Circulation. 2007;115:638-653
doi: 10.1161/CIRCULATIONAHA.106.618587
(Circulation. 2007;115:638-653.)
© 2007 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Contemporary Pacemaker and Defibrillator Device Therapy
Challenges Confronting the General Cardiologist
Mark H. Schoenfeld, MD
From the Cardiac Electrophysiology and Pacemaker Laboratory, Hospital of Saint Raphael, Yale University School of Medicine, New Haven, Conn.
Correspondence to Mark H. Schoenfeld, MD, FACC, FAHA, FHRS, Cardiac Electrophysiology and Pacemaker Laboratory, Hospital of Saint Raphael, Yale University School of Medicine, 330 Orchard St, Suite #210, New Haven, CT 06511. E-mail mschoenfeld{at}srhs.org
Key Words: pacemakers • pacing • cardioverter-defibrillator, implantable
 |
Introduction
|
|---|
Intracardiac pacemaker and defibrillator implantations were
initially described a half century and a quarter century ago,
respectively.
1,2 Originally conceived as devices for the treatment
of symptomatic bradycardia and sustained ventricular tachyarrhythmias,
these therapies have subsequently been applied to the management
of an increasing host of arrhythmia and other indications, including
the treatment of heart failure.
3 Although underuse of this technology
has occasionally been reported,
4 it has become abundantly clear
that the number of patients deriving benefit from device therapy
has risen exponentially; cardiac electrophysiology and pacing
has emerged as a subspecialty within cardiology to address the
growing needs of cardiac rhythm management.
5 It is, nonetheless,
incumbent on the general cardiologist to become proficient in
certain aspects of device therapy.
6 The goals of the present
review are to highlight some of the fundamental areas of knowledge
essential for follow-up, to provide an update on newer applications
of device therapy, and to address some of the more common challenges
and clinical scenarios encountered by the general cardiologist.
|
Changing Indications for Device Therapy
|
|---|
The implantable cardioverter-defibrillator (ICD) was originally
applied to patients surviving life-threatening ventricular tachyarrhythmias—so-called
secondary prevention. Subsequently, primary prevention trials
identified other patients who were at increased risk for sudden
cardiac death but who had yet to manifest such risk,
7 thereby
expanding the indications for ICD therapy. The most recent iteration
of guidelines for device implantation has identified additional
conditions in which pacemaker and/or ICD therapy are associated
with an enhancement of quality of life and/or survival.
3,8 In
particular, new ICD indications for primary prevention include
prophylactic implantation in patients with ischemic cardiomyopathy
and ejection fraction (EF) less than or equal to 30% (MADIT-II
[Multicenter Automatic Defibrillator Implantation Trial II]
criteria),
9 and in patients with Brugada syndrome.
10 The potential
importance of ICD therapy for patients with nonischemic cardiomyopathy,
EF less than 35%, and New York Heart Association class II or
III congestive heart failure (CHF) symptomatology was demonstrated
by the SCD-HeFT (Sudden Cardiac Death in Heart Failure) trial,
11 a primary prevention application published after the 2002 guidelines.
Potential new applications of cardiac pacing have been recognized, such as pacing in patients with neurocardiogenic syncope.3 Ironically, this application has been the subject of more recent debate: No benefit was found in the Second Vasovagal Pacemaker Study.12 Cardiac resynchronization therapy (CRT) has been identified as a class IIA therapy for patients with medically refractory New York Heart Association class III or IV CHF patients with cardiomyopathy, QRS interval of greater than or equal to 130 ms, and EF less than or equal to 35%.13,14 This latter application has allowed for a "marriage" of technologies in 1 device (CRT-ICD) that allows for treatment of CHF and protection against sudden cardiac death in selected patients.
Indications may flourish and, almost as rapidly, languish. The time-honored use of dual-chamber pacing to achieve physiological pacing15 has come under new scrutiny. This concept, as originally proposed, referred to pacing techniques that were designed to allow for normal cardiovascular physiology, preserve atrioventricular (AV) synchrony, and provide heart rate increases (rate adaptiveness) as required by exercise or other physiological demands.16 Although this improved symptoms in many patients and reduced the incidence of atrial fibrillation (AF) compared with single-chamber pacing, no benefit was identified in certain patient subsets,17–19 as in the PASE (Pacemaker Selection in the Elderly)17 and UKPACE (United Kingdom Pacing and Cardiovascular Events)18 trials. Furthermore, potential adverse consequences of right ventricular apical pacing have led to the evaluation of alternative sites for pacing the heart,20 and our definition of physiological pacing continues to evolve.21 All of these points attest to the importance of periodically revisiting and updating implantation indications and guidelines as new data from randomized clinical trials become available.7,8,22
|
Follow-Up of the Patient After Device Implantation
|
|---|
Much has been written on device follow-up, and training requirements
have been established for the selection, implantation, and follow-up
of cardiac implantable electronic devices.
23–26 Six-month
intervals for ICD follow-up seem to be safe
27; the same applies
to pacemaker follow-up. These follow-up intervals may be extended
as a result of innovations in remote monitoring
28,29 and device
automaticity. The latter may be defined as the automatic regulation
of device function by programmed algorithms (see below) that
are based on patient conditions and pacemaker/ICD system conditions,
without the need for clinician input.
30 Transtelephonic monitoring
of pacemakers has been available for nearly 3 decades. The technology
has shown that there is a relatively long trouble-free period
in the midst of a device’s life; most issues arise early
after implantation (wound healing, threshold changes) or toward
the device’s end of life.
30 These lessons have been applied
increasingly to the management of ICDs; depending on the manufacturer,
remote monitoring may be enabled through Internet-based systems
or through radiofrequency transmission from a transmitter in
the ICD via a phone device to a service center.
