Indications and Recommendations for Pacemaker Therapy GABRIEL GREGORATOS, M.D., University of California, San Francisco, School of Medicine, San Francisco, California

Each year, pacemaker therapy is prescribed to approximately 900,000 persons worldwide. Current pacemaker devices treat bradyarrhythmias and tachyarrhythmias and, in some cases, are combined with implantable defibrillators. In older patients, devices that maintain synchrony between atria and ventricles are preferred because they maintain the increased contribution of atrial contraction to ventricular filling necessary in this age group. In general, rate-responsive devices are preferred because they more closely simulate the physiologic function of the sinus node. Permanent pace- makers are implanted in adults primarily for the treatment of , acquired , and certain fascicular blocks. They also are effective in the prevention and treatment of certain tachyarrhythmias and forms of neurocardiogenic syncope. Biventricular pac- ing (resynchronization therapy) recently has been shown to be an effective treatment for advanced in patients with major intraventricular conduction effects, predominately left . Many studies have documented that pacemaker therapy can reduce symptoms, improve quality of life and, in certain patient populations, improve survival. (Am Fam Physician 2005;71:1563-70. Copyright© 2005 American Academy of Family Physicians.)

ince the first permanent pacemaker defined as a “documented bradyarrhythmia was implanted in 1958, device ther- that is directly responsible for the develop- apy has continued to grow. It is ment of the clinical manifestations of frank estimated that more than 300,000 syncope or near syncope, transient dizzi- S patients in the United States receive a per- ness or light-headedness, and confusional manent pacemaker each year, and about states resulting from cerebral hypoperfusion 900,000 pacemakers are implanted world- and attributable to low heart rates.”1 Other wide. The indications for pacemaker therapy symptoms that may result from severe bra- have expanded in the past 45 years and now dycardia include fatigue, reduced exercise include the treatment of bradyarrhythmias capacity, and frank congestive heart failure. and the electrical therapy of tachyarrhyth- Physiologic sinus , which can mias, certain types of syncope, and advanced occur in highly trained athletes, must be heart failure. Device technol- excluded and should not be confused with ogy also has evolved from sim- pathologic bradyarrhythmias. The decision to implant ple single-chamber, fixed-rate a pacemaker in a patient pacemakers to multichamber, ACC/AHA/NASPE Recommendations with abnormal atrioventric- rate-responsive (to meet physi- The American College of Cardiology (ACC) ular conduction depends on ologic needs) units capable and the American Heart Association (AHA) the presence of symptoms. of pacing, cardioversion, and published the first clinical guideline for per- defibrillation. In specific popu- manent pacemaker implantation in 1984. lations, clinical studies have demonstrated Three subsequent revisions have been pub- improvement of patient survival with the use lished, the latest being the 2002 update of these implantable devices. in collaboration with the North American The decision to implant a pacemaker usu- Society of Pacing and Electrophysiology ally is based on symptoms of a bradyar- (NASPE), on which this article is based.1 rhythmia or tachyarrhythmia in the setting The selected recommendations are pre- of heart disease. Symptomatic bradycardia sented in the usual three-class ACC/AHA is the most common indication. It has been format (Table 1).1

