Executive Summary
I. Introduction
The publication of major studies dealing with the
natural history of bradyarrhythmias and
tachyarrhythmias and major advances in the technology
of pacemakers and implantable cardioverter-defibrillators (ICDs) has
mandated this revision of the 1991 ACC/AHA Guidelines for Implantation
of Pacemakers and Antiarrhythmia Devices.
This executive summary appears in the April 7, 1998 issue of
Circulation. The full text of the guidelines, including the
ACC/AHA Class I, II, and III recommendations, is published in the April
1998 issue of the Journal of the American College of
Cardiology. Reprints of both the executive summary
and the full text are available from both organizations.
Following extensive review of the medical literature and related
documents previously published by the American College of
Cardiology, the American Heart Association, and the
North American Society for Pacing and Electrophysiology, the writing
committee developed recommendations that are evidence based whenever
possible.
Evidence supporting current recommendations is ranked as level A if the
data were derived from multiple randomized clinical trials
involving a large number of individuals. Evidence was ranked as level B
when data were derived from a limited number of trials involving
comparatively small numbers of patients or from well-designed data
analysis of nonrandomized studies or
observational data registries. Evidence was ranked as level
C when consensus of expert opinion was the primary source of
recommendation. The committee emphasizes that for certain conditions
for which no other therapies are available, the indications for device
therapies are based on years of clinical experience as well as expert
consensus and are thus well supported, even though the evidence was
ranked as level C.
These guidelines include expanded sections on selection of pacemakers
and ICDs, optimization of technology, cost, and follow-up of implanted
devices. The follow-up sections are relatively brief because in many
instances the type and frequency of follow-up examinations are device
specific. The importance of adequate follow-up, however, cannot be
overemphasized because optimal results from an implantable device can
be obtained only if the device is adjusted to changing clinical
conditions.
The text accompanying the list of indications should be read carefully
because it includes the rationale and supporting evidence for many
indications and in several instances includes a discussion of
alternative acceptable therapies. Terms such as "potentially
reversible," "persistent," "transient," and "not expected
to resolve" are frequently used. These terms are not specifically
defined because the time element varies in different clinical settings.
The treating physician must use appropriate clinical judgment and
available data in deciding whether a condition is persistent or when it
can be expected to be transient. The statement "incidental finding at
electrophysiological study" is used
several times in this document and does not imply such a study is
indicated. Appropriate indications for
electrophysiological studies have been
previously published.
The term "symptomatic bradycardia" is used frequently
throughout the guidelines and is defined as a documented
bradyarrhythmia that is directly responsible for the
development of frank syncope or near-syncope, transient dizziness or
light-headedness, and confusional states resulting from cerebral
hypoperfusion attributable to slow heart rate. Fatigue, exercise
intolerance, and frank congestive heart failure may also result from
bradycardia. These symptoms may occur at rest or with exertion.
Definite correlation of symptoms with a bradyarrhythmia is a
requirement to fulfill the criteria of symptomatic
bradycardia. Caution should be exercised not to confuse
physiological sinus bradycardia (as occurs in
highly trained athletes) with pathological
bradyarrhythmias.
The section on indications for ICDs has been extensively revised and
enlarged to reflect emerging developments in this field and the
voluminous literature attesting to the efficacy of these devices in the
treatment of sudden cardiac death and malignant ventricular
arrhythmias. Indications for ICDs are constantly changing and
can be expected to change further as ongoing large-scale trials are
reported. In these guidelines the term "mortality" is used to
indicate "all-cause" mortality unless otherwise specified. The
committee elected to use "all-cause" mortality because of the
variable definition of "sudden death" and the developing
consensus to use "all-cause" mortality as the most appropriate end
point of clinical trials.
The final recommendations for indications for device therapy are
expressed in the standard ACC/AHA format:
Class I: Conditions for which there is evidence and/or general
agreement that a given procedure or treatment is beneficial, useful,
and effective.
Class II: Conditions for which there is conflicting evidence
and/or a divergence of opinion about the usefulness/efficacy of
a procedure or treatment.
Class IIa: Weight of evidence/opinion is in favor of
usefulness/efficacy.
Class IIb: Usefulness/efficacy is less well established by
evidence/opinion.
Class III: Conditions for which there is evidence and/or general
agreement that a procedure/treatment is not useful/effective and in
some cases may be harmful.
II. Indications for Permanent Pacing
A. Pacing for Acquired Atrioventricular Block
in Adults
Nonrandomized studies strongly suggest that permanent pacing
improves survival in patients with third-degree AV block, particularly
if syncope has occurred. It is now recognized that marked first-degree
AV block can lead to symptoms even in the absence of higher degrees of
AV conduction disturbance and may be associated with a
"pseudopacemaker syndrome" because of close proximity of atrial
systole to the preceding ventricular systole. Small
uncontrolled trials have suggested some
symptomatic and functional improvement with pacing in
patients with PR intervals >0.30 second, especially those with left
ventricular (LV) dysfunction, some of whom may benefit from
dual-chamber pacing with short AV delay.
Type I second-degree AV block is unlikely to progress to advanced AV
block when the delay is within the AV node. Consequently, pacing is not
usually indicated in this situation. However, in patients with type II
second-degree AV block (either intra- or infra-His), symptoms are
frequent, prognosis is compromised, and progression to third-degree AV
block is common.