Nonetheless, there is no substitute for direct patient contact, with an essential role for the physician to uncover device-related issues.24 In addition to periodic routine visits, more urgent examination may be required, as in the case of an ICD patient with increasingly frequent ICD discharges (as opposed to a single ICD shock, which could be addressed through remote monitoring). History taking is crucial to ensure that symptoms prompting the original implantation remain ameliorated and that device therapy has not resulted in the creation of new symptoms, as in the so-called pacemaker syndrome.31 This syndrome, most commonly caused by the loss of optimal AV synchrony in patients with single-chamber ventricular pacing, consists of cardiovascular and neurological symptoms that include neck/abdominal pulsations, palpitation, fatigue, dyspnea, and/or presyncope; the pathophysiology reflects diminished cardiac output and is associated with signs of systemic hypotension, AV valvular regurgitation, unpleasant cannon A waves in the neck, and pulmonary/hepatic congestion.24
Examination of the wound is important early after implantation to address wound-healing as well as potential infection; the latter is particularly serious because it is rare for a patient to overcome device-related infections without extraction of the entire system.24 Pacing-induced complications such as diaphragmatic stimulation or myopectoral stimulation/inhibition also may be identified. Examination of chest radiographs is occasionally necessary to confirm lead integrity and position.32 The importance of 12-lead electrocardiography cannot be understated, not only for assessment of rhythm but also for confirmation of the appropriate QRS complex–paced morphology associated with various pacing lead locations (typically left bundle-branch block morphology and left-axis deviation with conventional right ventricular apical pacing). This examination is particularly important with the advent of alternative-site pacing, where less typical ECG patterns are observed.20,33
Magnet application to a pacemaker generator is a useful adjunct to follow-up and converts the pacemaker to the asynchronous pacing mode (not inactivation).23 The resulting asynchronous rate is manufacturer specific and changes over the life of the battery as it approaches a preset elective replacement indicator rate. Thus, magnet application is useful in following device longevity and in confirming capture at the programmed output. It may be used to temporarily induce asynchronous pacing in cases of electromagnetic interference (EMI), such as electrocautery. With EMI, external signals may be detected by the device and misconstrued as intracardiac, resulting in inhibition of pacing output, unless sensing is eliminated by either magnet application or device reprogramming. In contrast, magnet application to ICD generators does not affect pacing, but it may temporarily or permanently suspend antitachycardia therapies.
The importance of device interrogation and programmability has been appreciated since the inception of pacemaker therapy.34,35 Unfortunately, there is no universal pacemaker/ICD programmer to date; the manufacturer-specific nature of programmers constrains the nonelectrophysiologist who may not be familiar with or have access to the seemingly vast array of programmers required for follow-up. Ironically, allied professionals, often industry employed, may know more about a particular device and its associated programmer than a given physician; guidelines for such assisted follow-up have been established, and the physician must remain responsible for the device management and the patient’s overall care.36
Interrogation of a device provides a wealth of information, including but not limited to programmed parameters, such as the pacing rates and pacing mode (Table 1)37; real-time lead and battery impedance, as well as trends; event counters and histograms detailing the percentage of time sensed/paced, automatic mode-switch episodes, and atrial and/or ventricular arrhythmias; real-time and stored intracardiac electrograms; and marker channels that indicate what a device thinks it has seen or is seeing (Figure 1). Interrogation of programmed settings is essential in explaining phenomena that may be misinterpreted as device malfunction. For example, if a pacing rate is lower than the programmed lower tracking rate in a correctly functioning pacemaker, the phenomenon may be understood if interrogation also reveals that a hysteresis function has been programmed, allowing the patient’s native rhythm to be maintained and to dip down to lower rates before pacing is triggered at a faster rate; this reduces current drain and preserves native rhythm.
View larger version (88K):
[in this window]
[in a new window]
|
Figure 1. T-wave sensing, resulting in spurious detection of tachycardia; both QRS and T waves are sensed, resulting in double counting by the device and thereby triggering detection of a pseudotachycardia by the device. FS indicates fibrillation sensed (faster interval that falls within VF zone); VS, ventricular sensed; and EGM, electrogram.
|
|
The inability to perform telemetry could indicate that the wrong manufacturer’s programmer was used, that the telemetry wand has not been positioned adequately over the generator (some models also require a magnet applied to the wand), or that the generator has reached anticipated (or premature) end of life.38 Elevated lead impedances may suggest a fracture in the conductor coil(s), a loose-set screw site at the lead insertion into the header block, or a problem at the tissue–electrode interface39 (Figure 2). Reduction of lead impedance may indicate a breach in lead insulation, often seen at the site of transvenous insertion—the so-called subclavian crush syndrome.40 Analysis of impedance trends may actually provide historical insight as to when lead disruption may have occurred (Figure 3). Reduction in battery voltage and a rise in battery impedance are characteristic of generators over time, providing a method by which to assess generator longevity.
