was attempted in four of the five patients (patient 1 had epicardial leads). Only gentle traction was used. The leads were easily removed in patient 4, but the leads in the other three patients had been present for several years and had adhered to the endocardium. As a result, we elected not to remove the leads from these patients because more aggressive attempts to remove them carried an unjustifiable risk.

No complications related to the procedures occurred. The mean hospital stay was 2.6 days. All patients have been reassessed regularly for at least 18 months since the pacemaker was removed. No patient has had symptomatic bradycardia to warrant the reinstitution of cardiac pacing.

Case Highlights

Patient 1

At 34 years of age, patient 1 had patching of a ventricular septal defect. The procedure was complicated by third-degree atrioventricular block, and a dual-chamber pacemaker was implanted. Atrioventricular conduction subsequently improved. When the patient was 44 years of age, loss of capture in the ventricle was noted. The patient was referred at 45 years of age because of depletion of the pacemaker battery and frequent episodes of atrial flutter despite therapy with antiarrhythmic agents. During our evaluation, suboptimal sensing of the atrial lead was also noted. We were concerned that this suboptimal sensing, followed by inappropriate atrial pacing, might be contributing to the triggering of atrial flutter. Moreover, the patient had done well without a functioning ventricular lead for 1 year.

The pacemaker was removed. In the next 2 years, the patient did not have symptoms of bradycardia but atrial flutter continued to recur. The patient eventually had successful transcatheter ablation of the flutter circuit.

Patient 3

At 19 years of age, patient 3 developed third-degree atrioventricular block after cardiac surgery for the correction of complex congenital heart disease. At 37 years of age, he presented with twitching of the pectoral muscle. Electrophysiologic evaluation was done to assess the conduction system. With the patient sedated, 1:1 atrioventricular conduction was present, but conduction block in the atrioventricular node occurred during atrial pacing at a relatively slow heart rate (75 beats/min). The HV interval was 53 ms, suggesting normal conduction of the His-Purkinje system at baseline (normal range, 35 to 55 ms). Later in the study, when the patient was not sedated, conduction of the atrioventricular node improved. While the patient was receiving isoproterenol (1 µg/min), 1:1 atrioventricular conduction was sustained at 180 beats/min. Conduction block in the His-Purkinje system was not seen, even after protocols with bursts of rapid atrial pacing and intravenous procainamide (1000 mg) were used concomitantly to uncover possible dysfunction of the distal conduction system. The pacemaker was subsequently removed.

Patient 4

A permanent pacemaker had been implanted in patient 4 after he presented with third-degree atrioventricular block and narrow-complex escape rhythm associated with fatigue. Nine months later, at 53 years of age, the patient sought a second opinion because of rapid depletion of the pacemaker battery. An electrophysiologic evaluation was done. While the patient was sedated, atrioventricular-node block occurred at 110 beats/min during atrial pacing. The HV interval was normal (50 ms). When the effects of the sedative subsided and atropine was administered to diminish vagal effects on conduction properties, conduction of the atrioventricular node substantially improved; 1:1 conduction was sustained at 175 beats/min. Conduction block in the His-Purkinje system did not occur, even after procainamide was administered. The pacemaker was electively removed.

Discussion

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Review of Findings

The experience that we report suggests that in certain patients, long-term cardiac pacing can be safely discontinued. Despite differences in underlying cardiovascular disease, the patients in our series shared certain features. They were all relatively young and were referred because of battery depletion or a pacing-related complication. At the time of evaluation, all patients had sinus rhythm and a narrow QRS complex.

Several techniques were used to confirm the presence of an appropriate natural rhythm before and after removal of the pacemaker. Ambulatory electrocardiography (using event and Holter monitors) was done before the procedure when the pacing rate had been reduced to a safe minimum (30 to 40 beats/min) and after the procedure; using this method, recurrent symptoms could be correlated with the underlying heart rate. Electrophysiologic assessment of the conduction system was done in patients 3 and 4. Patients 2 and 5 had pacemakers that could keep track of the number of times a pacing stimulus was released or a native complex was sensed. This feature permitted an assessment of the degree to which the device was used for a specific time. All patients were followed closely after pacemaker removal for symptoms that suggested recurrence of bradycardia.

Terminating Cardiac Pacing

The decision to discontinue long-term cardiac pacing is difficult to make for several reasons. Available clinical tools for evaluating dysfunction of the sinus and atrioventricular nodes are not optimally sensitive for detecting the progression or regression of electric disease. Moreover, the natural history of some bradyarrhythmias that require cardiac pacing may be unpredictable. Finally, recurrence of bradycardia after pacemaker removal carries the risk for substantial illness and perhaps even death. Thus, when compared with the termination of other long-term therapies (such as digoxin in patients with heart failure), discontinuation of cardiac pacing may have a smaller margin for error and greater exposure to legal risk.

On the other hand, the cost and health risks of long-term cardiac pacing can be substantial. Therefore, our challenge is to identify the patients who would be least served by the replacement of a permanent pacemaker. Although our data are limited by referral bias and a relatively small patient population, we estimate that 2% to 4% of patients whose pacemakers are being replaced may not require permanent cardiac pacing.

Reassessment of the need for permanent cardiac pacing may be considered in patients who received their device for a class III indication [4], who continue to have the same symptoms despite an appropriately functioning pacemaker, or who seem to have had a reversal of the process that originally led to the need for cardiac pacing. Reversible dysfunction of the sinus or atrioventricular nodes has been described in various disease states. Potentially reversible causes of bradycardia that have been reported [9-19] include electrolyte disturbances, severe hypoxia, use of pharmacologic agents (almost all antiarrhythmic agents), cardiac surgery (aortic or mitral valve replacement, repair of congenital heart disease, and heart transplantation), myocardial infarction of the inferior wall, infections (endocarditis, myocarditis, and especially Lyme borreliosis), neurally mediated reflexes with a cardioinhibitory component, sleep apnea, cardiac contusion, and (rarely) cardiac neoplasms and rheumatic syndromes.

Limitations

Interpretation of the experience that we report is subject to several important limitations. We have described only a small number of cases and a relatively short follow-up period. Our patient sample is highly selected and may not represent all patients who receive permanent pacemakers. It seems that the discontinuation of cardiac pacing may be considered for only a small percentage of patients with permanent pacemakers. Finally, no currently available technique can unequivocally rule out intermittent failure of the conduction system.

Conclusion

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The presence of a permanent pacemaker may not necessarily imply a permanent need for cardiac pacing. Discontinuation of cardiac pacing may be justified if a preponderance of clinical findings suggests that pacing is no longer indicated or that the risks of the continuous replacement of the device outweigh the potential benefits of implantation. The method and timing of pacemaker removal need to be clarified by an expert panel and, ultimately, by a randomized trial.