Physiological AV block in the presence of
supraventricular tachyarrhythmias is not an
indication for pacemaker implantation except as specifically defined in
the recommendations below. Similarly, neurally mediated mechanisms in
young patients with AV block should be assessed before proceeding with
permanent pacing. Finally, permanent pacing for AV block after valve
surgery follows a variable natural history; therefore, the decision
for permanent pacing is at the physician's discretion.
Indications for Permanent Pacing in Acquired
Atrioventricular Block in Adults
Class I
Class IIa
Class IIb
Class III
B. Pacing for Chronic Bifascicular and Trifascicular Block
The PR and HV intervals have been identified as possible predictors of
third-degree AV block and sudden death in the presence of underlying
bifascicular block. However, the prolongation is often at the level of
the AV node, and frequently there is no correlation between the PR and
HV intervals and progression to third-degree AV block and incidence of
sudden cardiac death. Some investigators have suggested that
asymptomatic patients with bifascicular block and a
prolonged HV interval (
Indications for Permanent Pacing in Chronic Bifascicular and
Trifascicular Block
Class I
Class IIa
Class IIb
Class III
C. Pacing for Atrioventricular Block Associated
With Acute Myocardial Infarction
The decision to implant a permanent pacemaker for AV or
intraventricular conduction block complicating AMI
will depend on the type of conduction disturbance, location of
the infarction, and relation of the electrical disturbance to
infarct time. Thrombolytic therapy has decreased the
incidence of high-grade AV block in AMI, but mortality remains high in
this group of patients.
The impact of preexisting bundle branch block on mortality after AMI is
uncertain. However, left bundle branch block combined with advanced or
third-degree AV block and right bundle branch block combined with left
anterior or left posterior fascicular block carry a particularly
ominous prognosis.
Indications for Permanent Pacing After the Acute Phase of
Myocardial Infarction4
Class I
Class IIa
Class IIb
Class III
D. Pacing in Sinus Node Dysfunction
Trained athletes may have a physiological sinus
bradycardia of 40 to 50 bpm while awake and at rest and a sleeping
heart rate as low as 30 bpm with sinus pauses producing
asystolic intervals as long as 2.8 seconds. These findings are
due to increased vagal tone and are not an indication for permanent
pacing.
Permanent pacing in patients with sinus node dysfunction will
frequently relieve symptoms but may not necessarily result in improved
survival. Whether dual-chamber pacing improves survival compared with
ventricular pacing remains controversial. Multiple
prospective trials are ongoing to assess the superiority of
dual-chamber versus ventricular-based pacing systems in
patients with sinus node dysfunction.
Indications for Permanent Pacing in Sinus Node
Dysfunction
Class I
Class IIa
Class IIb
Class III
E. Prevention and Termination of Tachyarrhythmias
by Pacing
Indications for Permanent Pacemakers That Automatically Detect and
Pace to Terminate Tachycardias
Class I
Class IIa
Class IIb
Class III
Pacing Indications to Prevent Tachycardia
Class I
Class IIa
Class IIb
Class III
F. Pacing in Hypersensitive Carotid Sinus and Neurally
Mediated Syndromes
Ten to forty percent of syncopal episodes are due to a variety of
neurally mediated syndromes, the most common being vasovagal syncope.
Considerable controversy exists concerning the role of permanent pacing
in refractory neurally mediated syncope associated with significant
bradycardia or asystole because approximately 25% of patients have a
predominant vasodepressor reaction without significant bradycardia.
There is conflicting evidence in the literature regarding the efficacy
of permanent pacing in neurally mediated syncope, although a recent
randomized trial in highly symptomatic patients with
bradycardia demonstrated that permanent pacing increased the time to
the first syncopal event.
Indications for Permanent Pacing in Hypersensitive Carotid Sinus
Syndrome and Neurally Mediated Syncope
Class I
Class IIa
Class IIb
Class III
G. Pacing in Children and Adolescents
Symptomatic bradycardia is an indication for pacemaker
implantation, provided other causes of symptoms have been excluded. The
bradycardia-tachycardia syndrome is an increasingly
frequent problem in young patients after surgery for congenital heart
disease. Recurrent or chronic atrial flutter is responsible for
substantial morbidity and mortality in young patients, and long-term
atrial pacing at physiological rates and atrial
antitachycardia pacing have been used in this setting.
However, the results of permanent pacing to date have been equivocal
and the source of considerable controversy.
The indications for permanent pacing in congenital third-degree AV
block have evolved with some studies suggesting improved long-term
survival and prevention of syncopal episodes in
asymptomatic patients with congenital complete heart block
who meet specific criteria. High-grade second- or third-degree AV block
persisting for 7 to 14 days after cardiac surgery is an indication for
permanent pacing. The need for permanent pacing in patients with
transient postoperative AV block and residual bifascicular block has
not been established, whereas patients with AV conduction that returns
to normal have a favorable prognosis.
Indications for Permanent Pacing in Children and
Adolescents
Class I
Class IIa
Class IIb
Class III
H. Pacing in Specific Conditions
Pacing Indications for Hypertrophic
Cardiomyopathy
Class I
Class IIa
Class IIb
Class III
Several nonrandomized trials of patients with
symptomatic dilated cardiomyopathy
refractory to medical therapy have reported limited improvement of
symptoms with dual-chamber pacing with a short AV delay. However, at
this time no long-term data are available, and there is no consensus of
opinion for this indication. It has been hypothesized that a well-timed
atrial contraction primes the ventricles and decreases mitral
regurgitation, thus augmenting stroke volume and
arterial pressure. However, one randomized
controlled trial showed no significant benefit of DDD pacing
through a range of PR intervals despite the presence of both tricuspid
and mitral regurgitation. Preliminary data suggest that
simultaneous biventricular pacing may improve
cardiac hemodynamics and lead to subjective and
objective symptom improvement. This technique must still be considered
investigational at this time.