View larger version (29K):
[in this window]
[in a new window]
|
Figure 2. Detection of false signals on ventricular electrogram at nonphysiological intervals because of make-and-break connections in setting of loose-set screw, where lead interfaces with pacer generator, associated with elevated impedance. AS indicates atrial sensed; V EGM, ventricular electogram.
|
|
View larger version (22K):
[in this window]
[in a new window]
|
Figure 3. Graph of impedance trends in defibrillator patient, showing intermittent elevations of impedance attributable to make-and-break connections at header block of a pacemaker generator.
|
|
Device counters may allow for the quantification of events such as high atrial rates, high ventricular rates, and automatic mode-switch episodes, suggesting the interim occurrence of arrhythmias such as AF, supraventricular tachycardia (SVT), ventricular tachycardia (VT), or ventricular fibrillation (VF). Far-field sensing of ventricular depolarization, T waves, or noise by the atrial channel may result, however, in a false-positive incidence of high atrial rate or mode-switch episodes (Figure 4). Thus, pacemaker memory functions do not obviate the need for Holter or event monitoring in all patients with suspected arrhythmias. However, longer durations of individual episodes, on the order of many minutes to days, especially if confirmed by intracardiac electrograms, are more likely to correspond to true atrial dysrhythmias and an increased association with clinical events such as thromboemboli.41,42 Although device counters give a rough indication as to arrhythmia history, stored intracardiac electrograms have been increasingly used for validation of the true arrhythmia in pacemakers43 and ICDs44 (Figure 5).
View larger version (75K):
[in this window]
[in a new window]
|
Figure 4. Noise on atrial channel in setting of reduced atrial lead impedance from subclavian crush syndrome in a pacemaker, falsely sensed as atrial fibrillation and causing automatic mode switching. The 3 channels are marker channel, atrial electrogram, and ventricular electrogram. A indicates atrial paced; V, ventricular paced; P, atrial sensed; and AMS, automatic mode switch to ventricular-paced mode.
|
|
View larger version (83K):
[in this window]
[in a new window]
|
Figure 5. Ventriculoatrial dissociation during ventricular tachycardia in defibrillator patient; upper electrogram is atrial, lower is ventricular, with ventricular rate more than twice that of atrial rate; the last panel demonstrates delivery of a 29.9-J shock with restoration of sinus rhythm and 1:1 conduction.
|
|
|
Automatic Algorithms for Detection and Treatment: A Brief Synopsis
|
|---|
It is beyond the scope of this review to detail all the device-specific
algorithms available for sensing, discrimination, pacing, and
defibrillation. Certain algorithms have, however, been increasingly
used to automatically facilitate device function and follow-up
37;
these algorithms warrant some understanding on the part of the
general cardiologist.
Automatic algorithms that are intended to enhance sensitivity and optimize arrhythmia detection invariably encounter challenges regarding under- and oversensing.45 This is particularly important for ICDs where low-amplitude fibrillatory signals from the ventricle must be adequately sensed while avoiding oversensing in sinus rhythm. ICDs typically have algorithms to automatically adjust the gain or sensing threshold to sense reduced signals; it is, therefore, uncommon for current ICDs to miss VF. Conversely, oversensing may result in spurious discharge or inhibition of pacing output in ICD patients who are pacemaker dependent (Figure 6).
View larger version (54K):
[in this window]
[in a new window]
|
Figure 6. Myopotential sensing with inhibition of ventricular pacing output in patient with pacer dependence and complete heart block in an cardioverter-defibrillator, with spurious interpretation of myopotentials as fibrillatory signals (VF) triggering cardioverter-defibrillator charge; uppermost channel is atrial electrogram, middle is ventricular rate-counting electrogram, lower is shock electrogram, and marker channels are below. Note inhibition of ventricular signals.
|
|
Algorithms that allow for rhythm discrimination have become essential to ICD management. Inappropriate or spurious device discharges may be observed in up to 40% of patients, typically from misclassification of sinus tachycardia or from rapidly conducting supraventricular arrhythmias.46 For single-chamber devices, ventricular rate has served as the primary determinant of arrhythmia detection. Additional features such as sudden-onset criteria have aided discrimination of sinus tachycardia (gradual in onset) from VT or VF (typically sudden in onset) by comparing the interval at the onset of the tachycardia against an average of the previous intervals. This will not, however, distinguish VT from SVT. Rate-stability enhancements allow for measurement of beat-to-beat intervals, noting that monomorphic VT is typically regular, whereas AF and polymorphic VT or VF have wider variability when beat-to-beat variability is assessed. This feature proves to be particularly useful in discriminating AF from monomorphic VT. These enhancements reduce the likelihood of delivering spurious shocks for SVT without undersensing or delaying treatment for VT. Beyond this, certain algorithms have been developed to assess morphological characteristics of the electrogram during a patient’s baseline rhythm. The resulting template may then be compared with the morphological characteristics obtained during a tachycardia, thereby aiding in the discrimination of supraventricular and ventricular rhythms.47 Although it is unpleasant for a patient to receive spurious shocks for misclassified SVT, it is far more hazardous for VT to be undetected; this has led manufacturers to incorporate a programmable time limit for tachycardia duration that, when exceeded, will result in the delivery of VT therapy.
In dual-chamber ICDs, the presence of an atrial lead allows for comparison of ventricular and atrial rates during baseline rhythm and tachycardia, as well as the relative timing of atrial and ventricular activity. Ventricular rates exceeding atrial rates are typical for ventricular tachyarrhythmias with AV dissociation. Intracardiac electrograms are particularly useful in this regard (Figure 5). The Detect SVT trial reported a reduction of inappropriate SVT detection from 39.5% in the single-chamber detection arm compared with 30.9% in the dual-chamber arm.46 Arrhythmia detection by dual-chamber ICDs may be enhanced by combining various discriminators.48
A recent multicenter trial, Comparison of Empiric to Physician-Tailored Programming of Implantable Cardioverter-Defibrillators (EMPIRIC), reported that standardized empirical ICD programming was as effective as physician-tailored programming as long as the empirical strategy included avoidance of detection of nonsustained tacyhcardia, avoidance of detection of SVTs as VT, empirical antitachycardia pacing for slow and fast VTs, and high-output first shocks.49 Nonetheless, misclassification of arrhythmic events is an ongoing concern, and much work remains in the refinement of detection algorithms, particularly in delineating rapid SVTs.50,51
For the sake of completeness, it should be acknowledged that automatic sensing algorithms have been applied to a host of sensors unrelated to either atrial or ventricular depolarization, allowing for rate-adaptive pacing that is particularly well suited to patients exhibiting chronotropic incompetence.24,52 Thus, activity sensors, accelerometers, minute ventilation, and QT-interval sensing have been used alone or in combination to provide for more physiological rate modulation.
