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SYMPOSIUM
ON CARDIOVASCULAR DISEASES
CONTEMPORARY PACEMAKERS
Contemporary Pacemakers:
What the Primary Care Physician Needs to Know
KAROLY KASZALA, MD, PHD; JOSE F. HUIZAR, MD ; AND KENNETH A. ELLENBOGEN, MD
Pacemaker therapy is most commonly initiated because of symptomatic bradycardia, usually resulting from sinus node disease.
Randomized multicenter trials assessing the relative benefits of
different pacing modes have made possible an evidence-based
approach to the treatment of bradyarrhythmias. During the past
several decades, major advances in technology and in our understanding of cardiac pathophysiology have led to the development
of new pacing techniques for the treatment of heart failure in the
absence of bradycardia. Left ventricular or biventricular pacing
may improve symptoms of heart failure and objective measurements of left ventricular systolic dysfunction by resynchronizing
cardiac contraction. However, emerging clinical data suggest that
long-term right ventricular apical pacing may have harmful effects.
As the complexity of cardiac pacing devices continues to grow,
physicians need to have a basic understanding of device indications, device function, and common problems encountered by
patients with devices in the medical and home environment.
Mayo Clin Proc. 2008;83(10):1170-1186
AV = atrioventricular; CARE-HF = Cardiac Resynchronization in Heart
Failure; CRT = cardiac resynchronization therapy; CRTD = CRT pacemaker defibrillator; CRTP = CRT pacemaker; CTOPP = Canadian Trial of
Physiologic Pacing; DDD = dual-chamber pacing and sensing with
inhibition and atrial tracking; DDDR = DDD with rate modulation; ECG =
electrocardiography; LV = left ventricular; MOST = Mode Selection Trial
in Sinus-Node Dysfunction; NYHA = New York Heart Association; PASE =
Pacemaker Selection in the Elderly; PMT = pacemaker-mediated tachycardia; QALY = quality-adjusted life-year; UKPACE = United Kingdom
Pacing and Cardiovascular Events; VVI = ventricular inhibitory; VVIR =
VVI with rate modulation
D
uring the past 50 years, pacemaker therapy has remained the cornerstone of therapy for the treatment of
symptomatic bradyarrhythmias.1 Pacemakers were first
used for postsurgical patients with heart block and in
patients with Stokes-Adams attacks.2 Major advances in
technology over the past 5 decades have paralleled our
improved understanding of arrhythmias and cardiac pathophysiology. Newer research on basic cardiac hemodynamFrom Cardiac Electrophysiology, Division of Cardiology, McGuire VA Medical
Center, Richmond, VA (K.K., J.F.H., K.A.E); and Cardiac Electrophysiology,
Division of Cardiology, Medical College of Virginia/Virginia Commonwealth
University, Richmond (K.A.E.).
Dr Ellenbogen is a consultant to Boston Scientific and Sorin Biomedical; is a
recipient of research grants from Medtronic, Boston Scientific, and St. Jude
Medical; and has received honoraria from Medtronic, Boston Scientific, St.
Jude Medical, and Biotronik.
Address correspondence to Kenneth A. Ellenbogen, MD, Medical College of
Virginia, PO Box 980053, Richmond, VA 23298-0053 (kellenbogen
@mcvh-vcu.edu). Individual reprints of this article and a bound reprint of the
entire Symposium on Cardiovascular Diseases will be available for purchase
from our Web site www.mayoclinicproceedings.com.
© 2008 Mayo Foundation for Medical Education and Research
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ics has led to the development of dual-chamber pacing and
sensing with inhibition and atrial tracking (DDD) pacing,
rate-responsive pacing, and biventricular pacing. Advances
in electronics and miniaturization have led to an exponential increase in the number of pacemaker parameters that
can be programmed and in the quantity of data pacemakers
can collect and store. Although symptomatic atrioventricular (AV) block and sinus node disease remain the most
common etiologies for pacemaker therapy, knowledge to
support other, newer indications has evolved rapidly. The
primary goal of pacemaker therapy is symptom relief and
improvement in quality of life and functional status. More
than 200,000 pacemakers are implanted annually in the
United States alone.3 Ever-increasing sophistication (and
cost), together with an aging population and budgetary
constraints, have made an evidence-based approach to device therapy more important than ever. Our review discusses basic pacemaker function and indications.
BASIC FUNCTION AND TYPES
The pacemaker system consists of a pulse generator and 1,
2, or 3 leads (Figure 1). The generator contains the battery
and the electrical circuitry and is connected to the leads
through the header. The generator is typically implanted in
the left or right pectoral region. The subclavian, cephalic, or
axillary vein is accessed via standard percutaneous puncture
or cutdown to introduce the leads and provide access to the
chamber being paced: the right atrium, right ventricle, or
coronary sinus (for left ventricular [LV] stimulation). The
pulse generator emits electrical pulses that depolarize the
myocardium. Modern pacemakers sense electrical signals
from the cardiac chambers and respond to the sensed event
by either inhibition of pacing or tracking the sensed event
with a pacing pulse. The type and rate of pacing may be
further controlled by a series of algorithms that can alter the
mode and rate of pacing. Because of the complexity of
devices and programming, a uniform nomenclature has been
adopted (Table 1).4 A 5-letter code is used to describe the
pacemaker mode. The first letter refers to the chamber that is
paced (atrium, ventricle, dual), the second letter refers to the
chamber sensed (atrium, ventricle, dual), the third letter
refers to the response to sensing (inhibit, trigger, dual), the
fourth letter indicates the presence or absence of rate modulation, and the fifth letter indicates multisite pacing.
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CONTEMPORARY PACEMAKERS
FIGURE 1. Schematic of commonly used pacemaker systems. A, Single-chamber ventricular pacemaker;
B, Single-chamber atrial pacemaker; C, Dual-chamber pacemaker; D, Triple-chamber (biventricular)
pacemaker.
Single-chamber atrial or ventricular pacemakers sense
myocardial signals emanating from the corresponding cardiac chamber and deliver a pacing stimulus if no signal is
sensed at the programmed lower rate. Dual-chamber pacemakers sense and pace both the atrium and the ventricle.
Depending on the particular clinical situation and programming, sensed events trigger or inhibit pacing (Figure 2).
For example, in the DDD pacing mode and during atrio-
ventricular sequential pacing, atrial pacing takes place at
the lower rate limit. Atrial pacing triggers ventricular pacing once the programmed AV delay has timed out. Ventricular pacing is inhibited if a ventricular event is sensed
before the end of the paced AV delay. If the atrial rate is
faster than the programmed lower rate, atrial pacing is
inhibited. After the sensed atrial signal, ventricular pacing
would occur only if no ventricular event is sensed by the
TABLE 1. The Revised NASPE/BPEG Generic Code for Antibradycardia, Adaptive-Rate, and
Multisite Pacinga
Position
Category
Manufacturers’
designation only
I
II
III
IV
V
Chamber(s) paced
O = None
A = Atrium
V = Ventricle
D = Dual (A+V)
S = Single
(A or V)
Chamber(s) sensed
O = None
A = Atrium
V = Ventricle
D = Dual (A+V)
S = Single
(A or V)
Response to sensing
O = None
T = Triggered
I = Inhibited
D = Dual (T+I)
Rate modulation
O = None
R = Rate modulation
Multisite pacing
O = None
A = Atrium
V = Ventricle
D = Dual (A+V)
a
BPEG = British Pacing and Electrophysiology Group; NASPE = North American Society of Pacing and Electrophysiology.