Pacing Indications for Dilated
Cardiomyopathy
Class I
Class IIa
Class IIb
Class III
Bradyarrhythmias after cardiac transplantation are common,
occurring in 8% to 23% of patients with transplantation and are
usually associated with sinus node dysfunction. Although some
investigators have recommended more liberal use of cardiac pacing for
persistent postoperative bradycardia, approximately 50% of these
patients demonstrate significant improvement within 6 to 12 months
after transplantation, and therefore long-term pacing is often
unnecessary. However, patients with irreversible sinus node dysfunction
or AV block with previously stated Class I indications should have
permanent pacing.
Pacing Indications After Cardiac
Transplantation
Class I
Class IIa
Class IIb
Class III
I. Selection and Follow-up of Pacemaker Devices
It has been suggested that less sophisticated devices, eg,
single-chamber ventricular pacemakers or
non–rate-responsive pacemakers, should be considered for elderly
patients who require pacing. However, a large retrospective
analysis of elderly Medicare patients suggested that
dual-chamber pacing is associated with improved survival compared with
ventricular pacing even after correction for confounding
variables. On the basis of results of recently published
randomized and nonrandomized trials,
rate-responsive ventricular pacing and dual-chamber pacing
appear to offer benefits over fixed-rate ventricular pacing
with respect to quality of life in elderly patients. However, there may
be no benefit of dual-chamber pacing over rate-responsive
ventricular demand pacing.
The cost of a pacemaker increases with its degree of complexity and
sophistication. At this time little is known about the
cost-effectiveness of the additional features of the more complex
pacemakers. Several ongoing trials assessing the clinical benefits of
dual-chamber or rate-responsive pacing include economic
analysis to estimate the incremental cost-effectiveness of
these features. Optimal programming of output voltages, pulse widths,
and AV delays can markedly decrease battery drain and prolong generator
life. It has been shown that expert programming of pacemaker generators
may prolong their longevity by an average of 4.2 years compared with
nominal settings.
After implantation of a pacemaker, careful follow-up and continuity of
care are absolute requirements. Programming at implantation must be
reviewed before the patient is discharged and further refined at
subsequent follow-up visits as indicated by interrogation and testing.
Frequency of follow-up is dictated by multiple factors, including other
cardiovascular or medical problems managed by the
physician involved, the age of the pacemaker, and the results of
transtelephonic testing. Patients who are pacemaker dependent require
more frequent clinical evaluations than those who are not. Follow-up
evaluation usually includes assessment of battery status, pacing
threshold and pulse width, sensing function, and lead integrity. The
North American Society of Pacing and Electrophysiology and the Health
Care Financing Administration have published reports on antibradycardia
pacemaker follow-up and guidelines for monitoring of patients with
antibradycardia pacemakers, respectively.
III. Indications for Implantable Cardioverter-Defibrillator
Therapy
Three major therapeutic options are currently available to reduce
or prevent VT or ventricular fibrillation (VF) in patients
at risk for these arrhythmias: (1) antiarrhythmic drug therapy
selected by electrophysiological study or
ambulatory monitoring or prescribed empirically; (2) ablative
techniques used in cardiac surgery or percutaneously
with catheter techniques; and (3) implantation of an ICD. A combination
of ICD therapy with drugs or ablation is also frequently used. Both
early observational reports and more recent
prospective and sometimes randomized
single-center and multicenter trials with long-term outcome data
uniformly document sudden cardiac death recurrence rates of 1%
to 2% annually after device implantation compared with
recurrences of 15% to 25% without device therapy. Recent
studies have recorded major improvements in implantation risk,
system longevity, symptoms associated with arrhythmia
recurrences, quality of life, and diagnosis and management of
delivery of inappropriate device therapy. Furthermore, the ICD has
rapidly evolved from a short-lived nonprogrammable device requiring
thoracotomy for a lead insertion into a multiprogrammable
antiarrhythmia device inserted almost exclusively without
thoracotomy and now capable of treating bradycardia, VT, and VF.
ICDs have been extensively evaluated in prospective clinical
trials and clearly documented to revert sustained VTs, including pace
termination of sustained VT and shock reversion of VF. Early
retrospective reports documented significant improvements in
patient survival with the use of an ICD. However, these studies tended
to overestimate benefits by using device therapies
(antitachycardia pacing and shocks) as surrogate mortality
events. It has recently become apparent that delivery of device therapy
cannot be used as a surrogate mortality end point, because
arrhythmias other than VT/VF can activate the device,
and recurrent VT is not invariably fatal. Considerable controversy
exists about the appropriate end point for evaluation of ICD efficacy,
with many studies using sudden death. However, classification of the
cause of death is often difficult and imprecise; therefore, a consensus
has emerged that "all-cause" mortality is the appropriate primary
end point for judging ICD efficacy. Total mortality has varied
significantly between reports due to differences in disease status of
the population under study and LV function. Survival of ICD recipients
is greatly influenced by LV function. Patients with an LV ejection
fraction
A significant body of information is now available comparing the
efficacy of antiarrhythmic drug therapy and ICDs for the secondary
prevention of cardiac arrest and sustained VT. Evidence from both early
retrospective nonrandomized reports and more recent
prospective randomized studies comparing ICD therapy with
Class III antiarrhythmic drug therapy indicates a significant relative
risk reduction with ICD therapy at 1 and 3 years of follow-up. In a
recently reported large prospective trial, 98% of randomly
selected patients could be maintained on ICD therapy, with 25.4%
requiring the addition of drug therapy by 2 years. Therefore, the
addition of an antiarrhythmic drug for selected patients with ICDs may
improve their quality of life by reducing recurrence of
arrhythmias and the need for defibrillation.
