The use and sophistication of permanent pacemakers have increased steadily since the first pacemaker was implanted in 1958. Indications for their use have broadened as the technology has advanced, and pacemakers have become a mainstay of therapy. Those involved in arrhythmia management must have a good understanding of this discipline.

History of Pacing

Since the first epicardial pacing system was implanted in 1958, pacemaker technology has evolved rapidly. The sophistication of sensing circuitry led to the introduction of single-chamber demand pacing systems in 1963. Although atrial-synchronous systems and dual-chamber systems were described in the 1950s, clinical use of such devices did not occur for many years. In the 1970s, lithium batteries and programmability were introduced. Milestones of the 1980s include greater acceptance of dual-chamber pacing systems and the introduction of rate-adaptive pacing systems. The 1990s and the 2000s witnessed the introduction of advanced sensor technology, new pacemaker algorithms, and enhanced automaticity of many programmable features. The utilization of pacing has increased significantly from 46.7 per 100,000 in 1993 to 61.6 per 100,000 in 2009, with the percentage of dual-chamber devices increasing from 62% to 82% during this time period.

Pacemaker Nomenclature

Since the first introduction of a three-letter code describing basic pacemaker functions in 1974, the code has been updated periodically by a committee made up of members of the North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group (NASPE/BPEG). The most recent code has five letters ( Box 120.1 ). The first position indicates the chamber or chambers that are stimulated: A (atrium), V (ventricle), or D (dual-chamber, both A and V). The second position indicates the chamber or chambers in which sensing occurs: A (atrium), V (ventricle), or D (dual-chamber, both A and V). The third position indicates the function: I (inhibition), T (triggered), or D (a dual function of atrial tracking and ventricular inhibition). The fourth position of the code indicates that rate modulation is present by the letter R . Rate modulation is the use of a sensor to meet the patient’s metabolic demands, independent of intrinsic cardiac activity. The fifth position indicates whether multisite pacing is present: A (atrium), V (ventricle), or D (both A and V). Multisite pacing is defined as more than one stimulation site in any single chamber. In any of the positions, O indicates that pacing, sensing, or a function is not present.

BOX 120.1
Revised NASPE/BPEG Generic Code for Antibradycardia Pacing
BPEG, British Pacing and Electrophysiology Group; NASPE, North American Society of Pacing and Electrophysiology.

Chamber(s) Paced

  • O = None

  • A = Atrium

  • V = Ventricle

  • D = Dual (A + V)

  • S = Single (A or V) (manufacturers’ designation only)

Chamber(s) Sensed

  • O = None

  • A = Atrium

  • V = Ventricle

  • D = Dual (A + V)

  • S = Single (A or V) (manufacturer’s designation only)

Response to Sensing

  • O = None

  • T = Triggered

  • I = Inhibited

  • D = Dual (T + I)

Rate Modulation

  • O = None

  • R = Rate modulation

Multisite Pacing

  • O = None

  • A = Atrium

  • V = Ventricle

  • D = Dual (A + V)

Indications for Cardiac Pacing

Criteria established by a joint committee of the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS) have categorized indications for pacing as class I, which stands for generally indicated; class II, which means possibly indicated; and class III, or not indicated. Class II is further divided into class IIa for recommendations for which there is general agreement and class IIb for recommendations for which there is some disagreement. The evidence supporting the recommendations is ranked as follows: The weight of evidence is ranked A if there are multiple randomized trials involving a large number of subjects and B if data were derived from a limited number of trials involving a relatively small number of subjects. The weight of evidence is ranked C if expert consensus is the primary source of the recommendation. Although some indications for permanent pacing are relatively certain or unambiguous, others require considerable expertise and judgment. The clinician prescribing permanent pacing systems should be aware of the indications and controversies regarding indications.

Acquired Atrioventricular Block

Acquired atrioventricular (AV) block is most commonly idiopathic and related to aging, but the potential causes are many.

Class I indications for permanent pacing in patients with acquired AV block include any AV block with associated symptoms, as well as AV block after AV node ablation or persistent AV block after cardiac surgery. For some patients, heart failure may be a manifestation of AV block. In addition, some patients require medications that can cause symptomatic bradycardia and might need pacing. For postoperative AV block, the guidelines do not specify a period to wait postoperatively for recovery of conduction. Class I indications also include acquired AV block below the level of the AV node or associated with marked pauses, such as longer than 3.0 seconds or a ventricular escape rate of less than 40 beats/min. Permanent pacemaker implantation is also indicated in awake, symptom-free patients with atrial fibrillation (AF) and bradycardia with pauses of 5 seconds or more. Because the cardiovascular risk is felt to be particularly high in patients with second- or third-degree block and specific underlying conditions, permanent pacing is felt to be indicated in these patients even in the absence of symptoms. These conditions include neuromuscular diseases such as myotonic dystrophy, Kearns-Sayre syndrome, peroneal muscular atrophy, and Erb limb girdle dystrophy. Myotonic dystrophy has been associated with an increased risk for sudden death thought to be because of progressive conduction system disease.