Beyond sensing and detection, automatic algorithms have also been increasingly used in the treatment and prevention of arrhythmias. Pacing for bradycardia has been facilitated by automatic capture threshold assessment. The determination of ventricular capture threshold may be made at programmed intervals during the day or on a beat-by-beat basis with corresponding adjustments in output.53 Periodic and frequent assessments of thresholds are important from a safety standpoint because thresholds may change as a function of multiple factors, including changes in autonomic tone, electrolyte and metabolic abnormalities, and concomitant antiarrhythmic drug therapy. On the other hand, the ability to automatically down-regulate outputs when improved thresholds are detected extends device longevity.
Automatic modulation of the AV interval may be accomplished in various ways in current pacing systems. It has long been appreciated that optimal hemodynamics are achieved with shorter AV delay intervals after atrial-sensed compared with atrial-paced events,54 and hemodynamics may be further enhanced by rate-adaptive shortening of the paced AV interval at faster heart rates.55
Conventional right ventricular apical pacing may contribute to cardiac desynchronization and foster or exacerbate CHF in pacer patients.20,56,57 Thus, in the DAVID (Dual Chamber and VVI Implantable Defibrillator) trial,56 committed dual-chamber pacing was associated with increased death or hospitalization for CHF in ICD patients with depressed EF compared with patients programmed to an intentionally slow backup ventricular-paced mode. MOST (Mode Selection Trial) identified an increased rate of CHF hospitalization associated with ventricular-paced rhythm in pacemaker patients with sinus node dysfunction.57 What options, then, are available to minimize cardiac desynchronization induced by right ventricular apical pacing? Reprogramming to atrial pacing mode is one alternative, recognizing, however, that there is a finite, albeit small progression to AV block in patients with sick sinus syndrome, approximating 0.6% of patients per year.58 Programming a fixed long AV delay may minimize ventricular pacing, but it is not always feasible.59,60 In recognition of this, some manufacturers have incorporated conduction search algorithms that automatically search for intrinsic ventricular events that, if not sensed during an extension of the AV interval, will resume stimulation at the programmed AV delay61 (Figure 7).
View larger version (55K):
[in this window]
[in a new window]
|
Figure 7. Minimal ventricular pacing mode. Upper panel: When atrial is paced at 60 bpm, intrinsic conduction occurs with first-degree block, inhibiting ventricular pacing. Lower panel: Atrial pacing at 80 bpm: at this faster atrial rate, atrioventricular node conducts with second-degree block, with progressive prolongation of time between atrial-paced complex and ventricular-sensed complex. When the device detects nonconduction to the ventricle, it triggers an atrioventricular-paced beat (AP/VP) (seventh ventricular complex). AP indicates atrial paced; VS, ventricular sensed; and VP, ventricular paced.
|
|
In an effort to mimic naturally occurring circadian rhythms, some devices allow for programming of algorithms that will allow for slower pacing rates nocturnally.62 Another hysteresis function allows for pacing to kick in only when an abrupt rate drop is detected, applied with mixed results in the management of patients with neurocardiogenic syncope.12 Rate-smoothing programs are designed to prevent sudden changes in ventricular cycle length that may be responsible for either inducing pause-dependent arrhythmias or exacerbating symptoms of cardiac irregularity that are often encountered in AF.
Automatic mode switching is, undoubtedly, one of the most useful and widely applied algorithms currently available; it provides for the detection of atrial tachyarrhythmias and conversion from dual-chamber to single-chamber ventricular pacing to preempt pacer-mediated tachycardia, with reversion to dual-chamber pacing once the sinus mechanism has reemerged63,64 (Figure 8). Oversensing, which results in false-positive automatic mode-switching responses, may be observed, most commonly from far-field sensing of the end of the QRS complex by the atrial channel, especially in the setting of noise and low right atrial implants63 (Figure 4). An analysis of automatic mode-switching episodes may provide the clinician with an estimate of the incidence of atrial dysrhythmias, prompting clinical decisions such as institution of anticoagulation, antiarrhythmic drug therapy, or even ablation; the above limitations of algorithm analysis regarding sensitivity and specificity must, however, be considered.
View larger version (89K):
[in this window]
[in a new window]
|
Figure 8. Demonstration of patient with atrial flutter, with atrial electrograms at cycle length of 200 ms, initially tracking every other flutter wave with triggered ventricular-paced beat (2:1 lock-in) (A), then temporary inhibition of pacing by programmer showing flutter waves (B), followed by automatic mode switch to ventricular demand pacing (C); upper tracing is surface recording, lower is atrial electrogram. MS indicates mode switch; AS, atrial sensed; AR, atrial refractory; and VP, ventricular paced.
|
|
Finally, some commentary is warranted regarding the potential utility of pacing algorithms for the prevention and/or treatment of AF. A variety of different methodologies have been developed to increase the atrial pacing rate when the native rhythm emerges and to periodically reduce the search rate for intrinsic atrial activity (dynamic atrial overdrive),65 to transiently use higher rate pacing after mode-switch episodes or spontaneous atrial ectopy, and to pace rapidly alone or in combination with shock therapy to terminate established arrhythmias.66 In general, evidence-based data in this area are sparse, and much work is needed to clarify whether there is any role for the use of permanent pacing in the prevention or treatment of AF, as recently noted by a joint working group of the American Heart Association and the Heart Rhythm Society.67
|
Alternative Site Pacing and CRT
|
|---|
As previously noted, there has been growing evidence that cardiac
desynchronization induced by conventional right ventricular
apical pacing may have deleterious effects on cardiac function
and patient symptomatology, corresponding with an increased
risk of heart failure and death.
