American College of Cardiology

GREGORATOS ET AL., ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices
http://www.acc.org/clinical/guidelines/pacemaker/index.htm; 2002

ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices—Full Text

A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee on Implantation)

I. Indications for Permanent Pacing

A. Pacing for Acquired Atrioventricular Block in Adults

Atrioventricular (AV) block is classified as first-, second-, or third-degree (complete) block; anatomically, it is defined as supra-, intra-, or infra-His. First-degree AV block is defined as abnormal prolongation of the PR interval. Second-degree AV block is subclassified as type I and type II. Type I seconddegree AV block is characterized by progressive prolongation of the PR interval before a blocked beat and is usually associated with a narrow QRS complex. Type II second-degree AV block is characterized by fixed PR intervals before and after blocked beats and is usually associated with a wide QRS complex. When AV conduction occurs in a 2:1 pattern, block cannot be unequivocally classified as type I or type II, although the width of the QRS can be suggestive as just described. Advanced second-degree AV block refers to the block of two or more consecutive P waves but with some conducted beats, indicating some preservation of AV coneduction. Third-degree AV block (complete heart block) is defined as absence of AV conduction.

Patients with abnormalities of AV conduction may be asymptomatic or may experience serious symptoms related to bradycardia, ventricular arrhythmias, or both. Decisions regarding the need for a pacemaker are influenced importantly by the presence or absence of symptoms directly attributable to bradycardia. Furthermore, many of the indications for pacing have evolved over 40 years based on experience without the benefit of comparative randomized clinical trials, in part because no acceptable alternative options exist to treat most bradycardias.

Nonrandomized studies strongly suggest that permanent pacing does improve survival in patients with third-degree AV block, especially if syncope has occurred ^8-13. Although there is little evidence to suggest that pacemakers improve survival in patients with isolated first-degree AV block ¹⁴, it is now recognized that marked (PR more than 300 milliseconds) first-degree AV block can lead to symptoms even in the absence of higher degrees of AV block ¹⁵. Such marked first-degree AV block may follow catheter ablation of the fast AV nodal pathway with resultant slow pathway conduction. When marked first-degree AV block for any reason causes atrial systole in close proximity to the preceding ventricular systole and produces hemodynamic consequences usually associated with retrograde (ventriculoatrial) conduction, signs and symptoms similar to the pacemaker syndrome may occur ¹⁶. With marked first-degree AV block, atrial contraction occurs before complete atrial filling, ventricular filling is compromised, and an increase in pulmonary capillary wedge pressure and a decrease in cardiac output follow. Small, uncontrolled trials have suggested some symptomatic and functional improvement by pacing of patients with PR intervals more than 0.30 seconds by decreasing the time for AV conduction ¹⁵. Finally, a long PR interval may identify a subgroup of patients with left ventricular (LV) dysfunction, some of whom may benefit from dual-chamber pacing with a short(er) AV delay ¹⁷. These same principles also may be applied to patients with type I second-degree AV block who experience hemodynamic compromise due to loss of AV synchrony, even without bradycardia. Although echocardiographic or invasive techniques may be used to assess hemodynamic improvement before permanent pacemaker implantation, such studies are not required.

Type I second-degree AV block is usually due to delay in the AV node irrespective of QRS width. Because progression to advanced AV block in this situation is uncommon ^18-20, pacing is usually not indicated unless the patient is symptomatic. Nevertheless, controversy exists, and pacemaker implantation has been advocated for this finding ^21-23. On the other hand, type II second-degree AV block is usually infranodal (either intra- or infra-His), especially when the QRS is wide. In these patients, symptoms are frequent, prognosis is compromised, and progression to third-degree AV block is common ^1820,24. Thus, type II second-degree AV block and a wide QRS indicate diffuse conduction system disease and constitute an indication for pacing even in the absence of symptoms. However, it is not always possible to determine the site of AV block without electrophysiologic evaluation, because type I second- degree AV block can be infranodal even when the QRS is narrow ³⁴⁰. If type I second-degree AV block with a narrow or wide QRS is found to be intra- or infra-His at electrophysiologic study, pacing should be considered.

Because it may be difficult for both patients and their physicians to attribute ambiguous symptoms such as fatigue to bradycardia, special vigilance must be exercised to acknowledge the patient’s concerns that may be caused by a slow heart rate. Thus, in a patient with third-degree AV block, permanent pacing should be considered strongly even when the ventricular rate is more than 40 beats per minute (bpm), because the choice of a 40 bpm cutoff in these guidelines was not determined from clinical trial data. Indeed, it is not the escape rate that is necessarily critical for safety, but rather the site of origin of the escape rhythm (i.e., in the AV node, the His bundle, or infra-His).

AV block can sometimes be provoked by exercise. If not secondary to myocardial ischemia, AV block in this circumstance usually is due to disease in the His-Purkinje system and is associated with a poor prognosis. Thus, pacing is indicated ^343,344. Conversely, long sinus pauses and AV block can occur during sleep apnea. In the absence of symptoms, these abnormalities are reversible and do not require pacing ³⁴⁵. If symptoms are present, pacing is indicated as in other conditions.

Recommendations for permanent pacemaker implantation in patients with AV block in AMI, congenital AV block, and AV block associated with enhanced vagal tone are discussed in separate sections. Neurocardiogenic etiologies in young patients with AV block should be assessed before proceeding with permanent pacing. Physiologic AV block in the presence of supraventricular tachyarrhythmias does not constitute an indication for pacemaker implantation except as specifically defined in the recommendations that follow.

In general, the decision regarding implantation of a pacemaker must be considered with respect to whether or not AV block will be permanent. Reversible causes of AV block, such as electrolyte abnormalities, should be corrected first. Some diseases may follow a natural history to resolution (e.g., Lyme disease), and some AV block can be expected to reverse (e.g., hypervagotonia due to recognizable and avoidable physiologic factors, perioperative AV block due to hypothermia, or inflammation near the AV conduction system after surgery in this region).