From Pac Clin Electrophysiol.4
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CONTEMPORARY PACEMAKERS
A
B
C
FIGURE 2. Basic pacing behaviors of dual-chamber pacemakers in
dual-chamber pacing and sensing with inhibition and atrial tracking
(DDD) pacing mode. Order of panels in electrograms: Top, Standard lead II electrocardiogram (ECG); Middle, Marker channel;
Bottom, Ventricular electrogram (VEGM). A, Electrocardiogram illustrating atrial pacing (AP) with ventricular tracking. Atrial pacing
and atrial capture (pacing artifact followed by P wave) occur at the
lower rate limit (60 beats/min) at the beginning of the tracing.
Ventricular pacing (VP) is inhibited because intrinsic ventricular
activity is sensed before the expiration of the programmed atrioventricular delay (AVD, 280 ms). Once the intrinsic sinus rate
accelerates to 60 beats/min or more, AP is also inhibited, and
both atrial and ventricular events are sensed (AS and VS). B,
Electrocardiogram illustrating atrioventricular sequential dualchamber pacing. The AP artifact is well seen, followed by a P wave,
confirming atrial capture. Once the AVD times out, VP ensues. In
this example, it is difficult to identify the VP artifact on the surface
ECG, but pacing is confirmed by the local ventricular electrogram
(arrows). C, Electrocardiogram illustrating atriosynchronous VP.
Atrial-sensed events (AS) inhibit atrial pacing. Ventricular pacing
occurs at the programmed AVD with appropriate ventricular capture (QRS complex follows each VP stimulus).
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end of the programmed sensed AV delay (Figure 2). When
atrial tachyarrhythmias such as atrial fibrillation or atrial
flutter occur, AV synchrony cannot be maintained, and a
“nontracking” mode (ie, dual-chamber pacing without
atrial synchronous pacing [DDI] or ventricular inhibitory
[VVI] pacing) will be activated to avoid inappropriate
rapid ventricular pacing. Most dual-chamber pacemakers
are able to detect atrial arrhythmias and allow automatic
switching between different pacing modes activated by
changes in atrial rhythm (Figure 3).
If a blunted heart rate response to exercise occurs, rateadaptive pacemakers are useful.5 These devices have special sensor(s) that, when triggered during exercise, increase
the pacing rate (so-called sensor rate). Most commonly
used sensors monitor body movement by detecting vibration (activity sensor or accelerometer). Although compatible with any pacemaker lead system, these vibration-detecting sensors can be subject to substantial environmental
interactions. More physiologic sensors detect changes in
minute ventilation by measuring changes in thoracic impedance with ventilation or changes in QT interval that
reflect sympathetic drive.6-9 Some pacemakers incorporate
more than 1 sensor to limit disadvantages of individual
sensors and enhance specificity without compromising
sensitivity.7,9 A commonly used combination is an activity
sensor combined with a QT interval sensor or a minute
ventilation sensor. Careful programming of the “sensor
blend” and sensor response is often required to achieve
optimal clinical results.10
Modern pacemakers are able to capture and store a
wealth of information that may be helpful in clinical management, follow-up, and troubleshooting. Interrogation of
the pacemaker will reveal programmed parameters, such as
pacing mode and pacing rates, as well as battery and lead
parameters. Event counters, heart rate histograms, and
trends may shed light on pacing frequency, arrhythmias,
mode switches, activity level, fluid status, and heart rate
variability or be used to monitor automatic pacing threshold and sensing tests (Figure 4). Stored electrograms may
be used to correlate symptoms and identify atrial or ventricular arrhythmias (Figures 3 and 5).
ASSOCIATED MORBIDITY
It has been a challenge and overall goal of pacing therapy to
mimic the normal electrical activation of the heart. Although simple ventricular pacing prevents severe bradycardia, AV dissociation or retrograde atrial activation may
occur, resulting in pacemaker syndrome in up to 30% of
patients.11,12 The multifactorial causes of pacemaker syndrome include hemodynamic, neurohumoral, and autonomic changes.13,14 Ventricular pacing without proper atrial
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CONTEMPORARY PACEMAKERS
FIGURE 3. Atrial tachycardia in a Guidant Insignia I Entra pacemaker (Boston Scientific, Natick, MA). Upper channel shows
atrial electrogram (AEGM); lower channel shows ventricular electrogram (VEGM). Atrial tachycardia is appropriately detected
(marked as atrial tachycardia response [ATR]), and pacing mode is changed from dual-chamber pacing and sensing with
inhibition, atrial tracking, and rate modulation (DDDR) to nonatrial tracking with rate modulation (DDIR) mode (*). In this
particular algorithm, ventricular pacing (VP) rate decreases slowly to the programmed lower rate after the detection of the
arrhythmia (gradual fallback). AP-Ns = atrial pace–sense amp noise; AS = atrial-sensed event; ATR-FB = ATR fallback started;
EGM = electrogram; VS = ventricular-sensed event; VP-FB = VP in atrial tachycardia response; VP-MT = VP at maximum
tracking rate.
synchronization results in loss of the atrial contribution to
ventricular filling. The importance of the atrial contribution
to cardiac output has been described in different clinical
settings, and the hemodynamic advantages of dual-chamber pacing are well known.15-18 Dual-chamber pacing allows more “physiologic activation” by coordinating the
timing of atrial and ventricular systole and promoting
physiologic heart rate response in patients with intact sinus
node function and AV block. Optimal AV timing allows
better ventricular filling, improves cardiac output, prevents
AV valve regurgitation, and prevents increased atrial pressure by avoiding atrial contraction against closed AV
valves. Pacemaker syndrome can lead to disabling symptoms, including dizziness, weakness, heart failure, and
FIGURE 4. Long-term threshold record from a St. Jude Medical Integrity single-chamber pacemaker (St. Jude Medical, St
Paul, MN). The AutoCapture feature allows beat-to-beat analysis of adequate capture and automatic modification of
pacing output as required by changing clinical circumstances. The pacemaker-dependent patient whose long-term
threshold record is pictured in this figure had a sudden increase in pacing threshold (from 0.75 V to 3.5 V) due to
exacerbation of chronic heart failure (arrow). Once this increase was recognized, pacing output was appropriately
increased by the pacemaker. Conventional programming would have likely resulted in intermittent loss of capture. E/R =
evoked response; VVIR = ventricular inhibitory pacing with rate modulation.
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CONTEMPORARY PACEMAKERS
FIGURE 5. Ventricular tachycardia (V-Tachy) is recorded in a Guidant Insignia I Entra dual-chamber pacemaker (Boston
Scientific, Natick, MA). The recording shows local atrial (upper channel) and ventricular (lower channel) electrograms.