Exercise-related AV block is also felt to be an indication for pacing. Advanced second-degree AV block or alternating bundle branch block in the setting of bifascicular block is considered a class I indication. Asymptomatic type II second-degree AV block with a wide QRS is a class I indication. Transient, infranodal, high-grade AV block and associated bundle branch block is a class I indication.

Class IIa indications include asymptomatic type II second-degree AV block with a narrow QRS complex and asymptomatic second-degree AV block at intra-His or infra-His levels based on electrophysiologic (EP) testing. First-degree or second-degree AV block with hemodynamic compromise is also considered a class IIa indication because some patients develop pacemaker-like syndrome because of conduction delay. In patients with bifascicular block, asymptomatic severe prolongation of the His-ventricle interval (>100 ms), asymptomatic pacing-induced infra-His block that is not felt to be physiologic, or syncope when other causes such as ventricular tachycardia (VT) have been excluded are considered class IIa indications for pacing.

First-degree AV block in patients with neuromuscular disorders is considered a class IIb indication because the risk for progression to AV block is felt to be high. Another class IIb indication includes AV block that might have occurred because of drug use or toxicity, but there is a risk for recurrence of AV block. First-degree AV block in a patient with left ventricular (LV) dysfunction and congestive heart failure in whom hemodynamic improvement with AV interval optimization can be demonstrated is a class IIb indication. Asymptomatic persistent second-degree or third-degree block at the AV node level is classified as a class IIb indication.

Class III indications include asymptomatic first-degree AV block, asymptomatic second-degree AV block at the supra-His level or not known to be intra-His or infra-His, and AV block occurring in the setting of reversible conditions such as drug toxicity that is unlikely to recur, Lyme disease, transient increases in vagal tone, or during sleep apnea.

After a myocardial infarction, a pacemaker is generally considered to be indicated for persistent second-degree bilateral bundle branch block, third-degree AV block within or below the His bundle, or persistent symptomatic second-degree or third-degree AV block.

Congenital Complete Heart Block

Symptomatic congenital complete AV block remains a class I indication for pacing in pediatric patients. In addition, in pediatric patients with congenital complete AV block, the presence of a wide QRS escape rhythm, ventricular dysfunction, or complex ventricular ectopy is also a class I indication. In pediatric patients, an average heart rate less than 50 beats/min, pauses two to three times the basic cycle length, or symptoms associated with chronotropic incompetence are considered class IIa indications. In pediatric and adult patients with an adequate rate, narrow QRS complex, and normal ventricular function, pacing is a class IIb indication.

For adult patients with congenital complete AV block, the timing and indications for permanent pacing are more controversial and continue to evolve. As a result of data regarding the high incidence of unexpected syncope in adult patients with congenital complete AV block, prophylactic pacemaker implantation is often considered. ,

Sinus Node Dysfunction

Sinus node dysfunction may be manifested by abrupt sinus pauses or gradual sinus slowing. Symptomatic chronotropic incompetence and symptomatic sinus bradycardia occurring spontaneously or as the result of drug therapy are considered class I indications for pacing. In patients with minimal or no symptoms and chronic heart rates less than 40 beats/min, pacing is a class IIb indication.

Class III indications for pacing include asymptomatic sinus node dysfunction. Sinus pauses occurring during sleep are generally not considered indications for pacing. Many patients, particularly trained athletes, have high levels of vagal tone and have significant pauses greater than 3 seconds and periods of sinus bradycardia. These patients do not require permanent pacing.

Neurocardiogenic Syncope

Neurocardiogenic syncope (see Chapter 103 ) typically has both cardioinhibitory and vasodepressor components. Pacing during most episodes of neurocardiogenic syncope is still associated with a significant fall in blood pressure and symptoms because of the continued vasodepressor response. Therefore, even in the presence of significant bradycardia, pacing is usually not considered first-line therapy. A number of randomized trials have failed to show a substantial benefit in increasing the freedom from recurrent syncope. , As a result, neurocardiogenic syncope with documented bradycardia is considered a class IIb indication for pacing. Nevertheless, there are some recent studies that may indicate the selective use of pacing. In the Third International Study on Syncope of Uncertain Etiology (ISSUE-3) trial, in patients 40 years of age or older with at least three syncopal episodes in 2 years, and with documentation of syncope with 3 or more seconds of asystole or 6 or more seconds of asystole without syncope, 77 patients were randomized to dual-chamber pacing on or off with an algorithm to increase the pacing rate with a sudden decrease in heart rate. The syncope recurrence rate was 57% in the pacing off group and 25% in the pacing on group ( P = .039).