Conversely, some conditions may warrant pacemaker implantation owing to the possibility of disease progression even if the AV block reverses transiently (e.g., sarcoidosis, amyloidosis, and neuromuscular diseases). Finally, permanent pacing for AV block after valve surgery follows a variable natural history, and therefore the decision for permanent pacing is at the physician’s discretion ³⁴⁶.

Recommendations for Permanent Pacing in Acquired Atrioventricular Block in Adults

Class I

1. Third-degree and advanced second-degree AV block at any anatomic level, associated with any one of the following conditions:
   1. Bradycardia with symptoms (including heart failure) presumed to be due to AV block. (Level of Evidence: C)
   2. Arrhythmias and other medical conditions that require drugs that result in symptomatic bradycardia. (Level of Evidence: C)
   3. Documented periods of asystole greater than or equal to 3.0 seconds ²⁵ or any escape rate less than 40 bpm in awake, symptom-free patients ^26,27. (Level of Evidence: B, C)
   4. 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 ^28,29.
   5. Postoperative AV block that is not expected to resolve after cardiac surgery. (Level of Evidence: C) ^30,30a,346
   6. Neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy, with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) ^31-37
2. Second-degree AV block regardless of type or site of block, with associated symptomatic bradycardia. (Level of Evidence: B) ¹⁹

Class IIa

1. Asymptomatic third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster, especially if cardiomegaly or LV dysfunction is present. (Level of Evidence: B, C)
2. Asymptomatic type II second-degree AV block with a narrow QRS. When type II second-degree AV block occurs with a wide QRS, pacing becomes a Class I recommendation (see next section regarding Pacing for Chronic Bifascicular and Trifascicular Block).
   (Level of Evidence: B) ^21,23
3. Asymptomatic type I second-degree AV block at intra- or infra-His levels found at electrophysiologic study performed for other indications. (Level of Evidence: B) ^19,21-23
4. First- or second-degree AV block with symptoms similar to those of pacemaker syndrome. (Level of Evidence: B) ^15,16

Class IIb

1. Marked first-degree AV block (more than 0.30 seconds) 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) ¹⁷
2. Neuromuscular diseases such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: B) ^31-37

Class III

1. Asymptomatic first-degree AV block. (Level of Evidence: B) ¹⁴ (See also “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) ¹⁹
3. AV block expected to resolve and/or unlikely to recur ³⁸ (e.g., drug toxicity, Lyme disease, or during hypoxia in sleep apnea syndrome in absence of symptoms). (Level of Evidence: B)

B. Pacing for Chronic Bifascicular and Trifascicular Block

Bifascicular block refers to electrocardiographic (ECG) evidence of impaired conduction below the AV node in two fascicles of the right and left bundles. Alternating bundle-branch block (also known as bilateral bundle-branch block) refers to situations in which clear ECG evidence for block in all three fascicles is seen on successive ECGs. Examples are right bundle-branch block and left bundle-branch block on successive ECGs, or right bundle-branch block with associated left anterior fascicular block on one ECG and associated left posterior fascicular block on another ECG. A strict definition of trifascicular block is block documented in all three fascicles whether simultaneously or at different times. Alternating bundlebranch block also fulfills this criterion. This term has also been used to describe first-degree AV block in association with bifascicular block. Patients with such ECG abnormalities and symptomatic, advanced AV block have a high mortality rate and a significant incidence of sudden death ^9,39. Although third-degree AV block is most often preceded by bifascicular block, there is evidence that the rate of progression of bifascicular block to third-degree AV block is slow ³⁴⁷. Furthermore, no single clinical or laboratory variable, including bifascicular block, identifies patients at high risk of death from a future bradyarrhythmia due to bundle-branch block ⁴⁸.

Syncope is common in patients with bifascicular block. Although syncope may be recurrent, it is not associated with an increased incidence of sudden death ^40-52. Although pacing relieves the transient neurological symptoms, it does not reduce the occurrence of sudden death ⁴⁶. Electrophysiologic study may be helpful to evaluate and direct the treatment of inducible ventricular arrhythmias ^53,54 that are common in patients with bifascicular and trifascicular block. There is convincing evidence that in the presence of permanent or transient third-degree AV block, syncope is associated with an increased incidence of sudden death regardless of the results of electrophysiologic study ^9,54,55. Finally, if the cause of syncope in the presence of bifascicular or trifascicular block cannot be determined with certainty or if treatments used (such as drugs) may exacerbate AV block, prophylactic permanent pacing is indicated, especially if syncope may have been due to transient thirddegree AV block ^40,52.

Of the many laboratory variables, the PR and HV intervals have been identified as possible predictors of third-degree AV block and sudden death. Although PR interval prolongation is common in patients with bifascicular block, the delay is often at the level of the AV node. There is no correlation between the PR and HV intervals or between the length of the PR interval, progression to third-degree AV block, and sudden death ^43,45,49. Although most patients with chronic or intermittent third-degree AV block demonstrate prolongation of the HV interval during anterograde conduction, some investigators ^50,51 have suggested that asymptomatic patients with bifascicular block and a prolonged HV interval should be considered for permanent pacing, especially if the HV interval is greater than or equal to 100 milliseconds ⁴⁹. The evidence indicates that although the prevalence of prolonged HV is high, the incidence of progression to third-degree AV block is low. Because HV prolongation accompanies advanced cardiac disease and is associated with increased mortality, death is often not sudden or due to AV block but rather due to the underlying heart disease itself and nonarrhythmic cardiac causes ^{43,46-49,51,54-56}.

Atrial pacing at electrophysiologic study in asymptomatic patients as a means of identifying patients at increased risk of future high- or third-degree AV block is controversial. The probability of inducing block distal to the AV node (i.e., intra- or infra-His) with rapid atrial pacing is low ^{47,50,51,57-60}. Failure to induce distal block cannot be taken as evidence that the patient will not develop third-degree AV block in the future. However, if atrial pacing induces nonphysiologic infra-His block, some consider this an indication for pacing ⁵⁷.