Marker channel (what the pacemaker “sees”) is at the bottom and indicates 5 atrial-sensed (AS) and ventricular-paced
(VP) beats followed by a short 12-beat run of ventricular tachycardia (marked as premature ventricular contraction [PVC]
in the marker channel). There is atrioventricular dissociation (arrows indicate P wave; the asterisk indicates initiation of
V-Tachy). AEGM = atrial electrogram; EGM = electrogram; VEGM = ventricular EGM; VS = ventricular-sensed event.
presyncope or syncope; it also predisposes the patient to
the development of atrial fibrillation and increased incidence of stroke.19-22 Symptoms are sometimes mild and
nonspecific.18 Symptoms of pacemaker syndrome are
largely prevented or reversed by restoring AV synchrony.
Results of mode selection trials are discussed in “Specific
Indications for Use.”
The association between long-term right ventricular apical pacing and pathological changes and increased morbidity is increasingly recognized.23-25 Thus, ventricular dyssynchrony arising from right ventricular apical pacing may
cause cardiac dysfunction and heart failure.26-33 Avoidance
of right ventricular apical pacing by using pacing algorithms to promote intrinsic AV conduction in patients with
sick sinus syndrome or alternative-site pacing (eg, placement of the right ventricular lead in the mid-septum) has
been suggested as an alternative strategy.32,33 More data are
needed to clarify the overall benefits of these modalities.
Ventricular dyssynchrony, which may result from an
intrinsic conduction system disease such as left bundle
branch block, has been linked to adverse prognosis in
patients with heart failure and systolic dysfunction.34,35 Intraventricular conduction delay causes marked differences
in the timing of intraventricular contraction longitudinally
and radially along the LV myocardium and results in intraventricular dyssynchrony.36 Dyssynchrony leads to increased work of the LV, worsening mitral regurgitation
because of the delayed activation of the papillary muscle,
and shortened diastolic filling time.36-38 Biventricular pacing
(pacing of the right ventricle and LV) results in improved
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LV systolic and diastolic function by “synchronizing” timing of contraction. This is achieved by implantation of a third
pacing lead into a lateral branch of the coronary sinus (Figure 1). Biventricular pacing or cardiac resynchronization
therapy (CRT) has evolved as an additional therapeutic modality in medically optimized patients with New York Heart
Association (NYHA) class III or IV heart failure and evidence of conduction delay or bundle branch block.1
SPECIFIC INDICATIONS FOR USE
SINUS NODE DISEASE
Sinus node disease is currently the most common reason
for pacemaker implantation. Electrocardiographic features
include sinus bradycardia, sinoatrial block, sinus arrest, or
alternating periods of atrial tachycardia (eg, atrial flutter or
atrial fibrillation with a rapid ventricular response) and
bradycardia, often after termination of an atrial tachyarrhythmia. In some cases, sinus node disease manifests as
inadequate change in heart rate in response to physiologic
stress, such as exercise. Although most commonly caused
by idiopathic degeneration and fibrosis of the sinoatrial
node, sinus node disease may also result from certain infections, medication exposure, or other diseases such as amyloidosis or neurologic, endocrine, or liver disease. The
often nonspecific symptoms of sinus node disease include
dizziness, confusion, fatigue, syncope, and chronic heart
failure. Because sinus bradycardia and sinus pauses are not
uncommon, clinical symptoms should be correlated with
bradycardia to allow more definitive therapeutic recom-
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CONTEMPORARY PACEMAKERS
TABLE 2. Simplified Summary of Indications for Pacemaker Therapy
in Sinus Node Disease and Acquired AVB in Adultsa
Sinus node disease
Class I
Class II
Class III
Acquired AVB in adults
Class I
Class II
Class III
Symptomatic bradycardia
Symptomatic chronotropic incompetence
Heart rate <40 beats/min spontaneously or in the presence of essential medical therapy
when clinically important symptoms are not correlated with bradycardia
Syncope and abnormal sinus node function documented in electrophysiologic study
Heart rate <40 beats/min and minimal symptoms
Asymptomatic sinus node disease
Clear documentation that symptoms are unrelated to bradycardia
Sinus node disease due to nonessential drug therapy
Third-degree AVB
Symptoms
Asystole >3 s or escape rate <40 beats/min
Associated neuromuscular disease (eg, Kearns-Sayre, Erb dystrophy)
After atrioventricular node ablation
After cardiac surgery
Symptomatic second-degree AVB
Alternating bundle branch block type II second-degree AVB with underlying
bifascicular block
Third-degree AVB with LV dysfunction
Type II second-degree AVB
Syncope with underlying bifascicular block when VT excluded
Neuromuscular diseases with any AVB or fascicular block
Asymptomatic first-degree or type I second-degree AVB
AVB expected to resolve
Fascicular block with first-degree AVB or no AVB
a
AVB = atrioventricular block; LV = left ventricular; VT = ventricular tachycardia. Class I conditions are those for
which there is evidence and/or general agreement that a given procedure or treatment is useful and effective. Class
II conditions are those for which there is conflicting evidence and/or a divergence of opinion about the usefulness/
efficacy of a procedure or treatment. Class III conditions are those for which there is evidence and/or general
agreement that the procedure/treatment is not useful and in some cases may be harmful.
Adapted from J Am Coll Cardiol,1 with permission.
mendations, even though exact correlation between symptoms and abnormalities on electrocardiography (ECG) is
not always possible. The natural course of asymptomatic
sinus node disease is benign.39 In general, pacemaker
therapy is recommended only when symptoms are present
(Table 2). Although the effectiveness of pacemaker therapy
is widely accepted, very few randomized controlled trials
have measured the effectiveness of pacing therapy in patients with symptomatic sinus node disease. The Effects of
Permanent Pacemaker and Oral Theophylline in Sick Sinus
Syndrome (THEOPACE) study randomized 107 patients
with moderately symptomatic sinus node disease to be
controls or to receive oral theophylline therapy or dualchamber pacing.40 During the average follow-up of 19
months, syncope was less frequent in the pacemaker group
(6%) than in the controls (23%). Both pacing and theophylline therapy reduced the risk of heart failure. Because pacing
therapy is effective in ameliorating symptoms, future trials
are unlikely.
Pacemaker mode selection in sinus node disease may
markedly affect patient outcomes. Several retrospective
and observational studies have shown reduced rates of
atrial fibrillation, stroke, heart failure, and death with
Mayo Clin Proc.
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physiologic or atrial (DDD or atrial inhibitory) pacing
compared with ventricular (VVI) pacing.19-22 The results of
these retrospective studies are confounded by selection
bias and incomplete follow-up. Results of several large,
multicenter, randomized trials are available to help clinicians predict optimal patient selection for pacing in sinus
node disease. The first randomized trial was a small
single-center study from Denmark by Andersen et al
(henceforth referred to as “Danish study”).41 The investigators compared single-chamber atrial with single-chamber ventricular pacing in 225 patients with symptomatic
sinus node disease. Long-term follow-up showed reduction in atrial fibrillation, stroke, heart failure, and death
with atrial pacing.26 Subsequent large trials from the
United States and Canada compared dual-chamber pacing
with ventricular pacing for sinus node disease and found
no difference in stroke or all-cause mortality.11,12,42 However, individual trials and a meta-analysis43 suggested that
risk of atrial fibrillation, pacemaker syndrome, and heart
failure is reduced with physiologic pacing (summarized
in Table 3).