Patients with coronary artery disease constitute the majority
of patients receiving devices in most reports. Device implantation is
widely accepted today as improving the outcome of these patients. It
has been reported that patients with impaired LV function may obtain
greater benefit with ICDs than with drug therapy. Optimal
anti-ischemic therapy including (when possible) a ß-blocker
should be used concomitantly with an ICD. In patients with marked
elevation of LV filling pressures, abbreviated defibrillation threshold
testing is desirable.
Patients with idiopathic dilated cardiomyopathy
have a high mortality rate within 2 years of diagnosis. Approximately
half die suddenly and unexpectedly, and it has been shown that the
combination of poor LV function and frequent episodes of nonsustained
VT is associated with an increased risk of sudden death. In a recently
published large prospective trial, patients with idiopathic
dilated cardiomyopathy constituted 10% of the
study group and showed similar survival benefits with ICD therapy
compared with empiric amiodarone therapy as the entire cohort.
Similarly, ICD therapy has been shown to confer a significant survival
benefit in selected patients with the long QT syndrome, hypertrophic
cardiomyopathy, arrhythmogenic right
ventricular dysplasia, idiopathic VF, and syncope with
inducible sustained VT.
Pediatric patients represent <1% of persons with ICDs.
Nevertheless, ICD therapy is an important treatment option for young
patients, given the problems of noncompliance and drug-induced side
effects with lifelong pharmacological treatment. Sudden cardiac death
is uncommon in childhood and is mainly associated with three forms of
heart disease: (1) congenital heart disease, (2)
cardiomyopathy, and (3) primary electrical disease.
It is noteworthy that a lower percentage of children who undergo
resuscitation survive to hospital discharge compared with adults.
Sudden death has been estimated to occur in 1.5% to 2.5% of pediatric
patients after repair of tetralogy of Fallot, and the risk is even
higher for patients with transposition of the great arteries and aortic
stenosis. Most cases are presumed to be due to a malignant
ventricular arrhythmia associated either with
ischemia, ventricular dysfunction, or rapid
ventricular response to atrial flutter. The risk of sudden
cardiac death may be greatest in young patients with diseases such as
hypertrophic cardiomyopathy or the long QT
syndrome. Family history of sudden cardiac death may be an important
indication for implantation of an ICD in a pediatric patient with these
conditions. Limited experience with ICDs in young patients with
hypertrophic cardiomyopathy after resuscitation has
been encouraging.
ICD therapy is also used in patients with coronary artery
disease for the "primary prevention" of sudden cardiac death:
nonsustained VT in patients with prior MI and LV dysfunction carries a
2-year mortality estimate of 30%. Approximately half of this mortality
is thought to be due to malignant ventricular
arrhythmias. In general, improved patient survival with
conventional antiarrhythmic drug therapy has not been shown in this
setting. Empiric amiodarone therapy has also shown
inconsistent survival benefit, although a recent
meta-analysis suggests that total mortality may be reduced when
amiodarone is compared with other medical therapies. A recent
prospective randomized trial has documented improved
survival of patients with inducible and nonsuppressible
ventricular tachyarrhythmias treated with
ICDs when compared with antiarrhythmic drug therapy, including
amiodarone. However, routine insertion of ICDs in patients
thought to be at high risk of sudden death who are undergoing
aortocoronary bypass graft surgery has not improved
survival.
ICDs are not recommended for a number of patients, including those with
ventricular tachyarrhythmias in evolving
AMI or with electrolyte abnormalities, those without inducible or
spontaneous VT undergoing coronary bypass surgery, and those
with preexcitation syndrome presenting with VF as a result of
atrial fibrillation. Similarly, patients with terminal illnesses or
drug-refractory NYHA Class IV congestive heart failure who are not
candidates for cardiac transplantation are likely to obtain limited
benefit from ICD therapy. A history of psychiatric disorders, including
severe depression and substance abuse, that interfere with the
meticulous care and follow-up needed is also a relative
contraindication to device therapy.
In appropriately selected patients, ICDs have been found to be
cost-effective and comparable to other widely accepted noncardiac
therapies such as hemodialysis. A preliminary analysis of a
recent randomized clinical trial indicates that in this group of
patients, ICDs had a cost-effectiveness ratio of $27,000 per life-year
gained.
Indications for ICD Therapy
Class I
Class IIa
Class IIb
Class III
Footnotes
"ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary" was approved by the Board of Directors of the American College of Cardiology in October 1997 and the American Heart Association Science Advisory and Coordinating Committee in January 1998.
1 Representative of the American College of Physicians.
2 Representative of the Society of Thoracic Surgeons.
3 Representative of the North American Society of Pacing and Electrophysiology.
When citing this document, the ACC and the AHA request that the following format be used: Gregoratos G, Cheitlin MD, Conill A, Epstein AE, Fellows C, Ferguson TB Jr, Freedman RA, Hlatky MA, Naccarelli GV, Saksena S, Schlant RC, Silka MJ. ACC/AHA guidelines for implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998;31:1175–1206.