Recommendations for Permanent Pacing in Chronic Bifascicular and Trifascicular Block

Class I

1. Intermittent third-degree AV block. (Level of Evidence: B) ^8-13,39
2. Type II second-degree AV block. (Level of Evidence: B) ^18,20,24,348
3. Alternating bundle-branch block. (Level of Evidence: C) ³⁴⁹

Class IIa

1. Syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia (VT). (Level of Evidence: B) ^40-51,53-58
2. Incidental finding at electrophysiologic study of markedly prolonged HV interval (greater than or equal to 100 milliseconds) in asymptomatic patients. (Level of Evidence: B) ⁴⁹
3. Incidental finding at electrophysiologic study of pacing- induced infra-His block that is not physiologic. (Level of Evidence: B) ⁵⁷

Class IIb

Neuromuscular diseases such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy with any degree of fascicular block, with or without symptoms, because there may be unpredictable progression of AV conduction disease. (Level of Evidence: C) ^31-37

Class III

1. Fascicular block without AV block or symptoms. (Level of Evidence: B) ^43,45,48,49
2. Fascicular block with first-degree AV block without symptoms. (Level of Evidence: B) ^43,45,48,49

C. Pacing for Atrioventricular Block Associated With Acute Myocardial Infarction

Indications for permanent pacing after myocardial infarction (MI) in patients experiencing AV block are related in large measure to the presence of intraventricular conduction defects. Unlike some other indications for permanent pacing, the criteria for patients with MI and AV block do not necessarily depend on the presence of symptoms. Furthermore, the requirement for temporary pacing in AMI does not by itself constitute an indication for permanent pacing [see ACC/AHA Guidelines for Management of Patients With Acute Myocardial Infarction ³³⁵].

The long-term prognosis for survivors of AMI who have had AV block is related primarily to the extent of myocardial injury and the character of intraventricular conduction disturbancesdisturbances rather than the AV block itself ^11,61-64. Patients with AMI who have intraventricular conduction defects, with the exception of isolated left anterior fascicular block, have an unfavorable short- and long-term prognosis and an increased risk of sudden death ^11,24,61,63. This unfavorable prognosis is not necessarily due to development of highgrade AV block, although the incidence of such block is higher in postinfarction patients with abnormal intraventricular conduction ^61,65,350.

When AV or intraventricular conduction block complicates AMI, the type of conduction disturbance, location of infarction, and relation of electrical disturbance to infarction must be considered if permanent pacing is contemplated. Even with data available, the decision is not always straightforward, because the reported incidence and significance of various conduction disturbances vary widely ⁶⁶. Despite the use of thrombolytic therapy and primary angioplasty, which have decreased the incidence of AV block in AMI, mortality remains high if AV block occurs ^67-70.

Although more severe disturbances in conduction are in general associated with greater arrhythmic and nonarrhythmic mortality ^61-66>, the impact of pre-existing bundlebranch block on mortality after AMI is controversial ^52,66. A particularly ominous prognosis is associated with left bundle-branch block combined with advanced second- or thirddegree AV block and with right bundle-branch block combined with left anterior or left posterior fascicular block ^41,52,62,64. Irrespective of whether the infarction is anterior or inferior, the development of an intraventricular conduction delay reflects extensive myocardial damage rather than an electrical problem in isolation ⁶⁴. Although AV block that occurs during inferior MI can be associated with a favorable long-term clinical outcome, in-hospital survival is impaired, irrespective of temporary or permanent pacing in this situation ^67,68,71,72. Furthermore, pacemakers should not be implanted if the peri-infarctional AV block is expected to resolve or to not negatively impact long-term prognosis, as in the case of inferior MI ⁶⁹.

Recommendations for Permanent Pacing After the Acute Phase of Myocardial Infarction*

Class I

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) ^24,61-65
2. Transient advanced (second- or third-degree) infranodal AV block and associated bundle-branch block. If the site of block is uncertain, an electrophysiologic study may be necessary. (Level of Evidence: B) ^61,62
3. Persistent and symptomatic second- or third-degree AV block. (Level of Evidence: C)

Class IIb

Persistent second- or third-degree AV block at the AV node level. (Level of Evidence: B) ²³

Class III

1. Transient AV block in the absence of intraventricular conduction defects. (Level of Evidence: B) ⁶¹
2. Transient AV block in the presence of isolated left anterior fascicular block. (Level of Evidence: B) ⁶³
3. Acquired left anterior fascicular block in the absence of AV block. (Level of Evidence: B) ⁶¹
4. Persistent first-degree AV block in the presence of bundle-branch block that is old or age indeterminate. (Level of Evidence: B) ⁶¹*

*These recommendations generally follow the ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction ³³⁵.

D. Pacing in Sinus Node Dysfunction

Sinus node dysfunction (sick sinus syndrome) constitutes a spectrum of cardiac arrhythmias, including sinus bradycardia, sinus arrest, sinoatrial block, and paroxysmal supraventricular tachyarrhythmias alternating with periods of bradycardia or even asystole. Patients with this condition may be symptomatic from paroxysmal tachycardia or bradycardia or both. Correlation of symptoms with the above arrhythmias by use of an ECG, ambulatory ECG monitoring, or an event recorder is essential. This correlation may be difficult because of the intermittent nature of the episodes. In the electrophysiology laboratory, abnormal sinus node function may be confirmed by demonstration of prolonged corrected sinus node recovery times or prolonged sinoatrial conduction times. However, utility of electrophysiologic studies for sinus node dysfunction is limited by issues of sensitivity and specificity.

Sinus node dysfunction may express itself as chronotropic incompetence in which there is an inadequate sinus response to exercise or stress. Rate-responsive pacemakers have clinically benefited patients by restoring physiologic heart rate during physical activity ^73-75.