20,56,57,60 Programming techniques
have been used to minimize right ventricular pacing by lowering
the baseline rate, changing to atrial-paced mode, or extending
the AV delay.
60,61 Invasive strategies to approach this problem
have included upgrading from right ventricular apical pacing
to biventricular pacing,
68,69 alternative or selective site
pacing from the His bundle,
70 and primary CRT with left ventricular
or biventricular pacing in patients with CHF, as in the MUSTIC
(Multisite Stimulation in Cardiomyopathies),
13 MIRACLE (Multicenter
InSync Randomized Clinical Evaluation),
14 COMPANION (Comparison
of Medical Therapy, Pacing and Defibrillation in Heart Failure),
71 and CARE-HF (Cardiac Resynchronization-Heart Failure) trials,
72 or in non-CHF patients requiring pacing for standard indications
(the HOBIPACE [Homburg Biventricular Pacing Evaluation] study
73).
The general cardiologist may be called on to interpret chest radiographs and electrocardiograms that may become increasingly complex with these alternative pacing modalities. Recently, electrocardiographic demonstration of a ratio of 1 or greater in the R/S wave amplitude in lead V1 has been shown to reliably detect left ventricular capture in patients with cardiac resynchronization devices33 (Figure 9). Changes in morphology may also be appreciated during assessment of pacing thresholds in biventricular systems (Figure 10).
View larger version (153K):
[in this window]
[in a new window]
|
Figure 9. Twelve-lead electrocardiograms of patient with left bundle-branch block (A) and with biventricular pacing (B); note tall R wave in lead V1 during cardiac resynchronization therapy.
|
|
View larger version (61K):
[in this window]
[in a new window]
|
Figure 10. Assessment of thresholds, with initial capture of both right and left ventricle, followed by loss of capture on left ventricular lead, followed by biventricular loss of capture, with corresponding change in morphologies.
|
|
It is beyond the scope of the present article to detail the burgeoning area of CRT. Selection of optimal candidates for this therapy has typically included New York Heart Association class II or III CHF patients with a widened QRS complex. Although a wider baseline complex (greater than 150 ms versus 120 to 150 ms) in the PATH-CHF (Pacing Therapies in Congestive Heart Failure) study correlated with CRT benefit,74 other studies have demonstrated that QRS complex duration is a poor predictor of the response to CRT75; in addition, the extent of shortening of the QRS complex with biventricular pacing has not predicted better individual outcomes with CRT.76 Indeed, attention has been directed increasingly at baseline markers of mechanical dyssynchrony as assessed by echocardiography and tissue Doppler imaging.77,78 Thus, patients with a wide QRS complex, that is, electrical dyssychrony (but without evidence of mechanical dyssynchrony), may not prove to be ideal candidates for CRT. Mechanical dyssynchrony may exist in various forms, including AV dyssynchrony (delay between atrial and ventricular contraction), interventricular dyssynchrony (delayed activation of the left ventricle relative to the right ventricle), and intraventricular dyssynchrony (delayed activation of 1 segment of the left ventricle [LV] relative to another).
It remains unclear how the individual forms of dyssynchrony contribute to CHF; equally unclear is the extent to which echocardiographic optimization of these individual forms will ameliorate CHF, and when and how such optimization should be performed. Confounding this problem is the difficult issue of assessing the clinical response to CRT. There is no consensus on what constitutes an adequate response to CRT or on what defines a nonresponder.79,80 If, after 6 months of therapy, there is either a lack of symptomatic improvement or worsening CHF, a variety of contributing factors may be considered: poor patient selection, development of AF, change in cardiac substrate with worsening cardiomyopathy or ischemia, loss of LV or RV capture, and lack of ideal cardiac resynchronization (nonoptimal AV and VV delays, poor LV lead position).79 Optimization of the AV delay may increase stroke volume through an increase in preload and may be achieved by guiding programming AV-interval changes through simultaneous echocardiographic assessment of the mitral Doppler inflow pattern.77,81 Left bundle-branch block typically delays activation, resulting in fusion of the E and A waves. The optimal AV delay is the shortest possible delay that allows for complete diastolic ventricular filling without interfering with the atrial contribution; the echocardiographic representation of this is separation of the E and A waves without truncation of the A wave (Figure 11). This technique, though widely applied, has yet to be validated in LV-based pacing.82 Optimization of the VV interval, correcting for interventricular dyssynchrony between RV and LV contraction, is a programmable feature available in some devices that may contribute to hemodynamic and symptomatic improvement.83,84
View larger version (46K):
[in this window]
[in a new window]
|
Figure 11. Echocardiographic optimization of atrioventricular (AV) interval for cardiac resynchronization. An AV delay that is too long (160 ms) results in fusion of E and A waves, with reduction in filling time, prolongation of time between the end of the A wave and mitral valve closure, and presystolic mitral regurgitation; an AV delay that is too short (50 ms) results in separation of E and A waves, but the A wave is truncated by mitral valve closure, resulting in an interruption of atrial contribution to ventricular filling. The optimal AV delay should allow for completion of end-diastolic filling before ventricular contraction, resulting in the longest diastolic filling time. The end of the A wave should coincide with complete mitral valve closure; ventricular contraction should begin at the end of atrial contraction. E indicates wave associated with the early filling phase of transmitral flow; A, atrial contraction phase of transmitral flow.
|
|
Certain ICDs have the ability to assess changes in intrathoracic impedance as measured between the pacing lead and generator; an inverse correlation has been demonstrated between intrathoracic impedance and pulmonary capillary wedge pressure, often heralding the onset of fluid overload.85 Application of this technology may allow the practitioner to institute preemptive changes in medical therapy when such changes are detected, thereby avoiding hospitalization (Figure 12). Thus, management of CHF in patients with CRT devices may well require extensive collaboration among the general cardiologist, electrophysiologist, echocardiographer, and heart failure specialist.