When pacing is performed in this setting, dual-chamber pacing is necessary to preserve the atrial contribution to cardiac output. Modifications to the pacing strategy are being studied to make dual-chamber pacing more effective in ameliorating neurocardiogenic syncope. The heart rate may be adjusted according to measured changes in impedance to estimate myocardial contractility, using so-called closed-loop stimulation (CLS). Although retrospective data suggest that this approach may reduce the frequency of recurrence of syncope, further prospective studies are needed.

In patients with syncope of unknown origin, a randomized, multicenter study examined patients exhibiting a pause of 10 seconds or more when given an intravenous bolus of 20 mg adenosine triphosphate (ATP). These patients were randomized to atrial inhibited pacing (AAI) at 30 beats/min versus dual chamber antibradycardia (DDD) pacing at 70 beats/min. In the DDD pacing group, 21% of patients had recurrence of syncope compared with 66% of patients in the AAI group. Of note, the mean age in these studies was 76 years.

Carotid Sinus Hypersensitivity

Carotid sinus hypersensitivity has been shown to be a cause of syncope, particularly in the elderly. Nevertheless, because an abnormal response can occur even in asymptomatic persons, caution must be used when spontaneous bradycardia has not been demonstrated. In cases in which syncope has occurred during carotid sinus stimulation and carotid sinus pressure has resulted in pauses of 3 seconds or more, a class I indication is felt to be present. If such an abnormal carotid sinus pressure response is obtained but syncope did not occur in circumstances suggesting carotid sinus stimulation, a class IIa indication is present. In addition, there may be a role for pacing in patients with unexplained falls and evidence of carotid sinus hypersensitivity. A previous study showed that pacing reduced syncopal episodes, with no differences between ventricular-inhibited (VVI) pacing, dual-chamber rate-adaptive pacemakers (DDDRs), or DDDRs with a sudden bradycardia response.

Nonbradycardic Indications for Pacing

An increasing number of patients are receiving pacemakers for nonbradycardic indications. Cardiac resynchronization therapy (CRT) for refractory congestive heart failure is the major indication in this category. Dual-chamber pacing for medically refractory symptoms of hypertrophic obstructive cardiomyopathy and pacing therapy for prevention of AF are no longer considered major nonbradycardic indications for pacing.

Pacing for Atrial Fibrillation

There are numerous studies that examined various pacing algorithms to prevent AF. Most such algorithms involve increasing the pacing rate to suppress the atrial ectopy felt to trigger AF. Although most randomized studies have not demonstrated a beneficial effect, selected studies have suggested a modest decrease in the occurrence of AF. In the Study of Atrial Fibrillation Reduction (SAFARI) trial, patients with recorded AF were randomized to AF pacing prevention strategies. Overall, there was a small reduction in the occurrence of AF. In patients with a high burden of AF, the reduction in AF was greater. At present, pacing is not indicated for AF reduction (class III).

Resynchronization Therapy

Numerous randomized controlled trials have demonstrated the benefit of CRT in improving symptoms and outcomes in patients with drug-refractory heart failure. CRT is the pacing of the LV and right ventricle (RV) to improve the hemodynamics that are impaired because of bundle branch block. These randomized studies have shown improvement in New York Heart Association (NYHA) classes, 6-minute walk time, oxygen consumption, brain natriuretic peptide levels, neurohormonal levels, ejection fraction (EF), end-diastolic and end-systolic dimensions, heart failure hospitalizations, and all-cause mortality. The current indications for resynchronization therapy (class I) include left bundle branch block (LBBB); QRS duration of 150 ms or greater; LVEF of 35% or less; sinus rhythm; and class II, III, or ambulatory class IV heart failure symptoms on optimal medical therapy. Class IIa indications include an LVEF of 35% or less and NYHA class II, III, and ambulatory IV symptoms on optimal medical therapy with (1) LBBB, QRS duration of 120 to 149 ms, or (2) non-LBBB and a QRS duration of 150 ms or greater. Class IIa indications also include patients with an LVEF of 35% or less on optimal medical therapy and (1) who are undergoing new or replacement device implantation with anticipated 40% or more ventricular pacing or (2) have AF that requires ventricular pacing or meets other criteria and near 100% ventricular pacing. ,

Hypertrophic Cardiomyopathy

Early studies suggested that RV apical pacing resulted in a reduction in the outflow tract gradient and ameliorated symptoms. Nevertheless, a subsequent randomized multicenter trial failed to demonstrate a benefit. A subset of elderly patients might have exhibited some improvement. An analysis from the Cochrane Database concluded that clinical trial data are inconclusive for evidence of an effect of pacing on outcomes in this patient population. Therefore, at present, pacing in medically refractory symptomatic patients with a significant resting or provoked gradient because of hypertrophic cardiomyopathy is a class IIb indication. Many such patients should be considered for a dual-chamber implantable cardioverter-defibrillator (ICD) because of the risk for sudden death.

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