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Class I: Conditions for which evidence or general agreement exists that a given procedure or treatment is useful and or more consecutive P waves, whereas complete (third- effective Class II: Conditions for which conflicting evidence or a degree) AV block is defined as absence of all atrioven- divergence of opinion exists about the usefulness or efficacy tricular conduction. of a procedure or treatment First-degree and type I second-degree AV block usually IIa: Weight of evidence and opinion is in favor of usefulness are caused by delayed conduction in the AV node irre- and efficacy spective of QRS duration. Type II second-degree AV block IIb: Usefulness or efficacy is less well established by evidence and opinion usually is infra-nodal, especially when the QRS is wide. Class III: Conditions for which evidence and or general Third-degree AV block may occur at any anatomic level. agreement exists that a procedure or treatment is not useful The decision to implant a pacemaker in a patient with or effective and in some cases may be harmful abnormal AV conduction depends on the presence of symptoms related to bradycardia or ventricular arrhyth- ACC = American College of Cardiology; AHA = American Heart Association. mias and their prognostic implications. Observational *—Each recommendation is evidence based whenever possible and studies over the years strongly suggest that permanent is assigned an appropriate level of evidence. Level A is based on data pacing improves survival in patients with complete AV derived from multiple randomized trials involving a large number of block, especially if syncope has occurred.2-5 Therefore, individuals. Level B is based on data from a limited number of trials using a comparatively small number of patients or from well-designed, symptomatic third-degree AV block is a class I indica- nonrandomized studies or observational data registries. Level C is tion for permanent pacing, whereas asymptomatic third- based primarily on expert consensus and clinical experience. degree AV block is a class IIa indication. More recently, Adapted with permission from Gregoratos G, Abrams J, Epstein AE, Freed- it has been recognized that type II second-degree AV man RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 guideline 6,7 update for implantation of cardiac pacemakers and antiarrhythmia devices: block may be a precursor to complete AV block. a report of the American College of Cardiology/American Heart Association Type II second-degree AV block should be treated with a Task Force on Practice Guidelines. Circulation 2002;106:2146. permanent pacemaker even in an asymptomatic patient, particularly if it is associated with fascicular block, which also is a class IIa recommendation. ACQUIRED ATRIOVENTRICULAR Marked first-degree AV block (PR greater than AND FASCICULAR BLOCKS IN ADULTS 300 ms) can produce symptoms even in the absence of Atrioventricular (AV) block is classified as first-, second-, higher degrees of block. In this situation, symptoms are or third-degree. First-degree AV block is defined as caused by hemodynamic impairment resulting from the an abnormally prolonged PR interval. Second-degree, inappropriate timing of atrial systole, which may produce Mobitz type I AV block (Wenckebach) is manifested by symptoms similar to those of the “pacemaker syndrome” progressive prolongation of the PR interval eventuating (i.e., fatigue, syncope or presyncope, and malaise sec- in a dropped QRS complex. It usually is associated with ondary to low cardiac output, hypotension, and elevated a narrow QRS complex. Second-degree, Mobitz type II ventricular filling pressures that may develop when ven- AV block demonstrates a constant PR interval before a tricular pacing results in improper timing of atrial and dropped QRS and usually is associated with a wide QRS ventricular systole).8,9 Small, observational studies have complex. Advanced AV block refers to blockage of two suggested that patients with left ventricular dysfunction and markedly prolonged PR interval may benefit from pacing with a shorter AV conduction time.10 The Author Fascicular block refers to electrocardiographic (ECG) evidence of impaired conduction below the AV node in GABRIEL GREGORATOS, M.D., F.A.C.C., F.A.H.A., F.A.C.P., is emer- itus clinical professor of medicine at the University of California, the right bundle branch or in one or both fascicles of the San Francisco, School of Medicine. He was previously the director left bundle branch. refers to impaired of the clinical cardiology department and the cardiology training conduction in two of the three fascicles; for example, program at the University of California, Davis, School of Medicine. right bundle branch block and a block in the left ante- Dr. Gregoratos received his medical degree from New York Medical rior-superior division of the left bundle branch. Trifas- College, Valhalla, N.Y., and completed an internal medicine resi- dency at Tripler Army Medical Center, Honolulu, and a cardiology cicular block is diagnosed when block is documented in fellowship at Walter Reed Army Medical Center, Washington, D.C. all three fascicles, whether simultaneously or at different times. First-degree AV block in combination with bifas- Address correspondence to Gabriel Gregoratos, M.D., University of California School of Medicine, 505 Parnassus Ave., M314, San cicular block fulfills the criteria of , Francisco, CA 94143-0214 (e-mail: [email protected]. as does “alternating bundle branch block.” Alternating edu). Reprints are not available from the author. (bilateral) bundle branch block is diagnosed when in