Sinus bradycardia is accepted as a physiologic finding in trained athletes, who not uncommonly have a heart rate of 40 to 50 bpm while at rest and awake and may have a sleeping rate as slow as 30 bpm, with sinus pauses or type I seconddegree AV block producing asystolic intervals as long as 2.8 seconds ^76-78. These findings are due to increased vagal tone.

Although sinus node dysfunction is frequently the primary indication for implantation of permanent pacemakers ⁷³, permanent pacing in patients with sinus node dysfunction may not necessarily result in improved survival time ^26,79, although symptoms related to bradycardia may be relieved ^27,80 (see Section I, Selection of Pacemaker Devices). During monitoring, pauses are sometimes observed during sleep. Duration of sinus pauses and their clinical significance is uncertain. If due to sleep apnea, apnea should be treated. A small retrospective trial of atrial overdrive pacing in the treatment of sleep apnea demonstrated a decrease “in episodes of central or obstructive sleep apnea without reducing the total sleep time” ⁴⁴⁷⁾. Although this initial trial is encouraging, it is premature to propose pacing guidelines until a larger body of data is available. Otherwise, there is not sufficient evidence to distinguish physiologic from pathologic nocturnal bradycardia.

Recommendations for Permanent Pacing in Sinus Node Dysfunction

Class I

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) ^27,73,79
2. Symptomatic chronotropic incompetence. (Level of Evidence: C) ^27,73-75,79

Class IIa

1. Sinus node dysfunction occurring spontaneously or as a result of necessary drug therapy, with heart rate less than 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) ^{26,27,73,78-80}
2. Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in electrophysiologic studies. (Level of Evidence: C) ^351,352

Class IIb

In minimally symptomatic patients, chronic heart rate less than 40 bpm while awake. (Level of Evidence: C) ^{26,27,73,78-80}

Class III

1. Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia (heart rate less than 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.

E. Prevention and Termination of Tachyarrhythmias by Pacing

Under certain circumstances, an implanted pacemaker may be useful for treating patients with recurrent symptomatic ventricular and supraventricular tachycardias ^85-94. Pacing can be useful in preventing and terminating arrhythmias. Reentrant rhythms including atrial flutter, paroxysmal reentrant supraventricular tachycardia, and VT may be terminated by a variety of pacing patterns, including programmed stimulation and short bursts of rapid pacing ^95,96. These antitachyarrhythmia devices may detect tachycardia and automatically activate a pacing sequence, or they may respond only to an external instruction (for example, application of a magnet).

Prevention of arrhythmias by pacing has been demonstrated in certain situations. In some patients with the long-QT syndrome, recurrent pause-dependent VT may be prevented by continuous pacing ⁹⁷. A combination of pacing and beta-blockade has been reported to shorten the QT interval and help prevent sudden cardiac death ^98,99. ICD therapy in combination with overdrive suppression pacing should be considered in high-risk patients.

Atrial synchronous ventricular pacing may prevent recurrences of re-entrant supraventricular tachycardia ¹⁰⁰ although this technique is rarely used given the availability of catheter ablation and other alternative therapies. Although ventricular ectopic activity may be suppressed by such pacing in other conditions, serious or symptomatic arrhythmias are rarely prevented ¹⁰¹. In some patients with bradycardia- dependent atrial fibrillation, atrial pacing may be effective in reducing the frequency of recurrences ⁹². In the Mode Selection Trial (MOST), 2010 patients with sinus node dysfunction were randomized between DDDR and VVIR pacing. After a mean follow-up of 33 months, there was a 21% lower risk of atrial fibrillation (p = 0.008) in the DDDR group than in the VVVIR group ³⁵³. Other trials are under way to assess the efficacy of atrial overdrive pacing algorithms and algorithms that react to premature atrial complexes in preventing atrial fibrillation, but data to date are sparse. Dual-site right atrial pacing or alternate single-site atrial pacing from nonconventional sites (e.g., septal or Bachmann’s bundle) may offer additional benefits to single-site right atrial pacing from the appendage in patients with symptomatic drug-refractory atrial fibrillation and concomitant bradyarrhythmias ⁹³. In patients with sick sinus syndrome and intra-atrial block (P wave more than 180 milliseconds), biatrial pacing may lower recurrence rates of atrial fibrillation ⁹⁴.

Potential recipients of antitachyarrhythmia devices that interrupt arrhythmias should undergo extensive testing before implantation to ensure that the devices safely and reliably terminate the ectopic mechanism without accelerating the tachycardia or inducing ventricular fibrillation (VF). Patients for whom an antitachycardia pacemaker has been prescribed have usually been unresponsive to antiarrhythmic drugs or were receiving agents that could not control their cardiac arrhythmias. When permanent antitachycardia pacemakers detect and interrupt supraventricular tachycardia, all pacing should be done in the atrium, because adverse interactions have been reported ^85,102 with use of ventricular pacing to interrupt supraventricular arrhythmias. Permanent antitachycardia pacing as monotherapy for VT is not appropriate given that antitachycardia pacing algorithms are available in tiered-therapy ICDs that have the capability of cardioversion and defibrillation in cases when antitachycardia pacing is ineffective or causes acceleration of the treated tachycardia.

Recommendations for Permanent Pacemakers That Automatically Detect and Pace to Terminate Tachycardias

Class I

None.

Class IIa

Symptomatic recurrent supraventricular tachycardia that is reproducibly terminated by pacing in the unlikely event that catheter ablation and/or drugs fail to control the arrhythmia or produce intolerable side effects. (Level of Evidence: C) ^86-88,90,91

Class IIb

Recurrent supraventricular tachycardia or atrial flutter that is reproducibly terminated by pacing as an alternative to drug therapy or ablation. (Level of Evidence: C) ^85-88,90,91

Class III

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.