In the later trials,11,12,42 the deleterious effects of right
ventricular pacing may have negated the benefits of AV
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CONTEMPORARY PACEMAKERS
TABLE 3. Landmark Trials in Cardiac Pacing for Sinus Node Disease and AVBa
Reference
11
No. of
patients
Age (y),
mean ± SD or
median (IQR)
Indication (%)
SND
AVB
Pacing
mode
Follow-up
(mo)
Primary
end point
Mortality
Importance and main findings
HR, 0.97;
95% CI,
0.80-1.18
DDD pacing results in improvement
in QOL, CHF, and AF in SSS
compared with VP
MOST
2010
74
(67-80)
100
21
VVIR,
DDDR
33
Death or
stroke
PASE12
407
76±7
(65-96)
43
49
DDDR,
VVIR
18
QOL
16% vs
17%;
P=.95
Dual-chamber pacing improved QOL
(P=.045). No mortality difference
between pacing modes. Decreased
AF with AP in SSS
1065
72±12
100
21b
DDD; forced
VP vs minimized VP
20
Time to
persistent
AF
5.4% vs
4.9%;
P=.54
Avoidance of unnecessary VP reduces
AF in SSS
225
76±8
100
0
AAI,
VVI
40
Mortality,
AF, CHF,
embolism
19% vs
22%;
P=.74
First prospective, randomized trial to
suggest advantage of AP over VP.
Decreased AF and CHF with AP
CTOPP42
2568
73±10
41
51
VVIR, DDDR,
AAIR
36
Death or
stroke
HR, 0.91;
95% CI,
0.82-1.17
No difference in mortality, CHF, or
stroke. Less AF with physiologic
pacing
UKPACE44
2021
80±6
NR
100
VVI, VVIR,
DDDR
56
Death
HR, 1.04;
95% CI,
0.89-1.17
No difference between AP and VP
pacing in the incidence of CHF,
AF, stroke, or death in AVB
SAVEPACe33
Danish
trial41
a
AAI = atrial inhibitory; AAIR = atrial inhibitory with rate modulation; AF = atrial fibrillation; AP = atrial pacing; AVB = atrioventricular block; CHF = chronic heart
failure; CI = confidence interval; CTOPP = Canadian Trial of Physiologic Pacing; DDD = dual-chamber pacing and sensing with inhibition and atrial tracking; DDDR =
DDD with rate modulation; HR = hazard ratio; IQR = interquartile range; MOST = Mode Selection Trial in Sinus-Node Dysfunction; PASE = Pacemaker Selection in the
Elderly; QOL = quality of life; SAVE-PACe = Search AV Extension and Managed Ventricular Pacing for Promoting Atrioventricular Conduction; SND = sinus node
disease; SSS = sick sinus syndrome; UKPACE = United Kingdom Pacing and Cardiovascular Events; VP = ventricular pacing; VVI = ventricular inhibitory; VVIR =
VVI pacing and rate modulation.
b
First-degree AVB only.
synchrony. This notion is supported by the Dual Chamber
and VVI Implantable Defibrillator (DAVID) Trial,31 which
randomized recipients of dual-chamber implantable cardioverter-defibrillators to back-up VVI or DDD with rate
modulation (DDDR) pacing. The increased incidence of
hospitalization for heart failure or death in the dual-chamber group was thought to be caused by increased right
ventricular pacing. Post hoc analysis of the Mode Selection
Trial in Sinus-Node Dysfunction (MOST)29 revealed that in
patients with prepaced QRS duration of less than 120 ms,
incremental percentages of right ventricular pacing strongly
predicted hospitalization due to heart failure and development of atrial fibrillation. Of interest, the percentage of
ventricular pacing was increased in DDDR mode compared with the VVI and rate modulation (VVIR) mode
(90% vs 58%). The beneficial effects of AV synchrony
with dual-chamber pacing may have been counterbalanced
by the detrimental effects of right ventricular apical pacing
seen in the DDDR mode. The more recently published
Search AV Extension and Managed Ventricular Pacing for
Promoting Atrioventricular Conduction (SAVE-PACe)
trial33 confirmed these findings. Patients with sinus node
disease were randomized to conventional dual-chamber
pacing or dual-chamber pacing with a special algorithm
designed to minimize ventricular pacing; mean ± SD fol1176
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low-up was 1.7±1.0 years. In patients for whom the algorithm was used to minimize ventricular pacing (from 99%
in the dual-chamber group with short AV delay to 9% in the
intervention group), the incidence of persistent atrial fibrillation was reduced by 4.7%.
ATRIOVENTRICULAR CONDUCTION DISEASE AND HEART BLOCK
The AV node and His-Purkinje system are integral parts of
normal ventricular electrical activation. Abnormalities in
conduction may occur at different levels, and prognosis is
largely dependent on the level of block, the presence or
absence and reliability of escape rhythms, and underlying
cardiac disease. Progression of the disease may cause severe bradycardia or asystole and may be responsible for
sudden cardiac death. The causes of AV conduction disease are diverse (Table 4). Indications for pacemaker
therapy in AV conduction disease are directed by symptoms and by patient prognosis. In general, patients with
symptomatic AV node disease or with His-Purkinje disease
and high likelihood of progression benefit from pacing
(Table 2).
Intuitively, dual-chamber pacing in the treatment of AV
block is attractive in that it restores AV synchrony and
normal chronotropy (provided there is normal sinus node
function). Clinical outcomes of single-chamber (25% VVI
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CONTEMPORARY PACEMAKERS
and 25% VVIR) and DDD pacing (50% DDD or DDDR)
were examined in the multicenter, randomized United
Kingdom Pacing and Cardiovascular Events (UKPACE)
trial,44 in which 2021 patients (mean age, 79 years) with
second-degree or complete AV block were enrolled. After
a median follow-up of 4.6 years, no difference was observed in all-cause mortality or in the rates of atrial fibrillation, stroke or thromboembolism, and heart failure. These
results, in accordance with the observations from the Pacemaker Selection in the Elderly (PASE) trial12 and the Canadian Trial of Physiologic Pacing (CTOPP),42 suggest that
DDD pacing offers no significant clinical or survival advantage over single-chamber pacing in elderly patients
with high-grade AV block during a relatively short followup of 3 to 5 years. Meta-analysis of pooled data from 5
major trials (MOST, CTOPP, UKPACE, PASE, Danish
trial) confirmed no survival advantage with physiologic
pacing but showed a reduction in atrial fibrillation and
stroke.45
The benefits of dual-chamber pacing must be balanced
against increased cost (additional leads, more sophisticated
devices, more complex follow-up) and increased complication rates with dual-chamber systems.12,42,44 Cost-effectiveness analysis between single- and dual-chamber systems,
especially in the short term, is largely dependent on the
prevalence of pacemaker syndrome. Cost per quality-adjusted life-year (QALY) improves with longer therapy and
remains economically acceptable ($14,900 per QALY in
AV block and $16,600 in sick sinus syndrome for 5 years;
approximately $9600 per QALY in both populations for 10
years).46
These trials answer important questions but leave other
clinically relevant questions unanswered. Although death
or stroke reduction has not been seen with dual-chamber
pacing during a follow-up of 3 to 5 years, emerging data
suggest that physiologic pacing may reduce the incidence
of atrial fibrillation, especially in patients with sinus node
disease. Longer follow-up might be required to translate
these benefits to reduction in risk of stroke and perhaps
death. This question is especially important for younger
patients who are expected to be paced for long periods of
time.