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Figure 1. Electrocardiogram of a 79-year-old woman with severe conduction system disease. Precordial leads V1 through V3 show pattern (wide QRS of 140 ms and broad, deep S waves with no R waves). The QRS complexes in the limb leads are consistent with right bundle branch block (wide QRS of 120 ms, broad S waves in I, , etc.). In leads V4 through V6, the first QRS complex is similar to the QRS complexes in leads V1 through V3, whereas the second QRS after the nonconducted P wave is typical of right bundle branch block (wide QRS of 120 ms, small R waves, deep and broad S waves). The same changes can be seen in the V1 rhythm strip at the bottom of the trac- ing, which also illustrates the presence of alternating bundle branch block. The QRS complexes show left bundle branch block morphology until there is a nonconducted P wave (second-degree atrioventricular block). The following QRS has the morphology of right bundle branch block with a typical V1 RSRı pattern. This patient developed complete and required implantation of a pacemaker. different leads of the ECG or on successive ECG tracings Before a decision is made to implant a pacemaker for there is clear evidence of block in all three fascicles; for AV block, it is important to exclude and correct revers- example, right bundle branch block in one lead and left ible causes such as electrolyte abnormalities. Some types bundle branch block in another (Figure 1). of AV block can be expected to resolve and do not require Recurrent syncope is common in patients with bifas- pacing therapy; for example, perioperative block caused cicular block, but it is not associated with an increased by hypothermia or inflammation near the AV junction incidence of sudden death.11,12 Pacing therapy in such as a result of a surgical procedure in that area, or AV patients often relieves the transient neurologic symp- block developing during the acute phase of Lyme dis- toms (syncope) but does not prevent sudden death.13 On ease. Conversely, prophylactic pacing is recommended the other hand, syncope in the presence of permanent in certain conditions even if the AV block is transient, or transient third-degree AV block is associated with an because of the possibility of disease progression (for increased incidence of sudden death, and pacing therapy example, in sarcoidosis, amyloidosis, and certain neuro- definitely is indicated. Similarly, if the cause of syncope muscular diseases). The principal recommendations for in the presence of bifascicular or trifascicular block can- pacing in these conditions are listed in Tables 2 and 3.1 not be determined with certainty, prophylactic pacing is indicated.14 Pacing is not indicated for asymptomatic SINUS NODE DYSFUNCTION (SICK SINUS SYNDROME) bifascicular block because the rate of progression to Sinus node dysfunction is a syndrome manifested by a more advanced degrees of block is very slow. variety of cardiac , including sinus bradycar- Some investigators recommend pacing therapy for dia, , and paroxysmal supraventricular asymptomatic bifascicular block if there is evidence of , which frequently alternates with periods of severe intraventricular conduction delay on electrophysio- bradycardia or even (the so-called bradycardia- logic study. Patients with alternating bundle branch block tachycardia syndrome). Symptoms can result from the bra- have a high mortality rate and a significant incidence of dycardia, the paroxysmal supraventricular tachycardia, or sudden death if pacing therapy is not provided.15 both. It is important to correlate symptoms with one of the

April 15, 2005 ◆ Volume 71, Number 8 www.aafp.org/afp American Family Physician 1565 TABLE 2 Principal Recommendations for Permanent Pacing in Acquired Atrioventricular Block in Adults