Pacing Recommendations to Prevent Tachycardia

Class I

Sustained pause-dependent VT, with or without prolonged QT, in which the efficacy of pacing is thoroughly documented. (Level of Evidence: C) ^97,98

Class IIa

High-risk patients with congenital long-QT syndrome. (Level of Evidence: C) ^97,98

Class IIb

1. AV re-entrant or AV node re-entrant supraventricular tachycardia not responsive to medical or ablative therapy. (Level of Evidence: C) ^87,88,92
2. Prevention of symptomatic, drug-refractory, recurrent atrial fibrillation in patients with coexisting sinus node dysfunction. (Level of Evidence: B) ^{93,94,354,355}

Class III

1. Frequent or complex ventricular ectopic activity without sustained VT in the absence of the long-QT syndrome.
2. Torsade de Pointes VT due to reversible causes.

F. Pacing in Hypersensitive Carotid Sinus and Neurocardiogenic SyncopeSyndromes

The hypersensitive carotid sinus syndrome is defined as syncope or presyncope resulting from an extreme reflex response to carotid sinus stimulation. It is an uncommon cause of syncope. There are two components of the reflex:

1. Cardioinhibitory, resulting from increased parasympathetic tone and manifested by slowing of the sinus rate or prolongation of the PR interval and advanced AV block, alone or in combination.
2. Vasodepressor, secondary to a reduction in sympathetic activity resulting in loss of vascular tone and hypotension. This effect is independent of heart rate changes.

Before concluding that permanent pacing is clinically indicated, the physician should determine the relative contribution of the two components of carotid sinus stimulation to the individual patient’s symptom complex. Hyperactive response to carotid sinus stimulation is defined as asystole due to either sinus arrest or AV block of more than 3 seconds, or a substantial symptomatic decrease in systolic blood pressure, or both ¹⁰⁶. Pauses up to 3 seconds during carotid sinus massage are considered to be within normal limits. Such heart rate and hemodynamic responses may occur in normal subjects and patients with coronary artery disease. The cause-and-effect relation between the hypersensitive carotid sinus and the patient’s symptoms must be made with great caution ¹⁰⁷. Spontaneous syncope reproduced by carotid sinus stimulation should alert the physician to the presence of this syndrome. Minimal pressure on the carotid sinus in elderly patients or patients receiving digitalis may result in marked changes in heart rate and blood pressure yet not be of clinical significance. Permanent pacing for patients with pure excessive cardioinhibitory response to carotid stimulation is effective in relieving symptoms ^108,109. Because 10% to 20% of patients with this syndrome may have an important vasodepressor component of their reflex response, it is desirable to define this component before concluding that all symptoms are related to asystole alone. Among patients whose reflex response includes both cardioinhibitory and vasodepressor components, attention to the latter is essential for effective therapy in patients undergoing pacing.

Evidence has emerged that suggests that elderly patients who have sustained otherwise unexplained falls may have carotid sinus hypersensitivity ³⁵⁶. In a subsequent study, 175 elderly patients who had fallen without loss of consciousness and had pauses greater than 3 seconds during carotid sinus massage (thus fulfilling the diagnosis of carotid sinus hypersensitivity) were randomized to pacing or nonpacing therapy. The paced group had a significantly lower likelihood of subsequent falling episodes during follow-up ³⁵⁷.

Neurocardiogenic syncope and neurocardiogenic syndromes refer to a variety of clinical scenarios in which triggering of a neural reflex results in a usually selflimited episode of systemic hypotension characterized by both bradycardia and peripheral vasodilation ¹¹⁰. Neurocardiogenic syncope accounts for 10% to 40% of syncope episodes. Vasovagal syncope is a term used to denote one of the most common clinical scenarios within the category of neurocardiogenic syncopal syndromes. Patients classically have a prodrome of nausea and diaphoresis (often absent in the elderly), and there may be a positive familial history of the condition. Spells may be triggered by pain, anxiety, stress, or crowded conditions. Typically, no evidence of structural heart disease is present. Other causes of syncope such as LV outflow obstruction, bradyarrhythmias, and tachyarrhythmias should be excluded. Head-up tilt-table testing may be diagnostic.

The role of permanent pacing in refractory neurocardiogenic syncope associated with significant bradycardia or asystole is controversial. Approximately 25% of patients have a predominant vasodepressor reaction without significant bradycardia ¹¹¹. An additional large percentage of patients will have a mixed vasodepressor/vasoinhibitory component of their symptoms. While one group of investigators have noted some benefit of pacing in these patients ^112,113, another study using a pacing rate 20% higher than the resting heart rate demonstrated that pacing did not prevent syncope any better than pharmacotherapy ¹⁰⁶. Because most individuals with neurocardiogenic syncope have a slowing of heart rate after the fall in blood pressure, pacing may be ineffective in most patients. Dual-chamber pacing, carefully prescribed on the basis of tilt-table test results, may be effective in reducing symptoms if the patient has a significant cardioinhibitory component to the cause of their symptoms ¹¹⁴. Results from a randomized trial ^358,359 in highly symptomatic patients with bradycardia demonstrated that permanent pacing increased the time to first syncopal event. In one of these trials ³⁵⁸, the actuarial rate of recurrent syncope at 1 year was 18.5% for pacemaker patients and 59.7% for control patients. The specific modality of pacing under these circumstances is under active investigation. One study demonstrated that DDD pacing with rate-drop response function was more effective than beta-blockade in preventing recurrent syncope in highly symptomatic patients with vasovagal syncope and relative bradycardia during tilt-table testing ³⁶⁰. Although spontaneous or provoked prolonged pauses are a concern in this population, the prognosis without pacing is excellent ¹¹⁶. Several investigators have concluded that some patients with syncope of undetermined origin may benefit from pacing if findings strongly suggestive of bradycardic etiology are discovered or provoked at electrophysiologic study ^117,118,361.

The evaluation of patients with syncope of undetermined origin should take into account clinical status and not overlook other, more serious causes of syncope such as ventricular tachyarrhythmias.