Quality-of-life measures and decreased incidence of
pacemaker syndrome have suggested superiority of dualchamber pacing in the PASE and MOST studies. These
trials used software-based randomization. Each patient received a dual-chamber pacemaker that was randomly programmed to VVIR or DDDR mode. Pacemaker syndrome
has been infrequent in trials using hardware randomization
(such as UKPACE and CTOPP, in which a specific type of
single- or dual-chamber pulse generator was implanted).
Because changing of pacing mode required reoperation in
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TABLE 4. Common Causes of Acquired Atrioventricular Block
Degenerative disease
Lev disease
Lenègre disease
Secondary degeneration/calcification
Medications
β-Receptor blockers
Calcium channel antagonists
Digoxin
Other antiarrhythmic agents
Atherosclerotic heart disease
Myocardial ischemia
Myocardial infarction
Dilated cardiomyopathy
Infiltrative disease
Sarcoidosis
Amyloidosis
Metastasis
Infections
Endocarditis
Lyme disease
Chagas disease
Iatrogenic causes
After atrioventricular nodal ablation
After cardiac surgery
After radiation therapy
Enhanced parasympathetic activity
the latter trial design, the true incidence of pacemaker
syndrome may have been underestimated.
NEUROCARDIOGENIC SYNDROME
Syncope in neurocardiogenic syndrome is thought to be
due to a transient imbalance in the cardiovascular autonomic regulation that results in vasodilation with or without inappropriate bradycardia. In susceptible patients, these
events may be triggered by prolonged standing (vasovagal
syncope) or by compression of the carotid sinus (carotid
sinus hypersensitivity). The underlying mechanisms of vasovagal syncope and carotid sinus hypersensitivity have
been extensively studied but remain incompletely understood. Several studies have evaluated the role of pacemaker
therapy in patients with severe symptoms who did not benefit from medical therapy and had evidence of substantial
bradycardia during head-up tilt-table testing.47-51 Small observational and randomized trials suggested marked benefit
with dual-chamber pacing with use of rate hysteresis and
rate-drop response.49,52 These special algorithms allow increased pacing rate when a decrease in heart rate is detected.
The results of these studies are summarized in Table 5.
A multicenter, randomized, double-blind trial showed
no significant benefit in neurocardiogenic syncope with
pacing therapy, suggesting a substantial placebo effect in
prior unblinded studies.53 Therefore, pacing therapy should
be used only in very select patients who have not benefited
from other measures and who have substantial cardioin-
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CONTEMPORARY PACEMAKERS
TABLE 5. Landmark Trials in Pacing for Neurocardiogenic Syncopea
Reference
Trial design
50
42
Unblinded RCT
SYDIT51
93
Unblinded RCT
54
Unblinded RCT
VASIS
VPS
52
VPS II53
a
No. of
patients
100
Double-blind RCT
Entry criteria
Results
Recurrent syncope and cardioinhibitory
response during tilt-table testing
Recurrent syncope and cardioinhibitory
response during tilt-table testing
Recurrent syncope and cardioinhibitory
response during tilt-table testing
Recurrent syncope and cardioinhibitory
response during tilt-table testing
80% risk reduction with pacemaker therapy (DDI with
rate hysteresis)
87% risk reduction with pacing (vs atenolol)
85% risk reduction with pacemaker therapy (rate decrease)
No significant difference between DDD mode and ODO
mode
DDD = dual-chamber pacing and sensing with inhibition and atrial tracking; DDI = dual-chamber pacing without atrial synchronous ventricular pacing;
ODO = sensing only; RCT = randomized controlled trial; SYDIT = Syncope Diagnosis and Treatment Study; VASIS = Vasovagal Syncope International
Study; VPS = North American Vasovagal Pacemaker Study.
hibitory response (ie, predominant bradycardia) during tilttable testing. Patients with vasodilation as the primary
mechanism for hypotension would not benefit from cardiac
pacing. In pacemaker therapy for neurocardiogenic syndromes, ventricular pacing is obligatory due to frequent
AV block. Single-chamber ventricular pacing may frequently cause ventriculoatrial conduction and worsened
hemodynamics; therefore, although data are scarce, most
experts support dual-chamber pacing.
Small observational and randomized trials have assessed the effectiveness of pacemaker therapy for carotid
sinus hypersensitivity with encouraging results. One of the
2 largest randomized (but not blinded) trials by Brignole et
al54 randomized 60 patients with symptomatic carotid sinus
hypersensitivity to pacemaker (VVI or DDD) or no
therapy. During a mean ± SD follow-up of 36±10 months,
syncope occurred in 57% of the nonpaced and 9% of the
paced group. Although uncommon, carotid sinus hypersensitivity may be an important cause of falls and syncope in
elderly people. The Syncope And Falls in the Elderly—
Pacing And Carotid sinus Evaluation (SAFE PACE) trial55
studied 175 patients with frequent falls and a cardioinhibitory response to carotid sinus massage and randomized
them to dual-chamber pacemaker implantation or no
therapy. During 1 year of follow-up, pacemaker therapy
decreased the risk of falls and injury by 70%.
CHRONIC HEART FAILURE
Several trials have examined the role of pacing therapy for
heart failure and cardiomyopathy without bradycardia indication. Earlier studies focused on the potential role of dualchamber pacing and optimized LV filling.56 In selected
cases of dilated cardiomyopathy and severe heart failure,
DDD pacing with short AV delays has been shown to
provide hemodynamic benefit and symptomatic relief.56,57
Later studies failed to confirm any benefit of DDD pacing
in patients with dilated cardiomyopathy, suggesting that
initial results were likely a reflection of the powerful placebo effect of pacemaker implantation.58,59
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A large proportion (about 30%) of patients with heart
failure have dyssynchronous contraction of the LV myocardium in addition to LV filling abnormalities.60 Under
normal circumstances, ventricular depolarization is very
rapid, and the myocardium contracts nearly simultaneously. In left bundle branch block or conventional right
ventricular apical pacing, ventricular activation changes
markedly, with some myocardial regions activated early
and other regions activated late. Synchrony is important for
efficient cardiac function. Myocardial regions at early contraction sites waste energy because pressure is still low and
does not produce ejection, whereas activation and contraction in the rest of the heart cause “prestretching” and increased work in the late-activated regions.36 With right
ventricular pacing or left bundle branch block, late-activating areas are most commonly located in the posterolateral
LV wall. Preactivation of this late-activated area by LV
pacing has been used to improve synchrony.61,62 This may
be achieved by addition of an LV lead to a conventional
pacing system (biventricular pacing). In the United States,
most patients further undergo upgrade of the biventricular
pacemaker to a defibrillator by the addition of a defibrillation lead. Once required, epicardial LV lead placement
through thoracotomy is now reserved for special cases.