View larger version (21K):
[in this window]
[in a new window]
|
Figure 12. A decline in intrathoracic impedance measured between pacing lead and pacemaker generator, corresponding to "possible fluid accumulation" in a CHF patient. As fluid accumulates in the thoracic space, intrathoracic impedance decreases. The Optivol fluid index trend tracks the difference between daily measured impedances (averaged) and a daily calculated reference impedance. The index trend increases if the daily measured impedance is less than the reference impedance; if the increasing index trend exceeds a designated Optivol threshold, possible fluid accumulation is reported. P indicates time of last programming change in one or more pacemaker parameters; I, time of most recent interrogation of the device.
|
|
|
Drugs, Devices, and EMI
|
|---|
Pharmacological agents, especially antiarrhythmic drugs, may
be required in patients with devices
86; typical agents include
sotalol, amiodarone, mexiletine, and dofetilide. Among secondary
prevention patients with spontaneous or inducible VT who were
studied for 1 year in the OPTIC (Optimal Pharmacological Therapy
in Cardioverter Defibrillator Patients) trial, shocks were observed
in 38.5% of patients on ß-blockers alone, in 24.3%
of patients on sotalol, and in only 10.3% of patients treated
with amiodarone and a ß-blocker.
87 In another secondary
prevention study,
88 first ICD therapy occurred in patients whose
initial indication was sustained monomorphic VT (as opposed
to cardiac arrest) and LVEF
25%; subsequent therapy occurred
sooner and unpredictably, suggesting benefit of initiating antiarrhythmic
drug therapy soon after the first symptomatic ICD therapy. If
frequent nonsustained VT is evident at the time of implantation,
such drugs may be considered even sooner. What is less clear
is the role of prophylactic antiarrhythmic drugs in primary
prevention patients who have yet to demonstrate a sustained
arrhythmia.
Although antiarrhythmic drugs such as sotalol have proven useful in reducing the incidence of arrhythmia occurrences and ICD discharges,89 rate slowing of VT may be observed, resulting in underdetection of arrhythmias by ICDs. Although some antiarrhythmic drugs such as sotalol may reduce defibrillation thresholds, other agents (notably amiodarone and mexiletine) may elevate defibrillation thresholds90; the resulting compromise of safety margin between the energy that is required and the energy that is deliverable for defibrillation may have disastrous consequences. Flecainide is particularly noteworthy for elevating pacing thresholds. Thus, the addition of antiarrhythmic agents to the medical program of a patient with a device warrants periodic attention to programmed settings and sensing/pacing/defibrillation thresholds.
Potential sources of EMI are ubiquitous, especially in the hospital environment and workplace; therefore, it is critical for the general cardiologist to be aware of potential risks to the device patient and precautions that may be warranted23,91,92 (Table 2). In the surgical arena, electrocautery may be oversensed by a patient’s intracardiac device, resulting in transient inhibition of pacer output or in triggering of inappropriate ICD shocks (Figure 6). Particularly in the pacemaker-dependent patient, devices should be programmed to an asynchronous or triggered mode to preempt inhibition of pacing output, and the tachycardia-detection mode of an ICD should be temporarily inactivated. One of the most frequent settings in which this scenario arises is the endoscopy suite; notably, no studies have been published examining whether, or how often, cautery during endoscopy procedures interacts with ICDs. In general, electrocautery should be minimized; when electrocautery is required, it should use short bursts of bipolar cautery with the grounding pad placed distant from the generator. Rarely, electrocautery and defibrillation may produce irreversible damage to the generator or reset the device to a backup or noise-reversion mode (reprogramming of a device to an alternative mode); transient undersensing and rises in pacing thresholds may also be observed. When undertaking external cardioversion, anteroposterior paddles with the least possible energy should be used to minimize trauma to pacemaker systems. Devices should be interrogated postoperatively or after cardioversion to assess for threshold rises, reset modes, or changes in the tachycardia mode.
Other sources of EMI include magnetic resonance imaging (MRI), lithotripsy, radiofrequency ablation, and radiation therapy. Potential interactions with MRI include pacing inhibition, inappropriate ICD discharges, rapid pacing, mechanical pull and rotation of the device, and device reprogramming.93 It has been suggested that certain pacemaker and ICD systems may be MRI safe.94 Alternatively, certain strategies to minimize complications have been suggested, including the use of less powerful MRI machines; imaging limited to extremities (ie, remote from the device); careful reprogramming of the intracardiac device, including asynchronous modes and maximal pacing output; selection of appropriate spin sequences; limitation of MRI to patients who are not pacemaker dependent; and careful, continuous periprocedure monitoring.95 In general, however, the present use of MRI should be considered contraindicated in the patient with a pacemaker or ICD.
