Pacemaker longevity: are we getting what we are promised?

BACKGROUND: Although pacemaker manufacturers provide projections on longevity, these projections cannot be relied upon due to the assumptions of output parameters being far in excess of those programmed in clinical practice. OBJECTIVE: The purpose of this review was to compare the actual longevity to the calculated longevity of pacemakers based on battery cell characteristics taking into account individual programmed parameters, mode, degree of usage, and percent pacing. This was also compared to the manufacturers' own projected longevities. METHODS: Patients who had a pacemaker replaced between 1998 and 2003 were included (n = 124). Cell characteristics were obtained from manufacturers and programmed parameters were obtained at each visit. Stepwise calculations were done for each visit to find current drain during each interval, and then were used in a weighted average to find the total average lifetime current drain. This was subsequently used to find a calculated longevity for each pacemaker to be compared to the actual longevity observed. RESULTS: The pacemakers lasted 491+/-92 days (mean+/-SEM) less than calculated. There was also a difference between dual- and single-chamber devices (though not statistically significant). Moreover, it was found that there were significant differences between manufacturers. CONCLUSIONS: There appears to be a significant discrepancy between calculated and actual longevities, confirming that battery depletion occurs earlier than expected. This suggests that current drain expended for ancillary functions may be considerable. Another factor may be pre-implantation drain. Vigilance with programming of outputs, modes, sensors, heart rates, and ancillary functions could potentially extend longevity and postpone/obviate the need for costly repeat surgery with its attended risk of complications. Furthermore, the differences between manufacturers seem to parallel the clinical impressions.

Cardiac pacing device therapy for atrial dysrhythmias: how does it work?

Atrial fibrillation (AF) is the most common dysrhythmia in North America. Paroxysmal or persistent AF affects an estimated 2.8 million individuals, causes significant morbidity, and is associated with 1 billion dollars in healthcare costs each year in the United States. An aging population, the prevalence of hypertension, and the emergence of heart failure as the final common pathway of heart disease finds us in an age where the incidence of AF is ever increasing and the management challenges are indeed an expanding clinical problem. Although guidelines for selection of the appropriate pacing mode have been published, device therapy for the control of AF and paroxysmal AF is an emerging clinical management strategy. In 2001 The American College of Cardiology (ACC)/American Heart Association (AHA) published a document to revise the 1998 guidelines for device therapy, and even now these guidelines require elucidation and inclusion for the use of cardiac pacing device therapy for the control of atrial dysrhythmia. Choosing a complex system, in particular for the patient with persistent and symptomatic atrial dysrhythmia, is a most intricate challenge for the healthcare professional and the healthcare system. Rate dependent effects on refractoriness, reduction of ectopy, remodeling of the substrate, and prevention of pauses have been described as the potential mechanisms responsible for the rhythmic control effect attributed to atrial pacing. However, while permanent cardiac pacing is required for patients with symptomatic bradycardia with atrioventricular block and AF, the concept of pacing for the primary prevention of AF is novel. Pacing algorithms, single site, biatrial, and dual-site atrial pacing and site-specific pacing have all been studied as substrate modulators to prevent recurrent atrial dysrhythmia.A dilemma exists surrounding the primary approach for the control of symptomatic AF with rapid ventricular response. The question remains: should it be to maintain the sinus rhythm or to control the ventricular response rate to the AF and anticoagulate? Variations in the population studied, differences in the pacing algorithms and protocols, and a lack of definitive end points account for the variable results of the studies completed thus far. With the current data available, it appears that for individuals with sinus node dysfunction and paroxysmal AF in combination with a bradyarrhythmia indication for pacing, suppression algorithms may play an additive role with full atrial pacing in the management and reduction of episodes and burden of paroxysmal AF. The goal of these therapies is to reduce the symptoms and hopefully decrease the healthcare costs associated with paroxysmal and persistent AF with uncontrolled ventricular response.

Postpacemaker implant pericarditis: incidence and outcomes with active-fixation leads.

Pericarditis has been noted as a potential complication of pacemaker implantation. This study evaluated the risk of developing pericarditis following pacemaker implantation with active-fixation atrial leads. Included were 1,021 consecutive patients (mean age 73.4+/-0.4 years, range 16-101 years; 45.2% women) undergoing new pacemaker system implantation between 1991 and 1999 who were reviewed for the complication of pericarditis. The incidence and outcomes of postimplantation pericarditis in patients receiving active-fixation atrial leads were compared to those not receiving these leads. Of 79 patients who received active-fixation atrial leads, 4 (5%) developed pericarditis postpacemaker implantation. Of 942 patients with passive-fixation atrial leads or no atrial lead (i.e., a ventricular lead only), none developed pericarditis postoperatively (P < 0.001). Of patients receiving active-fixation ventricular leads only (n = 97), none developed pericarditis. No complications were apparent at the time of implantation in patients who developed pericarditis. Pleuritic chest pain developed between 1 and 28 hours postoperatively. Three patients had pericardial rubs without clinical or echocardiographic evidence of tamponade. They were treated conservatively with acetylsalicylic acid or ibuprofen and their symptoms resolved without sequelae in 1-8 days. One patient (without pericardial rub) died due to cardiac tamponade on postoperative day 6. Postmortem examination revealed hemorrhagic pericarditis with no gross evidence of lead perforation. Pericarditis complicates pacemaker implantation in significantly more patients who receive active-fixation atrial leads. It may be precipitated byperforation of the atrial lead screw through the thin atrial wall. Patients developing postoperative pericarditis should befollowed closely due to the risk of cardiac tamponade.

Evaluation of the appropriateness of pacemaker mode selection in bradycardia pacing: how closely are the ACC/AHA guidelines followed?

Although guidelines for selection of the appropriate pacing mode have been published, little data is available on how closely these are followed in the clinical setting. All 738 patients (men 412, women 326; age 73.4 +/- 0.46 years; range 19-101 years) who underwent pacemaker implantation from 1996 to 2000 were reviewed to determine if the appropriate mode was selected based on the ACC/AHA guidelines with the data collected prospectively. Demographic, investigational, and implantation data including the presence of sinus disease and/or atrioventricular block, diagnosis, indication for pacing, ACC/AHA class indication for device therapy, recommended ACC/AHA mode, implanted mode, and reason for not using the recommended mode were entered into an SPSS data base. Of 738 patients, 708 were cross-tabulated for a match to the guidelines of which 358 (50.6%) had a mode selected that did not conform. The reasons were advanced physical disability (16%), physician choice without identifiable reason (21%), rate modulation selected without identifiable indication (16%), DDD implanted instead of VDD (25%), advanced age (9%), rare need for pacing (6%), a need for specific device features (5%), and unstable stimulation thresholds or difficult venous access (2%). In the treatment of bradyarrhythmias, deviation from the ACC/AHA indicated mode occurred in a substantial proportion of pacing system implantations. However, in many, the deviation appeared appropriate considering the patient's clinical status. Nevertheless, in a smaller proportion of patients the deviation appeared inappropriate requiring rectification. The two outstanding categories were: (1) elderly denied a dual chamber system with no clinical explanation and (2) selection of rate-modulated devices without any indication of chronotropic incompetence.