Class I Third-degree and advanced second-degree AV block at any anatomic level, associated with any one of the following conditions: Bradycardia with symptoms (including heart failure) presumed to be caused by AV block. (C) Arrhythmias and other medical conditions requiring drugs that result in symptomatic bradycardia. (C) Documented periods of asystole greater than or equal to 3.0 seconds or any escape rate less than 40 beats per minute in awake, symptom-free patients. (B, C) After catheter ablation of the AV junction. (B, C) Postoperative AV block that is not expected to resolve after cardiac surgery. (C) 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, with or without symptoms, because there may be unpredictable progression of AV conduction disease. (B) Second-degree AV block regardless of type or site of block, with associated symptomatic bradycardia. (B) Class IIa Asymptomatic third-degree AV block at any anatomic site with average awake ventricular rates of 40 beats per minute or faster, especially if or LV dysfunction is present. (B, C) 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. (B) Asymptomatic type I second-degree AV block at intra- or infra-His levels found at electrophysiologic study performed for other indications. (B) First- or second-degree AV block with symptoms similar to those of pacemaker syndrome. (B) Class IIb 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. (C) 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, with or without symptoms, because there may be unpredictable progression of AV conduction disease. (B) Class III Asymptomatic first-degree AV block. (B) Asymptomatic type I second-degree AV block at the supra-His (AV node) level or not known to be intra- or infra-Hisian. (B, C) AV block expected to resolve or unlikely to recur (e.g., drug toxicity, Lyme disease, or during hypoxia in sleep apnea syndrome in absence of symptoms). (B)

NOTE: Level of evidence is given in parentheses. AV = atrioventricular; LV = left ventricular. Adapted with permission from Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2002;106:2146-8. above-mentioned arrhythmias by means of ECG, ambula- atrial overdrive pacing (pacing at a rate higher than tory ECG monitoring (Holter), or an event recorder. At the native sinus rate) may reduce episodes of obstruc- times, correlation can be difficult because of the intermit- tive sleep apnea in these patients.18 Another form of tent nature of the . Electrophysiologic studies sinus node dysfunction is “chronotropic incompetence,” can be used to diagnose sinus node dysfunction, but their defined as an inadequate sinus rate response to stress or utility is limited by low sensitivity and specificity. exercise. Clinical studies have shown that rate-responsive Trained athletes often manifest physiologic sinus bra- pacing clinically benefits patients by restoring physi- dycardia with resting heart rates as low as 40 to 50 beats ologic heart rate during exercise.19 per minute. During sleep, these athletes may have a heart Although sinus node dysfunction is the most com- rate as low as 30 beats per minute with associated pauses mon reason for pacemaker implantation,19 permanent or type I second-degree AV block resulting in asystole pacing in these patients may not improve survival, as long as 2.8 seconds.16,17 These findings are caused by despite symptom reduction and improvement in qual- increased vagal tone and usually do not indicate the need ity of life.20,21 Atrial-based pacing may be preferable in for pacing. In the general population, monitoring dur- patients with sinus node dysfunction,22 although con- ing sleep may reveal sinus pauses of variable duration. flicting data have been reported in various studies. A The clinical significance of such pauses is uncertain. In recent randomized trial23 reported reduced risk of atrial patients with sleep apnea, treatment of the apnea fre- recurrence with dual-chamber pacing com- quently will reduce the occurrence of pauses. In turn, pared with ventricular-based pacing in patients with

1566 American Family Physician www.aafp.org/afp Volume 71, Number 8 ◆ April 15, 2005 Pacemaker Therapy TABLE 3 Principal Recommendations for Permanent Pacing in Chronic Bifascicular and Trifascicular Block

Class I cardiac death28 in patients with the long QT syndrome. Intermittent third-degree AV block. (B) However, the insertion of an implantable defibrillator Type II second-degree AV block. (B) in combination with overdrive pacing should be consid- Alternating bundle branch block. (C) Class IIa ered in high-risk patients. The main recommendations Syncope not demonstrated to be caused by AV block when for the prevention and termination of tachyarrhythmias 1 other likely causes have been excluded, specifically ventricular by pacing are listed in Tables 5 and 6. tachycardia. (B) Class IIb SYNCOPE AND NEURALLY MEDIATED SYNDROMES Neuromuscular diseases such as myotonic muscular dystrophy, Syncope is commonly encountered in clinical practice, par- Kearns-Sayre syndrome, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy with any degree of fascicular block, ticularly in older patients. It usually results from a sudden, with or without symptoms, because there may be unpredictable transient reduction of cerebral blood flow. Older patients progression of AV conduction disease. (C) are particularly prone to syncope because of age-related Class III physiologic changes that reduce their ability to adapt to Fascicular block without AV block or symptoms. (B) Fascicular block with first-degree AV block without symptoms. (B)