Extracorporeal shockwave lithotripsy, in contrast, may be undertaken as long as there is appropriate distancing of the device from the focal point of lithotripsy, to minimize pacemaker inhibition or irregular sensing.96 Radiation therapy may pose the risk of random failure of individual components of the device, sudden loss of output, alternations in programming, rate runaway (nonphysiological rapid delivery of pacing stimuli to the heart), and premature battery depletion97,98; nonetheless, it may be unavoidable in certain device patients. Strategies to minimize this risk entail close discussion with the radiation therapist on appropriate shielding of the generator; rarely, repositioning of the generator or placement of a new system in the contralateral chest may be required.23 The EMI associated with radiofrequency current during catheter-ablation procedures may transiently cause reversion to asynchronous pacing or result in pacer inhibition. However, it is frequently the case that no significant impact on thresholds, impedances, or device function is observed.24,99 Reprogramming a pacemaker to asynchronous mode, inactivating antitachycardia therapies, and reassessing the device after the procedure are recommended approaches for patients undergoing radiofrequency ablation.
Although less common now, patients may have both a pacemaker and a separate ICD device. Clinical interactions between the 2 may include transient failure by the pacer to sense or capture post-ICD discharge; oversensing of the pacemaker stimulus by the ICD, leading to double counting; ICD failure to sense VF, resulting from pacer stimulus oversensing; and pacemaker reprogramming, caused by ICD discharge.100 In ICD patients who require a separate pacemaker, a bipolar pacing system is indicated to preempt these sensing issues. Other devices may rarely trigger device discharge in an ICD patient, notably, transcutaneous electronic nerve-stimulation units.101
In the nonmedical environment, it has been recognized that cellular telephones may interfere with the function of implanted devices, with the potential for any type of interference being 20% in one study with associated symptoms in 7.2% with the phone placed directly over the generator; the most common pacemaker interactions were tracking interference on the atrial channel, followed by asynchronous pacing and ventricular inhibition.102 Distancing the phone from the generator or using the contralateral ear is the recommended approach. Rarely, antitheft surveillance systems in retail centers may result in ICD discharge or pacemaker triggering. Patients should be advised to walk through the gates without leaning on them or lingering.103 When in doubt regarding the potential impact of any type of EMI, an inquiry with the manufacturer should be made.
|
Determinants of Frequent ICD Shocks and the Management of VT Storm
|
|---|
Electrical storm may be defined as recurrent VT or VF occurring
2 or more times in a 24-hour period and usually requiring electrical
cardioversion or defibrillation.
104 It is often difficult to
determine whether a patient presenting with VT is manifesting
a primary arrhythmogenic substrate or a secondary effect of
worsening CHF.
105 Clinical instability manifested as interim
hospitalizations for CHF or coronary events, as identified in
MADIT-II,
106 and severe depression, as demonstrated in the Triggers
of Ventricular Arrhythmias (TOVA) study,
107 seem to correlate
more strongly with recurrent VT. Also in the MADIT trial, electrophysiological
inducibility of VT was associated with increased likelihood
of VT, whereas noninducibility predicted a higher VF rate.
108 Electrical storm typically occurs late after ICD implantation
and may correlate with chronic renal failure and depressed EF.
104,109 What is less clear is whether there is any difference in appropriate
or inappropriate device therapy in primary versus secondary
prevention ICD patients.
110 Higher-risk patients may warrant
prophylactic administration of antiarrhythmic drug therapy with
agents such as amiodarone and ß-blockers, as in the
OPTIC trial,
87 or sotalol.
89 When patients are actually manifesting
frequent ICD shocks and/or storm, immediate management entails
reversal of electrolyte and/or metabolic abnormalities, intravenous
administration of amiodarone and ß-blockade, and addressing
potential acute coronary syndromes in the case of polymorphic
tachycardias. Slower VT may be totally asymptomatic or present
with symptoms of either palpitations or CHF if the duration
is prolonged and below the rate cutoff for device treatment.
It may be readily approached by reprogramming the detection
rate and incorporating antitachycardia pacing for treatment.
111 Strategies for the management of incessant spurious device discharge
include temporarily inactivating the device, rate control or
cardioversion in the case of AF or SVT, and reprogramming such
detection algorithms and rate cutoffs as previously outlined.
|
Device Advisories
|
|---|
Increased attention has been directed to the safety of implanted
devices, particularly because death may result from device failure
and/or complications; less commonly, death may result from unintended
pulse-generator inactivation (without reactivation).
112 System
failure can be associated with lead malfunction,
113 although
there is growing concern regarding generator performance.
38,114 The concept of a national database for tracking devices is not
new,
115 but most information regarding device survival and/or
malfunction is still limited to industry performance reports
of returned products and a meager collection of selected registries.
116 Although pacemaker malfunction replacement rate has declined,
ICD malfunction replacement rate has increased.
114 Equally alarming
are the risks inherent in replacement, whether warranted or
excessive, of devices under advisory; a disturbing incidence
of infections and deaths have been associated with system revision.
117 Specific recommendations for clinicians managing device advisory
notices are to consider device/lead replacement if the mechanism
of malfunction is known and potentially recurrent, if death
is a likely result of device malfunction, if the patient is
pacemaker dependent, if the risk of replacement is substantially
lower than the risk of device malfunction, and especially if
the device is nearing its elective replacement indicators.
118
|
Participation in Sports and Driving by the Patient With a Device
|
|---|
The clinician will often be asked to counsel a patient as to
what activities are allowable. Clearly, this will vary as a
function of the patient, the patient’s underlying condition,
the severity of the patient’s illness, and the potential
impact of an activity (such as driving) on others. Physician
recommendations to ICD patients regarding sports participation
vary widely; one survey of electrophysiologists reported 76%
recommending avoidance of contact and 45% recommending avoidance
of competitive sports
119; in the same study, shocks were cited
commonly, but adverse effects were rare. Nonetheless, the 36th
Bethesda Conference task force strongly suggests that athletes
with either primary or secondary prevention ICDs should be disqualified
from all competitive sports except for those of low intensity;
pacemaker-dependent patients are advised against participating
in most competitive sports that potentially involve body trauma.