Advances in technology and increased implantation experience have resulted in successful LV lead placement via a
transvenous approach through the coronary sinus. Lead
placement in the lateral or posterolateral branches is necessary to maximize benefits.63 Despite great variability in the
anatomy of the coronary sinus and tributary veins, optimal
lead positioning is usually achieved in 90% to 95% of cases
at centers handling high volumes of such cases.64,65
Several trials66-69 have examined the hemodynamic and
clinical benefits of CRT (Table 6). Most trials enrolled
patients with dilated cardiomyopathy (ischemic or
nonischemic etiology), ejection fraction of less than 35%,
electrical dyssynchrony as evidenced by prolonged QRS
duration of more than 120 to 130 ms (most commonly left
bundle branch block), presence of sinus rhythm, and
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CONTEMPORARY PACEMAKERS
TABLE 6. Landmark Trials in Cardiac Resynchronization Therapya
Inclusion criteria
Reference
No. of
patients
NYHA
class
LVEF
(%)
QRS
(ms)
Follow-up
(mo)
Primary
end point
COMPANION64
1520
III-IV
35
120
CRT,
CRTD
14.4
Death or
hospitalization
CARE-HF65
813
III-IV
35
120b
CRT
29.4
Death or
hospitalization
MIRACLE70
453
III-IV
35
130
CRT
6.0
QOL, NYHA
class, 6MWT
MIRACLE ICD71
369
III-IV
35
130
CRTD
6.0
QOL, NYHA
class, 6MWT
CONTAK CD72
490
II-IV
35
120
CRTD
6.0
Death or CHF
hospitalization
or VT/VF
Device
Results
Summary
Improved survival
and reduced
hospitalization
Improved survival
and reduced
hospitalization
Improvement in
all primary end
points
Improved QOL
and NYHA class
candidates
No difference in
primary end
point
Symptomatic and survival
benefit with CRTD
therapy
Symptomatic and survival
benefit with CRTP
therapy
Large randomized trial
to show symptomatic
improvement with CRT
Symptomatic improvement with CRT in ICD
Symptomatic improvement with CRT in
patients with NYHA
class III and IV heart
failure
a
CARE-HF = Cardiac Resynchronization in Heart Failure; CHF = chronic heart failure; COMPANION = Comparison of Medical Therapy, Pacing, and
Defibrillation in Heart Failure; CRT = cardiac resynchronization therapy; CRTD = CRT with additional defibrillation capability; CRTP = CRT
pacemaker; ICD = implantable cardioverter-defibrillator; LVEF = left-ventricular ejection fraction; 6MWT = 6-minute walk test; MIRACLE =
Multicenter InSync Randomized Clinical Evaluation; NYHA = New York Heart Association; QOL = quality of life; VF = ventricular fibrillation; VT =
ventricular tachycardia.
b
The CARE-HF trial included patients with QRS duration of more than 150 ms or patients with echocardiographic evidence of left ventricular dyssynchrony
and QRS duration from 120 to 149 ms.
NYHA class III to IV heart failure symptoms despite optimal medical therapy. Because patients with these clinical characteristics are also at risk of sudden cardiac
death, many trials included CRT pacemaker defibrillator
(CRTD) devices. The overall results of the randomized
trials confirmed substantial symptomatic benefits, such as
improved ejection fraction, decreased LV volume, and decreased mitral regurgitation as assessed by NYHA class,
quality-of-life score, 6-minute walk test, admission for
heart failure, and/or reverse ventricular remodeling.61-65,70-72
In a recent meta-analysis of available CRT trials cumulatively enrolling more than 9000 patients, CRT was found
to improve LV ejection fraction by an average of 3%
and functional status by 1 or more NYHA classes (in
60% of patients) and to decrease hospitalization rates by
37%.73
EFFECTS OF CRT ON SURVIVAL
Two large trials were adequately powered to assess the
effects of CRT therapy on survival,64,65 and the results of
these trials are summarized in Table 6. In the Comparison
of Medical Therapy, Pacing, and Defibrillation in Heart
Failure (COMPANION) study,64 1520 patients with ischemic or nonischemic cardiomyopathy, NYHA class III
to IV heart failure, QRS duration greater than 120 ms, PR
interval less than 150 ms, ejection fraction less than 35%,
and hospitalization due to heart failure within 12 months
were randomized in a 1:2:2 design to optimal medical
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therapy, resynchronization therapy with a CRT pacemaker
(CRTP), or resynchronization therapy with a defibrillator
(CRTD). In line with other randomized trials, CRT therapy
significantly improved NYHA class, the distance walked in
6 minutes, and quality of life. The primary combined end
point of death or hospitalization due to heart failure was
significantly reduced in both the CRTD and CRTP groups
(controls, 68%; CRTP, 56%; P=.015; CRTD, 56%;
P=.011). Overall mortality rates were reduced with CRTD
(relative risk reduction, 36%; P=.003) but not with CRTP
(relative risk reduction, 24%; P=.059). The trial was terminated early because of the substantial survival benefit with
CRTD therapy. The shortened follow-up may account for
the lack of survival benefit with CRTP.
The Cardiac Resynchronization in Heart Failure (CAREHF) study,65 the first trial to address the effects of CRTP
therapy on mortality, used dyssynchrony parameters for patient selection as well as QRS duration. The 813 patients
enrolled in the study had NYHA class III or IV heart failure
despite optimal medical therapy, dilated cardiomyopathy
with LV ejection fraction of 35% or less, and QRS duration
of more than 150 ms or QRS duration of 120 to 150 ms with
echocardiographic evidence of dyssynchrony. The mean follow-up was 29.4 months. The primary end point of death or
cardiovascular hospitalization was significantly reduced
with CRTP (39% CRTP vs 55% control; relative risk reduction, 37%; P<.001). All-cause mortality was significantly
lower (hazard ratio, 0.64; 95% confidence interval, 0.48-
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CONTEMPORARY PACEMAKERS
TABLE 7. Patient Selection
for Cardiac Resynchronization Therapya
Candidates
Optimal medical therapy for heart failure
Weaned intravenous inotropic therapy for 4 wk
QRS duration >120-130 ms (primarily studied in patients with left
bundle branch block)
NYHA class III-IV heart failure symptoms
Dilated left ventricle
Optimal candidates
Idiopathic cardiomyopathy
QRS duration >150 ms
Echocardiographic evidence of dyssynchrony
Absence of scar in the left ventricular posterolateral region
Absence of severe organic mitral regurgitation
Absence of competing morbidities (ie, severe pulmonary or renal
disease)
a
NYHA = New York Heart Association.
0.85; P<.002) in the CRTP group (1 year, 9.7%; 2 years,
18%) than in the medical therapy group (1 year, 12.6%; 2
years, 25.1%). The CARE-HF study also found that CRT
therapy maintained or further promoted reverse remodeling, ie, improvements in ejection fraction, LV size, degree
of mitral regurgitation, and biomarker levels (N-terminal
propeptide of brain-type natriuretic peptide). Sudden cardiac death, which occurred in 7% of patients with CRTP,
could have been reduced by back-up defibrillator capability (CRTD).