Recommendations for Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope

Class I

Recurrent syncope caused by carotid sinus stimulation; minimal carotid sinus pressure induces ventricular asystole of more than 3 seconds’ duration in the absence of any medication that depresses the sinus node or AV conduction. (Level of Evidence: C) ^108,109

Class IIa

1. Recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response. (Level of Evidence: C) ^108,109
2. Significantly symptomatic and recurrent neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table testing. (Level of Evidence: B) ^358-360,362

Class III

1. A hyperactive cardioinhibitory response to carotid sinus stimulation in the absence of symptoms or in the presence of vague symptoms such as dizziness, lightheadedness, or both. (Level of Evidence: C)
2. Recurrent syncope, lightheadedness, or dizziness in the absence of a hyperactive cardioinhibitory response. (Level of Evidence: C)
3. Situational vasovagal syncope in which avoidance behavior is effective. (Level of Evidence: C)

G. Pacing in Children, Adolescents, and Patients With Congenital Heart Disease

The indications for permanent cardiac pacemaker implantation in the child, adolescent, or young adult with congenital heart disease may be considered broadly as 1) symptomatic sinus bradycardia, 2) the bradycardia-tachycardia syndromes, 3) congenital third-degree AV block, and 4) advanced second- or third-degree AV block, either surgical or acquired. Although the general indications for pacemaker implantation in children are similar to those in adults, there are several important considerations in young patients. First, an increasing number of patients are surviving complex surgical procedures for congenital heart disease that result in palliation rather than correction of circulatory physiology. The residua of impaired ventricular function and abnormal physiology may result in symptomatic bradycardia at rates that do not produce symptoms in persons with normal cardiovascular physiology. Hence, the indications for pacemaker implantation in these patients need to be based on the correlation of symptoms with relative bradycardia rather than absolute heart rate criteria. Second, the clinical significance of bradycardia is age dependent; whereas a heart rate of 45 bpm may be a normal finding in an adolescent, the same rate in a newborn or infant indicates profound bradycardia.

Bradycardia and associated symptoms in children are often transient (e.g., paroxysmal AV block or sinus arrest) and difficult to document. Although sinus node dysfunction (sick sinus syndrome) is increasingly recognized in pediatric patients, it is not itself an indication for pacemaker implantation. In the young patient with sinus bradycardia, the primary criterion for a pacemaker is the concurrent observation of a symptom (e.g., syncope) with bradycardia (e.g., heart rate less than 40 bpm or asystole more than 3 seconds) ^25,27,119. In general, correlation of symptoms with bradycardia is determined by 24-hour ambulatory or transtelephonic electrocardiography. Symptomatic bradycardia (as defined) is considered an indication for pacemaker implantation, provided that other causes of the symptom(s) have been excluded. Alternative causes to be considered include seizures, breath holding, apnea, or neurocardiogenic mechanisms.

The bradycardia-tachycardia syndrome (sinus bradycardia alternating with atrial flutter or re-entrant atrial tachycardia) is an increasingly frequent problem in young patients following surgery for congenital heart disease. Substantial morbidity and mortality have been observed in young patients with recurrent or chronic atrial flutter, with the loss of sinus rhythm an independent risk factor for subsequent development of atrial flutter ^120,121. Thus, both long-term atrial pacing at physiologic rates as well as atrial antitachycardia pacing have been reported for treatment of sinus bradycardia and prevention or termination of recurrent episodes of tachycardia ^122,123. To date, the results of pacing for the bradycardia- tachycardia syndrome in children have been equivocal and the source of considerable controversy ^124,125. It is clear that long-term drug therapy (e.g., sotalol or amiodarone) deemed essential for the control of atrial flutter may result in symptomatic bradycardia in some patients, whereas the use of other antiarrhythmic agents (e.g., quinidine) may potentially increase the risk of ventricular arrhythmias or sudden death in the presence of profound bradycardia. Thus, in young patients with recurrent arrhythmias associated with the bradycardia-tachycardia syndrome, permanent pacing should be considered as an adjunctive form of therapy. As an alternative therapy to antiarrhythmic medications that result in profound bradycardia and the need for pacemaker implantation, radiofrequency catheter ablation may modify the anatomic substrate of tachycardia in select patients with congenital heart disease.

Indications for permanent pacing in young patients with congenital complete AV block continue to evolve, based on improved definition of the natural history of the disease as well as advances in pacemaker technology and diagnostic methods. In several studies it has been observed that pacemaker implantation may improve long-term survival and prevent syncopal episodes among asymptomatic patients with congenital complete AV block ^126,127. Periodic evaluation of ventricular function is required in patients with congenital AV block, even after pacemaker implantation ³⁶³. Several criteria (average heart rate, pauses in the intrinsic rate, associated structural heart disease, prolonged QT interval, and exercise tolerance) must be considered in the asymptomatic patient with congenital complete AV block ^128-130.

The use of cardiac pacing with beta-blockade for prevention of symptoms in patients with the congenital long-QT syndrome is supported by observational studies ^98,131,364. The primary benefit of pacemaker therapy may be in patients with pause-dependent initiation of ventricular tachyarrhythmias ¹³² or those with sinus bradycardia or advanced AV block in association with the congenital long- QT syndrome ^133,134. Although pacemaker implantation may reduce the incidence of symptoms in these patients, long-term benefit on risk of sudden cardiac arrest remains to be determined ^98,131,133.

A poor prognosis has been established for patients with permanent postsurgical AV block who do not receive permanent pacemakers for rate support ¹³⁵. The presence of advanced second- or third-degree AV block persisting for 7 to 14 days after cardiac surgery is considered a Class I indication for pacemaker implantation ¹³⁶. The need for pacing in patients with transient advanced AV block with residual bifascicular block is less certain, whereas patients in whom AV conduction returns to normal generally have a favorable prognosis ¹³⁷.