NOTE: Level of evidence is given in parentheses. TABLE 4 AV = atrioventricular. Recommendations for Permanent Pacing Adapted with permission from Gregoratos G, Abrams J, Epstein in Sinus Node Dysfunction AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and Class I antiarrhythmia devices: a report of the American College of Cardiol- Sinus node dysfunction with documented symptomatic ogy/American Heart Association Task Force on Practice Guidelines. bradycardia, including frequent sinus pauses that produce Circulation 2002;106:2148. 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 sinus node dysfunction. The main pacing recommenda- alternatives. (C) tions for this syndrome are listed in Table 4.1 Symptomatic chronotropic incompetence. (C) Class IIa PREVENTION AND TERMINATION OF TACHYARRHYTHMIAS Sinus node dysfunction occurring spontaneously or as a result of necessary drug therapy, with heart rate less than 40 beats Permanent pacing may prevent or terminate certain per minute when a clear association between significant ventricular and supraventricular arrhythmias in selected symptoms consistent with bradycardia and the actual patients,24,25 although it usually is not considered as presence of bradycardia has not been documented. (C) first-line therapy. Re-entrant rhythms (, re- Syncope of unexplained origin when major abnormalities of sinus node function are discovered or provoked in entrant paroxysmal supraventricular tachycardia, and electrophysiologic studies. (C) ) may be terminated by specific Class IIb pacing patterns available in special antitachyarrhythmia In minimally symptomatic patients, chronic heart rate less than devices. These devices may detect the tachycardia and 40 beats per minute while awake. (C) automatically initiate a pacing sequence to terminate it or Class III may require that the patient initiate activation by applica- Sinus node dysfunction in asymptomatic patients, including those in whom substantial (heart rate less tion of an external magnet. than 40 beats per minute) is a consequence of long-term Atrial synchronous pacing may prevent recurrences of drug treatment. re-entrant paroxysmal supraventricular tachycardia,26 Sinus node dysfunction in patients with symptoms suggestive of but catheter ablation is used more commonly and is bradycardia that are clearly documented as not associated with a slow heart rate. more effective. In patients with sinus node dysfunc- Sinus node dysfunction with symptomatic bradycardia caused tion and paroxysmal , one randomized by nonessential drug therapy. study23 demonstrated a 21 percent lower risk of atrial fibrillation recurrence with atrial-based pacing. Per- NOTE: Level of evidence is given in parentheses. manent pacing has been shown to prevent arrhythmias Adapted with permission from Gregoratos G, Abrams J, Epstein AE, Freed- in other situations. In some patients with the long QT man RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: syndrome, ventricular tachycardia may be prevented by a report of the American College of Cardiology/American Heart Association continuous pacing.27 A combination of beta blockade and Task Force on Practice Guidelines. Circulation 2002;106:2149-50. pacing can shorten the QT interval and prevent sudden