On the basis of the COMPANION and CARE-HF trials,
we conclude that CRT with or without a defibrillator not
TABLE 8. Summary of Common Complications
of Pacemaker Implantation
Complications related to implantation
Vascular access–related
Inadvertent arterial puncture
Hematoma
Air embolization
Pneumothorax
Lead placement to the systemic circulation
Other
Infection
Pocket pain
Lead dislodgement
Perforation of cardiac chamber
Coronary sinus perforation
Extracardiac stimulation
Arrhythmia
Long-term complications
Mechanical
Exit block
Lead fracture
Device failure
Perforation
Other
Erosion/infection
Deep venous thrombosis/venous occlusion
Lead migration
Pacemaker syndrome
Arrhythmia
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only leads to substantial symptomatic improvement but
also reduces overall mortality in selected patients. These
robust benefits are seen in addition to those provided by
optimal medical therapy. For example, data from the CAREHF trial suggest that implantation of only 9 devices prevents
1 death and 3 cardiovascular hospitalizations. Meta-analysis
showed a similar reduction in mortality of 22%.73 Although
the choice between CRTP and CRTD should be made as
appropriate to the individual case, CRTD therapy is usually
favored in the United States because risk of sudden cardiac
death may be further reduced.
Several questions regarding CRT therapy remain unanswered. Despite impressive overall benefits, only 60% to
70% of patients clinically respond to CRT therapy. Suboptimal response has been linked to clinical features (Table
7), such as lack of dyssynchrony,74,75 presence of scar tissue
at the optimal LV lateral pacing site,76 competing comorbidities, or development of atrial tachyarrhythmia
(with loss of AV synchrony or rapid ventricular response
and lack of ventricular pacing). Technical problems, such
as anterior or suboptimal lead placement,63,77,78 lead
dislodgement, and loss of capture, may also contribute to
the lack of response. Nominal (“out-of-the-box”) programming of the AV delay is frequently suboptimal, especially
in cases of substantial intra-atrial conduction delay. Changing the timing delay between the right ventricular and LV
pacing impulse also has been shown to improve response
in some subsets of patients. Although cumbersome,
echocardiography may aid the determination of correct
timing of the AV delay and the timing delay between the
right ventricular and LV pacing stimulus (known as the
VV delay).79,80 Extensive research is focused on methods
for identifying nonresponders in advance and for optimizing response after implantation. Studies are under way to
evaluate the role of CRT therapy in patients with severe
symptoms, dyssynchrony, and narrow QRS complex.
One report suggests a lack of benefit of CRT therapy in
patients with QRS duration of less than 120 ms.81 Longterm benefit is currently being evaluated in patients with
dyssynchrony and NYHA class I or II heart failure. Clinical
features of optimal candidates for CRT therapy are summarized in Table 7.
FOLLOW-UP
Pacemaker recipients should be followed up regularly to
monitor for changes in clinical status, perform assessments, and optimize the pacemaker system.1 The follow-up
intervals should be determined on the basis of the individual patient’s needs and should be driven by clinical
circumstances. Common complications related to pacemaker implantation are summarized in Table 8. In the early
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CONTEMPORARY PACEMAKERS
postimplantation period, problems are usually related to
wound healing or changes in postoperative lead parameters. Once lead maturation is reached at 6 months, less
frequent evaluations may be appropriate. Transtelephonic
monitoring or wireless remote follow-up may be used between clinic visits. These systems allow transmission of
ECG strips via regular telephone lines or wireless devices
at the patient’s home. Transtelephonic monitoring makes
use of the fact that the magnet rate changes as the pacemaker battery is depleted. Information provided by the
baseline rhythm and magnet rate allows remote evaluation
of basic pacing function and battery status. Internet-based
remote follow-up provides extensive device information,
including battery status, automatic pacing threshold, sensing measurements (if available), and underlying heart
rhythm. Although this new technology may substantially
enhance resource use and patient safety, it is not yet widely
available (it will likely be so in the future), and its effects
on long-term outcome for patients with pacemakers are not
fully understood. The reliability of pacemaker systems has
improved during the past decade, but more frequent follow-up is still recommended toward the end of battery life.
The pacemaker pocket and leads should also be inspected
for signs of erosion or infection.
IDENTIFYING MALFUNCTIONS
Assessment of proper programming and functioning of the
pacemaker system requires thorough understanding of interactions between the pulse generator and the pacemaker
leads as well as of the clinical circumstances of the patient.
Meticulous evaluation of each of these components is required when malfunction is suspected.
Clinical history in particular is a key component for
identifying pacemaker-related problems. During routine
visits, clinicians should inquire about potential pacemakerrelated symptoms, such as palpitation, light-headedness,
syncope, or change in exercise tolerance. Baseline information can be obtained from a postimplantation 12-lead
ECG during pacing and an overpenetrated posteroanterior
and lateral chest radiograph and used for comparison if
temporal changes occur. A standard 12-lead ECG will also
document pacing site (eg, left bundle branch block–like
morphology in right ventricular pacing vs right bundle
branch block pattern in inadvertent LV lead placement,
Figure 6, C). Chest radiography will document lead position and lead-pin connection. Careful documentation of
battery, lead, and programming parameters during pacemaker follow-up visits can greatly facilitate troubleshooting (Figure 7).
When a pacemaker abnormality is suspected, physical
examination, ECG, chest radiography, and pacemaker
interrogation are standard tests to clarify the diagnosis
Mayo Clin Proc.
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A
B
C
FIGURE 6. Electrocardiographic recordings of dual-chamber and triplechamber (biventricular) pacing. A, Electrocardiogram illustrating atrioventricular sequential pacing. Black arrows point to atrial pacing
artifact. Atrial capture is confirmed by P wave following atrial pacing
artifact. White arrows point to ventricular pacing artifact. Ventricular
capture is confirmed by QRS complex following the ventricular pacing
artifact. The QRS axis and morphology (left axis deviation, left bundle
branch–like morphology in V1) is consistent with right ventricular
apical pacing. B, Electrocardiogram illustrating atrial synchronous
biventricular pacing. Note rightward QRS axis, Q wave in lead I, and R
wave in V1. C, Electrocardiogram illustrating left ventricular pacing
due to inadvertent ventricular lead positioning via patent foramen
ovale. Note monophasic R wave (right bundle branch block–like
morphology) in lead V1.
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CONTEMPORARY PACEMAKERS
lems related to electromagnetic interference are summarized in Table 9. Other causes of oversensing include lead
or pulse generator malfunction (lead fracture, loose set
screw, component failure).
Failure to capture or pace may be related to the pacer
lead (lead dislodgement, lead fracture), the pulse generator
(battery depletion, loose set screw), or change in leadtissue interface (fibrosis, electrolyte changes, effect of
medications, infarction at the lead tip). Pacing at an unexpected interval or rate is most commonly the result of a
trigger from a sensed event or special algorithm, such as rate
smoothing, overdrive pacing, rate drop feature, and rate
hysteresis. Pacemaker-mediated tachycardia (PMT) should
also be considered. It is commonly initiated by a premature
ventricular stimulus that is conducted retrograde via the AV
node to the atrium. The retrograde atrial signal then is sensed
by the atrial channel and triggers pacing in the ventricle.