A single reprint of this document (executive summary) is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0136. To obtain a reprint of the full text of the guidelines published in the April issue of the Journal of the American College of Cardiology, ask for reprint No. 71-0137. To purchase additional reprints, specify version reprint number: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or . To make photocopies for personal or educational use, call the Copyright Clearance Center, 508-750-8400.
4 These recommendations generally follow the ACC/AHA Guidelines for the Management of Patients with Acute Myocardial Infarction.
© 1998 American Heart Association, Inc.
ACC/AHA Practice Guidelines
ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary
A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation)
Key Words: AHA Medical/Scientific Statements • pacemakers • pacing • arrhythmia
Patients with abnormalities of atrioventricular
(AV) conduction may be asymptomatic or may experience
serious symptoms related to bradycardia, ventricular
arrhythmias, or both. Decisions about the need for a pacemaker
are necessarily influenced by the presence or absence of symptoms that
are directly attributable to bradycardia.
1. Third-degree AV block at any anatomic level associated with any
one of the following conditions:
a. Bradycardia with symptoms presumed to be due to AV block.
(Level of evidence: C)
b. Arrhythmias and other medical conditions that require
drugs that result in symptomatic bradycardia. (Level
of evidence: C)
c. Documented periods of asystole 
3.0 seconds or any escape
rate <40 beats per minute (bpm) in awake, symptom-free patients.
(Level of evidence: B, C)
d. After catheter ablation of the AV junction. (Level of
evidence: B, C) There are no trials to assess outcome without
pacing, and pacing is virtually always planned in this situation unless
the operative procedure is AV junction modification.
e. Postoperative AV block that is not expected to resolve.
(Level of evidence: C)
f. Neuromuscular diseases with AV block such as myotonic muscular
dystrophy, Kearns-Sayre syndrome, Erb's dystrophy (limb-girdle), and
peroneal muscular atrophy. (Level of evidence: B)
2. Second-degree AV block regardless of type or site of block,
with associated symptomatic bradycardia. (Level of
evidence: B)
1. Asymptomatic third-degree AV block at any anatomic
site with average awake ventricular rates of 40 bpm or
faster. (Level of evidence: B, C)
2. Asymptomatic type II second-degree AV block.
(Level of evidence: B)
3. Asymptomatic type I second-degree AV block at
intra- or infra-His levels found incidentally at
electrophysiological study for other
indications. (Level of evidence: B)
4. First-degree AV block with symptoms suggestive of pacemaker
syndrome and documented alleviation of symptoms with temporary AV
pacing. (Level of evidence: B)
1. Marked first-degree AV block (>0.30 second) in patients with LV
dysfunction and symptoms of congestive heart failure in whom a shorter
AV interval results in hemodynamic improvement,
presumably by decreasing left atrial filling pressure. (Level of
evidence: C)
1. Asymptomatic first-degree AV block. (Level of
evidence: B) (See "Pacing for Chronic Bifascicular and
Trifascicular Block.")
2. Asymptomatic type I second-degree AV block at the
supra-His (AV node) level or not known to be intra- or infra-Hisian.
(Level of evidence: B, C)
3. AV block expected to resolve and unlikely to recur (eg, drug
toxicity, Lyme disease). (Level of evidence: B)
Symptomatic advanced AV block that develops in
patients with underlying bifascicular and trifascicular block is
associated with a high mortality rate and a significant incidence of
sudden death. However, there is considerable evidence that the rate of
progression of bifascicular block to third-degree AV block is slow.
Syncope is common in patients with bifascicular block, and there is
evidence that syncope in this setting is associated with an increased
incidence of sudden cardiac death. Therefore, if the cause of syncope
in the presence of bifascicular or trifascicular block cannot be
determined with certainty, prophylactic permanent pacing is
indicated. 100 milliseconds) should be considered for
permanent pacing. However, the incidence of progression to third-degree
AV block is low, even in the setting of prolonged HV interval. Death is
often not sudden or due to advanced AV block but rather due to the
underlying heart disease itself and nonarrhythmic cardiac
causes.
1. Intermittent third-degree AV block. (Level of
evidence: B)
2. Type II second-degree AV block. (Level of evidence: B)
1. Syncope not proved to be due to AV block when other likely causes
have been excluded, specifically ventricular
tachycardia (VT). (Level of evidence: B)
2. Incidental finding at
electrophysiological study of markedly
prolonged HV interval (100 milliseconds) in asymptomatic
patients. (Level of evidence: B)
3. Incidental finding at
electrophysiological study of
pacing-induced infra-His block that is not
physiological. (Level of evidence: B)
None.
1. Fascicular block without AV block or symptoms. (Level of
evidence: B)
2. Fascicular block with first-degree AV block without symptoms.
(Level of evidence: B)
The long-term prognosis of survivors of acute myocardial
infarction (AMI) who develop AV block is related primarily to the
extent of myocardial damage and the character of
intraventricular conduction disturbances
rather than the AV block itself. Indications for permanent pacing in
this setting do not necessarily depend on the presence of symptoms.
Patients with AMI who develop intraventricular
conduction defects (with the exception of isolated left anterior
fascicular block) have an unfavorable short- and long-term prognosis
and an increased incidence of sudden death.