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Class I in control patients.32 Head-up tilt-table testing may be Sustained pause-dependent ventricular tachycardia, with or diagnostic in this condition and help the physician select without prolonged QT, in which the efficacy of pacing is thoroughly documented. (C) patients who may benefit by pacing therapy. Asymptom- Class IIa atic spontaneous or provoked prolonged sinus pauses in High-risk patients with congenital long-QT syndrome. (C) this group of patients have an excellent prognosis even Class IIb without pacing therapy.33 AV re-entrant or AV node re-entrant supraventricular tachycardia An uncommon cause of syncope is the hypersensitive not responsive to medical or ablative therapy. (C) carotid sinus syndrome, which is defined as syncope Prevention of symptomatic, drug-refractory, recurrent atrial or presyncope resulting from an extreme response to fibrillation in patients with coexisting sinus node dysfunction. (B) carotid sinus stimulation. As in vasovagal syncope, there Class III usually are vasodepressor and cardioinhibitory compo- None nents of this reflex. Therefore, before pacing therapy is recommended for carotid sinus hypersensitivity, the rel- NOTE: Level of evidence is given in parentheses. ative contribution of the two reflex components must be AV = atrioventricular. determined. The basic criterion for a diagnosis of hyper- Adapted with permission from Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 sensitive carotid sinus syndrome is asystole in excess of guideline update for implantation of cardiac pacemakers and anti- 3 seconds caused by sinus arrest or advanced AV block arrhythmia devices: a report of the American College of Cardiology/ as a result of carotid sinus stimulation.31 Pauses up to American Heart Association Task Force on Practice Guidelines. Circula- tion 2002;106:2151. 3 seconds during carotid sinus stimulation are consid- ered to be physiologic. Recent studies have reported that many older patients who sustain unexplained falls may have a hypersensitive carotid sinus,34 and that pacing sudden blood pressure drops. Syncope may be caused by therapy can reduce subsequent falls significantly.35 The a variety of cardiac and noncardiac conditions, and the main recommendations for pacing therapy in these syn- precise cause often is difficult to identify. In patients with dromes are listed in Table 7.1 heart disease, an arrhythmic cause should be excluded. Neurocardiogenic syncope and neurally mediated syndromes account for 10 to 40 percent of syncopal TABLE 6 episodes. Vasovagal syncope is one of the most common Principal Pacing Recommendations for Detection types of neurocardiogenic syncopal syndromes. Classi- and Termination of cally, it is preceded by a prodrome of nausea and diapho- resis and is associated with severe bradycardia. Episodes Class I usually are triggered by pain, anxiety, or stress. A family None history of syncope may be present. Class IIa Pacing therapy for patients with refractory neuro- Symptomatic recurrent supraventricular tachycardia that is cardiogenic syndromes associated with severe bra- reproducibly terminated by pacing in the unlikely event dycardia or asystole is controversial. Approximately that catheter ablation or drug therapy fail to control the arrhythmia or produce intolerable side effects. (C) 25 percent of patients have a predominant vasodepres- Class IIb sor response (loss of vascular tone and hypotension Recurrent supraventricular tachycardia or atrial flutter that is without significant bradycardia).29 These patients would reproducibly terminated by pacing as an alternative to drug not benefit from pacing. Another large subset have a therapy or ablation. (C) mixed vasodepressor and cardioinhibitory response Class III (i.e., sinus bradycardia, prolongation of the PR interval, Tachycardias frequently accelerated or converted to fibrillation by pacing or advanced AV block). Although some studies have shown significant reduction of syncopal episodes with NOTE: Level of evidence is given in parentheses. 30 pacing therapy, others have reported that pacing did Adapted with permission from Gregoratos G, Abrams J, Epstein not prevent syncope any better than drug therapy.31 In AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE a recent randomized trial of symptomatic patients with 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: a report of the American College of Cardiol- bradycardia, permanent pacing decreased the one-year ogy/American Heart Association Task Force on Practice Guidelines. recurrence rate of syncope to 19 percent in patients Circulation 2002;106:2150. treated with a pacemaker, compared with 60 percent