Additional details that need to be considered in pacemaker implantation in young patients include risk of paradoxic embolism due to thrombus formation on an endocardial lead system in the presence of residual intracardiac defects and the lifelong need for permanent cardiac pacing ^138,139. Decisions about pacemaker implantation must also take into account implantation technique (transvenous versus epicardial) and long-term vascular access.

Recommendations for Permanent Pacing in Children, Adolescents, and Patients With Congenital Heart Disease

Class I

1. Advanced second- or third-degree AV block associated with symptomatic bradycardia, ventricular dysfunction, 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) ^25,27,119
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) ^365,366
4. Congenital third-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy, or ventricular dysfunction. (Level of Evidence: B) ^127,129,363
5. Congenital third-degree AV block in the infant with a ventricular rate less than 50 to 55 bpm or with congenital heart disease and a ventricular rate less than 70 bpm. (Level of Evidence: B, C) ^129,130
6. Sustained pause-dependent VT, with or without prolonged QT, in which the efficacy of pacing is thoroughly documented. (Level of Evidence: B) ^{97,98,131,132}

Class IIa

1. Bradycardia-tachycardia syndrome with the need for long-term antiarrhythmic treatment other than digitalis. (Level of Evidence: C) ^123,124
2. Congenital third-degree AV block beyond the first year of life with an average heart rate less than 50 bpm, abrupt pauses in ventricular rate that are two or three times the basic cycle length, or associated with symptoms due to chronotropic incompetence. (Level of Evidence: B) ¹²⁸
3. Long-QT syndrome with 2:1 AV or third-degree AV block. (Level of Evidence: B) ^133,134
4. Asymptomatic sinus bradycardia in the child with complex congenital heart disease with resting heart rate less than 3540 bpm or pauses in ventricular rate more than 3 seconds. (Level of Evidence: C)
5. Patients with congenital heart disease and impaired hemodynamics due to sinus bradycardia or loss of AV synchrony. (Level of Evidence: C)

Class IIb

1. Transient postoperative third-degree AV block that reverts to sinus rhythm with residual bifascicular block. (Level of Evidence: C) ¹³⁷
2. Congenital third-degree AV block in the asymptomatic infant, child, adolescent, or young adult with an acceptable rate, narrow QRS complex, and normal ventricular function. (Level of Evidence: B) ^126,127
3. Asymptomatic sinus bradycardia in the adolescent with congenital heart disease with resting heart rate less than 3540 bpm or pauses in ventricular rate more than 3 seconds. (Level of Evidence: C)
4. Neuromuscular diseases with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease.

Class III

1. Transient postoperative AV block with return of normal AV conduction. (Level of Evidence: B) ^136,137
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 with longest RR interval less than 3 seconds and minimum heart rate more than 40 bpm. (Level of Evidence: C) ¹⁴⁰

H. Pacing in Specific Conditions

1. Hypertrophic Obstructive Cardiomyopathy
Early nonrandomized studies demonstrated a fall in the LV outflow gradient with dual-chamber pacing and a short AV delay and symptomatic improvement in some patients with hypertrophic obstructive cardiomyopathy ^141-143,154. One long-term study ¹⁵³ in eight patients supported the long-term benefit of dual-chamber pacing in this group of patients. The outflow gradient was reduced even after cessation of pacing, suggesting that some ventricular remodeling had occurred consequent to pacing. Two randomized trials ^152,154 demonstrated subjective improvement in approximately 50% of study participants but there was no correlation with gradient reduction, and a significant placebo effect was present. A third randomized trial ³⁶⁷ failed to demonstrate any overall improvement in quality of life with pacing, although there was a suggestion that elderly patients (aged more than 65 years) may derive more benefit from pacing.

In a small group of patients with symptomatic, hypertensive cardiac hypertrophy with cavity obliteration, VDD pacing with premature excitation statistically improved exercise capacity, cardiac reserve, and clinical symptoms ³⁶⁸. Dual-chamber pacing may improve symptoms and LV outflow gradient in pediatric patients. However, rapid atrial rates, rapid AV conduction, and congenital mitral valve abnormalities may preclude effective pacing in some patients ¹⁵⁵.

There are currently no data available to support the contention that pacing alters the clinical course of the disease or bivenimproves survival or quality of life. Therefore, routine implantation of dual-chamber pacemakers should not be advocated in all patients with symptomatic hypertrophic obstructive cardiomyopathy. Patients who may benefit the most are those with significant gradients (more than 30 mm Hg at rest or more than 50 mm Hg provoked ^154,369-371. In highly symptomatic patients, septal myectomy or percutaneous septal alcohol ablation should be considered instead of dual-chamber pacing ³⁷². For the patient with hypertrophic obstructive cardiomyopathy who is at high risk for sudden death and has a definite indication for pacemaker implantation, the clinician should weigh the long-term advantages of implantation instead an ICD, even if the patient’s condition might not warrant an ICD implant at that point in time (see Section II-E).

Pacing Recommendations for Hypertrophic Cardiomyopathy

Class I

Class I indications for sinus node dysfunction or AV block as described previously. (Level of Evidence: C)

Class IIb

Medically refractory, symptomatic hypertrophic cardiomyopathy with significant resting or provoked LV outflow obstruction. (Level of Evidence: A) ^{142,145,146,152,154,367}

Class III

1. Patients who are asymptomatic or medically controlled.
2. Symptomatic patients without evidence of LV outflow obstruction.

2. Idiopathic Dilated Cardiomyopathy
Several observational studies have shown limited improvement in patients who have symptomatic dilated cardiomyopathy refractory to medical therapy with dual-chamber pacing with a short AV delay ^156-159. Theoretically, a short AV delay may optimize the timing of mechanical AV synchrony and ventricular filling time. In patients with prolonged PR intervals more than 200 milliseconds, diastolic filling time may be improved by dual-chamber pacing with a short AV delay ¹⁷. In one study ¹⁵⁷, cardiac output was increased 38% by shortening AV delay when the average PR interval was 283 milliseconds before pacing. When the PR interval was shorter, no benefit of pacing was noted. Permanent pacing in symptomatic patients with drug-refractory dilated cardiomyopathy and a prolonged PR interval may be useful if short-term benefit is demonstrated in acute studies. At this time no long-term data are available, and there is no consensus for this indication. The mechanisms by which dual-chamber pacing might benefit patients with dilated cardiomyopathy are poorly understood. One hypothesis is that a well-timed atrial contraction primes the ventricles and decreases mitral regurgitation, thus augmenting stroke volume and arterial pressure.