1. Persistent second-degree AV block in the His-Purkinje system with
bilateral bundle branch block or third-degree AV block within or below
the His-Purkinje system after AMI. (Level of evidence: B)
2. Transient advanced (second- or third-degree) infranodal AV block
and associated bundle branch block. If the site of block is uncertain,
an electrophysiological study may be
necessary. (Level of evidence: B)
3. Persistent and symptomatic second- or third-degree AV
block. (Level of evidence: C)
None.
1. Persistent second- or third-degree AV block at the AV node level.
(Level of evidence: B)
1. Transient AV block in the absence of
intraventricular conduction defects. (Level
of evidence: B)
2. Transient AV block in the presence of isolated left anterior
fascicular block. (Level of evidence: B)
3. Acquired left anterior fascicular block in the absence of AV
block. (Level of evidence: B)
4. Persistent first-degree AV block in the presence of bundle branch
block that is old or age indeterminate. (Level of evidence:
B)
Correlation of symptoms with arrhythmias resulting from
sinus node dysfunction (eg, sinus bradycardia, sinus arrest, paroxysmal
supraventricular tachycardia alternating with
periods of bradycardia or even asystole) is essential in deciding
whether a permanent pacemaker is indicated. This correlation may be
difficult because of the intermittent nature of the episodes. Sinus
node dysfunction may also express itself as chronotropic incompetence.
Rate-responsive pacemakers have clinically benefited patients by
restoring physiological heart rate during physical
activity in this setting.
1. Sinus node dysfunction with documented
symptomatic bradycardia, including frequent sinus pauses
that produce symptoms. In some patients, bradycardia is iatrogenic and
will occur as a consequence of essential long-term drug therapy of a
type and dose for which there are no acceptable alternatives.
(Level of evidence: C)
2. Symptomatic chronotropic incompetence. (Level
of evidence: C)
1. Sinus node dysfunction occurring spontaneously or as a result of
necessary drug therapy with heart rate <40 bpm when a clear
association between significant symptoms consistent with
bradycardia and the actual presence of bradycardia has not been
documented. (Level of evidence: C)
1. In minimally symptomatic patients, chronic heart rate
<30 bpm while awake. (Level of evidence: C)
1. Sinus node dysfunction in asymptomatic patients,
including those in whom substantial sinus bradycardia (heart rate <40
bpm) is a consequence of long-term drug treatment.
2. Sinus node dysfunction in patients with symptoms suggestive of
bradycardia that are clearly documented as not associated with a slow
heart rate.
3. Sinus node dysfunction with symptomatic bradycardia
due to nonessential drug therapy.
Pacing can be useful in terminating a variety of
tachyarrhythmias, including atrial flutter, paroxysmal
reentrant supraventricular tachycardia, and VT.
A variety of pacing patterns have been used, including programmed
stimulation and short bursts of rapid pacing.
Antitachyarrhythmia devices may detect the
tachycardia and automatically activate a pacing
sequence or may respond to an external instruction (eg, application of
a magnet). Similarly, prevention of tachyarrhythmias by
pacing has been demonstrated in several situations (eg, patients with
the long QT syndrome and recurrent pause-dependent VT). Combined
therapy of pacing and ß-blockade has been reported to shorten the QT
interval and help prevent sudden cardiac death. Atrial synchronous
ventricular pacing may prevent recurrences of
reentrant supraventricular tachycardia, but
this technique is rarely used today, given the availability of catheter
ablation and other alternative therapies. In some patients with
bradycardia-dependent atrial fibrillation, atrial pacing may also be
effective in reducing the frequency of recurrence. Dual-site
and biatrial pacing are actively being investigated as therapies for
symptomatic drug-refractory atrial fibrillation with
concomitant bradyarrhythmias.
1. Symptomatic recurrent supraventricular
tachycardia that is reproducibly terminated by pacing after
drugs and catheter ablation fail to control the arrhythmia or
produce intolerable side effects. (Level of evidence: C)
2. Symptomatic recurrent sustained VT as part of an
automatic defibrillator system. (Level of evidence: B)
None.
1. Recurrent supraventricular tachycardia or
atrial flutter that is reproducibly terminated by pacing as an
alternative to drug therapy or ablation. (Level of evidence:
C)
1. Tachycardias frequently accelerated or converted to
fibrillation by pacing.
2. The presence of accessory pathways with the capacity for rapid
anterograde conduction whether or not the pathways participate
in the mechanism of the tachycardia.
1. Sustained pause-dependent VT, with or without prolonged QT, in
which the efficacy of pacing is thoroughly documented. (Level of
evidence: C)
1. High-risk patients with congenital long QT syndrome. (Level
of evidence: C)
1. AV reentrant or AV node reentrant supraventricular
tachycardia not responsive to medical or ablative therapy.
(Level of evidence: C)
2. Prevention of symptomatic, drug-refractory, recurrent
atrial fibrillation. (Level of evidence:
C)
1. Frequent or complex ventricular ectopic activity
without sustained VT in the absence of the long QT
syndrome.
2. Long QT syndrome due to reversible causes.
Hypersensitive carotid sinus syndrome is an uncommon cause
of syncope or presyncope. Symptoms in this setting are mediated through
both cardioinhibitory and vasodepressor reflexes. It is
necessary to ascertain the relative contribution of these two
components of carotid sinus stimulation before concluding that
permanent pacing is clinically indicated. Patients with symptoms due
entirely to the cardioinhibitory response of carotid sinus
stimulation can be effectively treated with permanent pacing. However,
because 10% to 20% of patients also have an important vasodepressor
component in their reflex response, this component must be addressed as
well.