120 The authors acknowledge that little direct evidence in this
area is available; their concern is based on the uncertainties
associated with device performance at peak exercise, the likelihood
of triggering discharges from sinus tachycardia or other arrhythmias,
and the potential for injury resulting from an ICD shock during
competitive activity.
Patients presenting with impaired consciousness while driving a motorized vehicle, in the absence of intoxication or falling asleep, are frequently found to have arrhythmias as the putative cause, as identified by tilt-table testing and/or electrophysiological study.121 It is not uncommon for patients to have arrhythmia-type symptoms while driving; nonetheless, motor vehicle accidents are infrequent, even when associated with ICD discharge. Thus, in the AVID (Antiarrhythmics Versus Implantable Defibrillators) trial, 55 accidents were reported during 1619 patient-years of follow-up after resumption of driving by patients with documented sustained VT/VF (3.4% per patient-year), and only 11% of these accidents were preceded by symptoms of possible arrhythmia (0.4% per patient-year).122 Extensive recommendations regarding driving and related activities were published 1 decade ago.123 ICD patients with sustained VT or VF with structural heart disease were precluded from commercial driving but could resume private driving 6 months after device implantation if they were persistently free from ICD discharge. Pacemaker patients who were pacemaker dependent were only restricted from driving for the first week (private driving) or first month (commercial driving) after implantation. These recommendations predate the era of primary prevention ICD implantation, for which greater leniency may be anticipated; as such, the recommendations warrant updating and are, in any case, subject to the vagaries of local statutes. Of interest, when surveyed more than a decade ago, only 8 states in the United States had specific laws for patients with arrhythmias, and 74% of physician respondents (either general cardiologists or electrophysiologists) did not know their own state’s laws regarding driving by patients with ventricular arrhythmias.124
|
Conclusion
|
|---|
The size and mobility of the patient population with implanted
pacemakers and/or defibrillators is steadily increasing, as
is the complexity associated with these devices. Recognizing
that there are manpower limitations inherent in providing electrophysiological
expertise to all these deserving patients,
5 it has become abundantly
clear that the general cardiologist must attend to a variety
of clinical situations in which such expertise may not be immediately
available. The present review addresses some of the nuances
associated with device management.
|
Acknowledgments
|
|---|
Disclosures
A member of Dr Schoenfeld’s household is a shareholder for Boston Scientific.
|
References
|
|---|
- Furman S, Schwedel JB. An intracardiac pacemaker for Stokes-Adams seizures. N Engl J Med. 1959; 261: 943–948.[Medline]
[Order article via Infotrieve]
- Mirowski M, Reid PR, Mower MM, Watkins L, Gott VL, Schauble JF, Langer A, Heilman MS, Kolenik SA, Fischell RE, Weisfeldt ML. Termination of malignant ventricular arrhythmias with an implanted automatic defibrillator in human beings. N Engl J Med. 1980; 303: 322–324.[Medline]
[Order article via Infotrieve]
- Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, Kerber RE, Naccarelli GV, Schoenfeld MH, Silka MJ, Winters SL. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation. 2002; 106: 2145–2161.[Free Full Text]
- Voigt A, Ezzeddine R, Barrington W, Obiaha-Ngwu O, Ganz LI, London B, Saba S. Utilization of implantable cardioverter-defibrillators in survivors of cardiac arrest in the United States from 1996 to 2001. J Am Coll Cardiol. 2004; 44: 855–858.[Abstract/Free Full Text]
- Schoenfeld MH. Manpower concerns in cardiac electrophysiology and pacing. Pacing Clin Electrophysiol. 1995; 18: 1977–1979.[CrossRef][Medline]
[Order article via Infotrieve]
- Stevenson WG, Chaitman BR, Ellenbogen KA, Epstein AE, Gross WL, Hayes DL, Strickberger SA, Sweeney MO. Clinical assessment and management of patients with implanted cardioverter-defibrillators presenting to nonelectrophysiologists. Circulation. 2004; 110: 3866–3869.[Abstract/Free Full Text]
- Goldberger Z, Lampert R. Implantable cardioverter-defibrillators: expanding indications and technologies. JAMA. 2006; 295: 809–818.[Abstract/Free Full Text]
- Schoenfeld MH. Updating the guidelines for pacemaker/defibrillator device implantation: an historical perspective and a guide to their interpretation. J Cardiovasc Electrophys. 2002; 13: 1200–1201.[CrossRef][Medline]
[Order article via Infotrieve]
- Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, Daubert JP, Higgins SL, Brown MW, Andrews ML. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002; 346: 877–883.[Abstract/Free Full Text]
- Priori SG, Napolitano C, Gasparini M, Pappone C, Della Bella P, Giordano U, Bloise R, Giustetto C, De Nardis R, Grillo M, Ronchetti E, Faggiano G, Nastoli J. Natural history of Brugada syndrome: insights for risk stratification and management. Circulation. 2002; 105: 1342–1347.[Abstract/Free Full Text]
- Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005; 352: 225–237.[Abstract/Free Full Text]
- Connolly SJ, Sheldon R, Thorpe KE, Roberts RS, Ellenbogen KA, Wilkoff BL, Morillo C, Gent M. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope: Second Vasovagal Pacemaker Study (VPS II): a randomized trial. JAMA. 2003; 289: 2224–2229.[Abstract/Free Full Text]
- Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, Garrigue S, Kappenberger L, Haywood GA, Santini M, Bailleul C, Daubert JC; Multisite Stimulation in Cardiomyopathies (MUSTIC) Study Investigators. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med. 2001; 344: 873–880.[Abstract/Free Full Text]
- Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, Kocovic
Top
Introduction
Changing Indications for Device...