Thirty to fifty percent of patients with congestive heart failure have intraventricular conduction defects ^373,374. These conduction abnormalities progress over time, lead to discoordinated contraction of an already hemodynamically compromised ventricle, and are an independent predictor of mortality ³⁷⁵. Delayed activation of the LV during right ventricular pacing also leads to significant dyssynchrony in both LV contraction and relaxation. Biventricular pacing can provide a more coordinated pattern of ventricular contraction, reduce the QRS duration, and reduce intraventricular and interventricular asynchrony. Biventricular pacing was initially demonstrated to improve cardiac index acutely, decrease systemic vascular resistance and pulmonary capillary wedge pressure, increase systolic blood pressure, and lower V-wave amplitude compared with right ventricular or AAI pacing in several trials ^376-378. Advances in lead design have allowed the insertion of endocardial leads into distal branches of the coronary sinus to pace the LV. These advances have led to several small and large prospective trials to study the efficacy of biventricular pacing in patients with congestive heart failure and intraventricular conduction defects. Auricchio et al. ³⁷⁹ demonstrated that pacing in the mid-lateral LV augments positive pulse pressure changes more than pacing other areas. In the Pacing Therapies for Congestive Heart Failure trial ³⁸⁰, increases in LV dP/dt and pulse pressure were significantly better with biventricular than with right ventricular pacing. Convincing data from several prospective, randomized trials ^381-384 support the hemodynamic and subjective improvement that was noted in multiple previous anecdotal and smaller trials ^385-387. These trials demonstrate that in patients with New York Heart Association (NYHA) class III or IV congestive heart failure, decreased ejection fraction, and prolonged QRS duration, biventricular pacing decreases QRS duration and improves 6-minute walk distance, NYHA class, and quality-of-life scores. In the Multisite Stimulation in Cardiac Insufficiency trial ³⁸¹, rehospitalizations from congestive heart failure were also reduced. No data exist demonstrating that biventricular pacing improves survival, although early data suggest trends in improvement in decreasing spontaneous ventricular ectopy and ICD shocks ^388-390. Ongoing studies will determine whether a combination of biventricular pacing with an ICD will result in an improvement in subjective symptoms plus improved survival.

Pacing Recommendations for Dilated Cardiomyopathy

Class I

Class I indications for sinus node dysfunction or AV block as described previously. (Level of Evidence: C)

Class IIa

Biventricular pacing in medically refractory, symptomatic NYHA class III or IV patients with idiopathic dilated or ischemic cardiomyopathy, prolonged QRS interval (greater than or equal to 130 milliseconds), LV end-diastolic diameter greater than or equal to 55 mm, and ejection fraction less than or equal to 35%. (Level of Evidence: A) ^381,383

Class III

1. Asymptomatic dilated cardiomyopathy.
2. Symptomatic dilated cardiomyopathy when patients are rendered asymptomatic by drug therapy.
3. Symptomatic ischemic cardiomyopathy when the ischemia is amenable to intervention.

3. Cardiac Transplantation
The incidence of bradyarrhythmias after cardiac transplantation varies from 8% to 23% ^165-167. The majority of bradyarrhythmias are associated with sinus node dysfunction. Because of symptoms and impaired recovery and rehabilitation, some transplant programs recommend more liberal use of cardiac pacing for persistent postoperative bradycardia. About 50% of patients show resolution of the bradyarrhythmia within 6 to 12 months, and long-term pacing is often unnecessary in a large number of patients ^168-170. Significant bradyarrhythmias and asystole have been associated with reported cases of sudden death ¹⁷¹. No predictive factors have been identified to indicate which patients will develop post-transplantation bradyarrhythmias. In some patients, the need for pacing may be transient. The benefits of the atrial contribution to cardiac output and chronotropic competence may optimize the patient’s functional status. Attempts to treat the bradycardia temporarily with measures such as theophylline ¹⁷² may minimize the need for pacing. Post-transplant patients who have irreversible sinus node dysfunction or AV block with previously stated Class I indications should have permanent pacemakers.

Pacing Recommendations After Cardiac Transplantation

Class I

Symptomatic bradyarrhythmias/chronotropic incompetence not expected to resolve and other Class I indications for permanent pacing. (Level of Evidence: C)

Class IIb

Symptomatic bradyarrhythmias/chronotropic incompetence that, although transient, may persist for months and require intervention. (Level of Evidence: C)

Class III

Asymptomatic bradyarrhythmias after cardiac transplantation.

I. Selection of Pacemaker Device

Once the decision has been made to implant a pacemaker in a given patient, the clinician must decide among a large number of available pacemaker generators and leads. Generator choices include single- versus dual-chamber devices, unipolar versus bipolar configuration, presence and type of sensor for rate response, advanced features such as automatic mode switching, size, battery capacity, and cost. Lead choices include polarity, type of insulation material, fixation mechanism (active versus passive), and presence of steroid elution. Some lead models typically show low (300-500 Ohms) and some high (greater than 1000 Ohms) pacing impedance, and this can have implications with regard to the generator’s battery longevity. Other factors that importantly influence the choice of pacemaker system components include the capabilities of the pacemaker programmer, which provides the link between the pacemaker system and the physician, and local availability of technical support.

Even after selecting and implanting the pacing system, the physician has a number of options for programming the device. In modern single-chamber pacemakers, programmable features include pacing mode, lower rate,