1. Recurrent syncope caused by carotid sinus stimulation; minimal
carotid sinus pressure induces ventricular asystole of >3
seconds' duration in the absence of any medication that depresses the
sinus node or AV conduction. (Level of evidence:
C)
1. Recurrent syncope without clear, provocative events
and with a hypersensitive cardioinhibitory response.
(Level of evidence: C)
2. Syncope of unexplained origin when major abnormalities of sinus
node function or AV conduction are discovered or provoked in
electrophysiological studies. (Level
of evidence: C)
1. Neurally mediated syncope with significant bradycardia reproduced
by a head-up tilt with or without isoproterenol or other
provocative maneuvers. (Level of evidence: B)
1. A hyperactive cardioinhibitory response to carotid
sinus stimulation in the absence of symptoms.
2. A hyperactive cardioinhibitory response to carotid
sinus stimulation in the presence of vague symptoms such as dizziness,
light-headedness, or both.
3. Recurrent syncope, light-headedness, or dizziness in the absence
of a hyperactive cardioinhibitory response.
4. Situational vasovagal syncope in which avoidance behavior is
effective.
Permanent pacing in children or adolescents is generally indicated
in (1) symptomatic sinus bradycardia, (2) recurrent
bradycardia-tachycardia syndromes, (3) congenital AV block,
and (4) advanced second- or third-degree surgically induced or acquired
AV block. Important differences between indications for permanent
pacing in children and adults include (1) age dependency of
physiological heart rate and (2) impact of residual
ventricular dysfunction and abnormal circulatory physiology
after surgical palliation of complex congenital cardiac defects.
1. Advanced second- or third-degree AV block associated with
symptomatic bradycardia, congestive heart failure, or low
cardiac output. (Level of evidence: C)
2. Sinus node dysfunction with correlation of symptoms during
age-inappropriate bradycardia. The definition of bradycardia varies
with the patient's age and expected heart rate. (Level of
evidence: B)
3. Postoperative advanced second- or third-degree AV block that is
not expected to resolve or persists at least 7 days after cardiac
surgery. (Level of evidence: B, C)
4. Congenital third-degree AV block with a wide QRS escape
rhythm or ventricular dysfunction. (Level of
evidence: B)
5. Congenital third-degree AV block in the infant with a
ventricular rate <50 to 55 bpm or with congenital heart
disease and a ventricular rate <70 bpm. (Level of
evidence: B, C)
6. Sustained pause-dependent VT, with or without prolonged QT, in
which the efficacy of pacing is thoroughly documented. (Level of
evidence: B)
1. Bradycardia-tachycardia syndrome with the need for
long-term antiarrhythmic treatment other than digitalis. (Level
of evidence: C)
2. Congenital third-degree AV block beyond the first year of life
with an average heart rate <50 bpm or abrupt pauses in
ventricular rate that are two or three times the basic
cycle length. (Level of evidence: B)
3. Long QT syndrome with 2:1 AV or third-degree AV block.
(Level of evidence: B)
4. Asymptomatic sinus bradycardia in the child with
complex congenital heart disease with resting heart rate <35 bpm or
pauses in ventricular rate >3 seconds. (Level of
evidence: C)
1. Transient postoperative third-degree AV block that reverts to
sinus rhythm with residual bifascicular block. (Level of
evidence: C)
2. Congenital third-degree AV block in the asymptomatic
neonate, child, or adolescent with an acceptable rate, narrow QRS
complex, and normal ventricular function. (Level of
evidence: B)
3. Asymptomatic sinus bradycardia in the adolescent with
congenital heart disease with resting heart rate <35 bpm or pauses in
ventricular rate >3 seconds. (Level of evidence:
C)
1. Transient postoperative AV block with return of normal AV
conduction within 7 days. (Level of evidence: B)
2. Asymptomatic postoperative bifascicular block with or
without first-degree AV block. (Level of evidence:
C)
3. Asymptomatic type I second-degree AV block.
(Level of evidence: C)
4. Asymptomatic sinus bradycardia in the adolescent when
the longest RR interval is <3 seconds and the minimum heart rate is
>40 bpm. (Level of evidence: C)
In patients with severely symptomatic hypertrophic
cardiomyopathy, early nonrandomized
studies demonstrated that implantation of a dual-chamber pacemaker with
a short AV delay decreased the magnitude of LV outflow obstruction and
improved symptoms. However, recent observational studies
suggest that a decrease in LV outflow gradient produced by a temporary
dual chamber may adversely affect ventricular filling and
cardiac output. Recent randomized trials have yielded
variable results: one study demonstrated that DDD pacing reduced
outflow tract gradient and improved New York Heart Association (NYHA)
functional class, whereas another randomized double-blind
study demonstrated no significant subjective or exercise capacity
improvement in the paced versus nonpaced patient group at 2 to 3 months
of follow-up, despite a significant decrease in LV outflow gradient. As
a result, pacing indications for hypertrophic
cardiomyopathy remain controversial.
Class I indications for sinus node dysfunction or AV block
as previously described. (Level of evidence:
C)
None.
1. Medically refractory, symptomatic hypertrophic
cardiomyopathy with significant resting or provoked
LV outflow obstruction. (Level of evidence:
C)
1. Patients who are asymptomatic or medically
controlled.
2. Symptomatic patients without evidence of LV outflow
obstruction.