Ventricular pacing causes retrograde conduction to the atria,
and the PMT circuit is established. Most pacemakers have
FIGURE 7. Ventricular lead fracture. Top, Long-term lead parameters. The arrow points to sudden increase in ventricular lead
impedance. Bottom, Radiograph of the pacemaker system confirming ventricular lead fracture (arrow).
(Figures 6-9). Pacemaker system malfunctions may be
grouped as abnormalities in sensing or in pacing. Recording artifacts, magnet response, and suboptimal programming should be considered.
Abnormalities in sensing include undersensing and
oversensing. Undersensing may occur because of leadrelated changes (dislodgement, lead fracture) or change in
the lead-myocardium interface (change in activation sequence as in new bundle branch block or premature ventricular contractions, electrolyte abnormality, new medication, lead maturation and fibrosis, infarction at the pacer
lead tip). Oversensing is sensing of inappropriate signals.
These signals may be other parts of the normal ECG, such
as P wave, R wave, T wave, or pacing artifact. They may be
skeletal muscle signals such as myopotentials (seen in diaphragmatic oversensing). Electromagnetic interference occurs when the pacemaker is subjected to a strong electrical
field (eg, arc welding). The approaches to common prob1182
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A
B
FIGURE 8. Pacemaker syndrome due to pacing mode change at
pacemaker battery depletion. Patient with sinus node disease and
atrial pacing presented with symptoms of heart failure. Baseline
electrocardiogram shows atrial pacing and 1:1 atrioventricular conduction and narrow QRS complex (A). On presentation, there was
ventricular pacing with 1:1 retrograde atrial conduction (B). Arrows
point to retrograde P waves. Symptoms of heart failure were related
to pacemaker syndrome. Ventricular pacing occurred because the
pacemaker reached elective replacement indicator and switched to
ventricular inhibitory mode. Symptoms completely resolved after
pacemaker generator change.
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CONTEMPORARY PACEMAKERS
Pacemaker malfunction suspected
Yes
Capture present?
No
Pacing stimulus
present?
Intrinsic rhythm
present?
No
Interrogate device
Consider artifact,
mechanical failure,
drug/metabolic effect
Pacing appropriate?
Yes
Yes
No
Yes
No
Application of magnet
restores pacing?
Rate appropriate
to inhibit pacer?
Yes
Yes
No
No
Application of magnet
restores pacing?
No
Normal
function
If slow: oversensing,
mechanical failure
If rapid: undersensing,
tracking, sensor rate,
runaway pacer
Oversensing:
electromagnetic
interference,
crosstalk, myopotential,
insulation defect
Mechanical
failure
Yes
Normal
function
FIGURE 9. Simplified algorithm for evaluation of pacemaker malfunction.
algorithms to recognize and terminate PMT. Pacemaker
component failures are responsible for other unusual but
dangerous causes of high pacing rate, such as runaway pacemaker and sensor-driven tachycardia.
TROUBLESHOOTING: A BASIC APPROACH
Primary care physicians may be faced with situations in
which subspecialty support is not immediately available to
help with pacemaker troubleshooting. A general approach
to troubleshooting is summarized in the next paragraphs
and in Figure 9.
When pacemaker malfunction is suspected, ECG, preferably 12-lead ECG, should be performed. The next step is
to identify the presence of pacing stimulus. Digital recording systems may filter out pacing artifacts, and pacing
artifacts may be absent on the recording. In this case,
reviewing QRS morphology and axis may be helpful.
Pacing Stimulus Present. If there are pacing artifacts,
appropriate capture has to be assured. Lack of capture
usually indicates suboptimal programming, mechanical
failure, or metabolic or medication effect. If there is capture
and rate is appropriate, pacing malfunction is unlikely. If
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there is capture but pacing rate is inappropriately slow, then
oversensing and mechanical failure should be considered.
On the other hand, pacing rate may be rapid due to tracking,
undersensing, sensor response, or mechanical failure (such
as in runaway pacemaker).
Pacing Stimulus Absent. If intrinsic rhythm is present
at a rate that is appropriate to inhibit the pacemaker, a
magnet may be applied over the device to assure appropriate (asynchronous) pacing and capture. If the intrinsic rate
is slow or there is no intrinsic rhythm, response to magnet
application will differentiate between oversensing and mechanical failure (Figure 9). Ultimate evaluation of the pacemaker system should be performed by a dedicated programmer. The response of implantable cardioverter
defibrillators to magnet application is entirely different;
further discussion of this issue is beyond the scope of this
review.
PERIOPERATIVE MANAGEMENT
Perioperative management of patients in hospital settings
merits special mention. Commonly encountered interac-
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CONTEMPORARY PACEMAKERS
TABLE 9. Approach to Common Problems Related to Electromagnetic Interference
in Patients With Pacemakers
Problem
Solution
Cellular telephones
Keep telephone in contralateral pocket
Place telephone over contralateral ear when talking
Household appliances (eg, microwave oven,
television, stereo, toaster, electric blanket)
Dental office
Theft detection equipment at stores
Magnetic resonance imaging
Surgery (electrocautery)
Transcutaneous electrical nerve stimulation
Radiation therapy
Direct-current cardioversion
No specific concerns
No specific concerns
Do not loiter when passing through device
Absolute/relative contraindication except when special precautions are used
Program device to asynchronous mode
Alternative: place magnet over device during surgery
Place grounding pad away from the device
Monitor pulse pressure on telemetry
Check device after surgery
May need to program pacemaker in asynchronous mode in some patients
Discuss with radiotherapist
May need to move device in pacemaker-dependent patients
Place pads in anteroposterior position, at least 5 cm from the pulse generator
Have programmer present
Check device for increased pacing thresholds after cardioversion
tions are related to electromagnetic interference or interference with rate-response sensors. Unless special steps are
taken, electromagnetic interference during electrocautery
may result in temporary or (rarely) permanent pacemaker
malfunction. Electromagnetic interference from electrocautery may cause oversensing in the ventricular channel
and inhibit pacing. It may also result in oversensing in the
atrial channel and cause accelerated ventricular pacing (if
pacemaker is programmed in tracking mode).
The clinician should take the following precautions in
the perioperative setting: (1) obtain pacemaker programming information from the clinic in advance; (2) identify
pacemaker-dependent patients and monitor them closely,
occasionally using invasive measures (magnet may be
placed over the device to inhibit sensing or the pacemaker
may be programmed to asynchronous mode before surgery); (3) ensure availability of temporary pacing support
in case of an emergency; (4) use low energy and short
bursts of electrocautery (preferably bipolar configuration);
(5) avoid electrocautery near the device and place grounding pads away from the device; (6) turn off program rate
modulation during surgery; and (7) interrogate and reprogram pacemaker after surgery.
CONCLUSION
Cardiac pacing remains an important tool in the treatment
of various cardiac conditions. The general practitioner
should understand the current indications, limitations, and
basic functions of pacemakers. Further technological advances and results of ongoing clinical trials will further our
understanding of cardiac pathophysiology and extend the
indications for evidence-based pacemaker therapy.
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The Symposium on Cardiovascular Diseases will continue in the November issue.
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