1568 American Family Physician www.aafp.org/afp Volume 71, Number 8 ◆ April 15, 2005 Pacemaker Therapy TABLE 7 TABLE 8 Recommendations for Permanent Pacing in Pacing Recommendations for Dilated Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope Class I Class I Class I indications for sinus node dysfunction or atrioventricular Recurrent syncope caused by carotid sinus stimulation; minimal block as described previously. (C) carotid sinus pressure induces ventricular asystole of more than Class IIa 3 seconds’ duration in the absence of any medication that Biventricular pacing in medically refractory, symptomatic New depresses the sinus node or atriventricular conduction. (C) York Heart Association class III or IV patients with idiopathic Class IIa dilated or , prolonged QRS interval Recurrent syncope without clear, provocative events and with (greater than or equal to 130 ms), left ventricular end-diastolic a hypersensitive cardioinhibitory response. (C) diameter greater than or equal to 55 mm, and ejection fraction less than or equal to 35 percent. (A) Significantly symptomatic and recurrent neurocardiogenic syncope associated with bradycardia documented Class IIb spontaneously or at the time of tilt-table testing. (B) None Class IIb Class III None Asymptomatic . Class III Symptomatic dilated cardiomyopathy when patients are A hyperactive cardioinhibitory response to carotid sinus rendered asymptomatic by drug therapy. stimulation in the absence of symptoms or in the presence Symptomatic ischemic cardiomyopathy when the is of vague symptoms such as dizziness, light-headedness, or amenable to intervention. both. (C) Recurrent syncope, light-headedness, or dizziness in the NOTE: Level of evidence is given in parentheses. absence of a hyperactive cardioinhibitory response. (C) Adapted with permission from Gregoratos G, Abrams J, Epstein AE, Situational vasovagal syncope in which avoidance behavior Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 is effective. (C) guideline update for implantation of cardiac pacemakers and antiar- rhythmia devices: a report of the American College of Cardiology/

NOTE: Level of evidence is given in parentheses. American Heart Association Task Force on Practice Guidelines. Circula- tion 2002;106:2154-5. Adapted with permission from Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and anti- arrhythmia devices: a report of the American College of Cardiology/ Pacemaker Selection and Patient Follow-Up American Heart Association Task Force on Practice Guidelines. Circula- tion 2002;106:2151-2. Pacemakers that maintain synchrony between atria and ventricles are particularly advantageous in older adults because the hemodynamics of aging include a reduction of ventricular compliance and increased dependence of HEART FAILURE AND DILATED CARDIOMYOPATHY ventricular filling on atrial contraction. Similarly, rate- Thirty to 50 percent of patients with advanced conges- responsive pacemakers are preferred in patients with tive heart failure have major intraventricular conduc- sinus node dysfunction and chronotropic incompetence. tion defects.36 These defects and especially complete left Although single-lead atrial-based pacing has the advan- bundle branch block have been shown to be indepen- tage of simplicity and lower cost, concerns about subse- dent predictors of mortality. Delayed activation of the quent development of AV block limit its application. A left as a result of left bundle branch block has detailed description of the types of pacemakers available been shown to produce significant dyssynchrony in left and indications for implantation of a particular device ventricular contraction and relaxation. The dyssyn- are beyond the scope of this review. chrony can be minimized by biventricular pacing. This Careful follow-up and monitoring of implanted device pacing technique has been shown in several prospective function are essential elements of care after a patient has randomized trials to reduce heart failure symptoms, and received a pacemaker. The frequency and method of improve hemodynamics and left ventricular indices of such follow-up depend on many factors, including the systolic function.37-39 However, there is no convincing age of the patient, number and severity of comorbid con- evidence that biventricular pacing improves survival. ditions being treated, and age of the device. Telephone Many patients with severe left ventricular dysfunction and in-person clinic follow-up can be equally effective who meet criteria for biventricular pacing currently are when performed appropriately. receiving devices that combine pacemaker and cardio- The author thanks Noah Schwartz, B.S., for assistance in the preparation verter-defibrillator modalities. It is fair to say that the of the manuscript. indications for biventricular pacing are still evolving. The author indicates that he does not have any conflicts of interest. Current pacing recommendations for dilated cardiomy- Sources of funding: none reported. opathy are listed in Table 8.1 Figure 1 used with permission from Gabriel Gregoratos,M.D.

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1570 American Family Physician www.aafp.org/afp Volume 71, Number 8 ◆ April 15, 2005