Class I indications for sinus node dysfunction or AV block
as previously described. (Level of evidence:
C)
None.
1. Symptomatic, drug-refractory dilated
cardiomyopathy with prolonged PR interval when
acute hemodynamic studies have demonstrated
hemodynamic benefit of pacing. (Level of
evidence: C)
1. Asymptomatic dilated
cardiomyopathy.
2. Symptomatic dilated
cardiomyopathy when patients are rendered
asymptomatic by drug therapy.
3. Symptomatic ischemic
cardiomyopathy.
1. Symptomatic
bradyarrhythmias/chronotropic incompetence not expected to
resolve and other Class I indications for permanent pacing.
(Level of evidence: C)
None.
1. Symptomatic bradyarrhythmias/chronotropic
incompetence that, although transient, may persist for months and
require intervention. (Level of evidence:
C)
1. Asymptomatic bradyarrhythmias after cardiac
transplantation.
Once a decision has been reached to implant a pacemaker, the
clinician may choose from a large number of pacemaker generators and
leads. Generator choices include single- versus dual-chamber devices,
unipolar versus bipolar configuration, presence of rate responsiveness
and type of sensor used, advanced features such as automatic mode
switching, generator size, battery capacity, and cost. Lead choices
include polarity, type of insulation material, active versus passive
fixation mechanism, presence of steroid elution, and typical pacing
impedance. Other factors that frequently influence the choice of a
pacemaker system include the capabilities of the pacemaker programmer
and local availability of technical support. Current single-chamber
pacemakers incorporate a number of programming features such as pacing
mode, lower rate, pulse width and amplitude, sensitivity, and
refractory period. Additional features of current dual-chamber
pacemakers include maximum tracking rate and AV delays. Rate-responsive
pacemakers require programmable features to regulate the relation
between sensor output and pacing rate and to limit the maximum
sensor-driven pacing rate. These programmable parameters
must be individualized for each patient. Many of these considerations
are beyond the scope of this document. The
Table
presents brief guidelines for
selecting the appropriate pacemaker for the most commonly encountered
indications for pacing. Fig 1 depicts a
decision tree for selecting a pacing system for a patient with AV
block. Fig 2 depicts a decision tree for
selecting a pacing system for a patient with sinus node
dysfunction.
View this table:
[in a new window]
Table 1. Guidelines for Choice of Pacemaker Generator in Selected
Indications for Pacing
View larger version (24K):
[in a new window]
Figure 1. Selection of pacemaker systems for patients with
atrioventricular block. AV indicates
atrioventricular.
View larger version (17K):
[in a new window]
Figure 2. Selection of pacemaker systems for patients with
sinus node dysfunction. AV indicates
atrioventricular. 
30% have reduced survival rates compared with those with
higher ejection fractions. However, both populations appear to derive a
significant survival benefit from ICD implantation.
1. Cardiac arrest due to VF or VT not due to a transient or
reversible cause. (Level of evidence: A)
2. Spontaneous sustained VT. (Level of evidence:
B)
3. Syncope of undetermined origin with clinically relevant,
hemodynamically significant sustained VT or VF induced
at electrophysiological study when drug
therapy is ineffective, not tolerated, or not preferred. (Level
of evidence: B)
4. Nonsustained VT with coronary disease, prior MI, LV
dysfunction, and inducible VF or sustained VT at
electrophysiological study that is not
suppressible by a Class I antiarrhythmic drug. (Level of
evidence: B)
None.
1. Cardiac arrest presumed to be due to VF when
electrophysiological testing is precluded
by other medical conditions. (Level of evidence:
C)
2. Severe symptoms attributable to sustained ventricular
tachyarrhythmias while awaiting cardiac
transplantation. (Level of evidence: C)
3. Familial or inherited conditions with a high risk for
life-threatening ventricular
tachyarrhythmias such as long QT syndrome or
hypertrophic cardiomyopathy. (Level of
evidence: B)
4. Nonsustained VT with coronary artery disease, prior
MI, and LV dysfunction, and inducible sustained VT or VF at
electrophysiological study. (Level of
evidence: B)
5. Recurrent syncope of undetermined etiology in the presence of
ventricular dysfunction and inducible
ventricular arrhythmias at
electrophysiological study when other
causes of syncope have been excluded. (Level of evidence: C)
1. Syncope of undetermined cause in a patient without inducible
ventricular tachyarrhythmias. (Level
of evidence: C)
2. Incessant VT or VF. (Level of evidence:
C)
3. VF or VT resulting from arrhythmias amenable to surgical
or catheter ablation; for example, atrial arrhythmias
associated with the Wolff-Parkinson-White syndrome, right
ventricular outflow tract VT, idiopathic left
ventricular tachycardia, or fascicular VT. (Level of
evidence: C)
4. Ventricular tachyarrhythmias due to a
transient or reversible disorder (eg, AMI, electrolyte imbalance,
drugs, trauma). (Level of evidence: C)
5. Significant psychiatric illnesses that may be aggravated by
device implantation or may preclude systematic follow-up. (Level
of evidence: C)
6. Terminal illnesses with projected life expectancy 6 months.
(Level of evidence: C)
7. Patients with coronary artery disease with LV
dysfunction and prolonged QRS duration in the absence of spontaneous or
inducible sustained or nonsustained VT who are undergoing
coronary bypass surgery. (Level of evidence:
B)
8. NYHA Class IV drug-refractory congestive heart failure in
patients who are not candidates for cardiac transplantation.
(Level of evidence: C)
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