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AV block occurs when atrial conduction to the ventricle is blocked at a time when the AV junction is not physiologically refractory. This can be caused by conduction block in the atrium, AV node, and/or His-Purkinje system. Using His-bundle electrogram recordings, three anatomic sites of AV block can be identified: AV nodal, intra-Hisian, or infra-Hisian. Block at the AV nodal level implies a favorable prognosis, whereas block at or below the His-bundle level implies an unfavorable prognosis. Surface ECGs often provide adequate information to make a diagnosis regarding the site of the block, whereas intracardiac recordings are often necessary to define the level of the block at or below the His.
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Pathophysiology of Atrioventricular Block
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Transient or persistent AV block of varying degrees can occur in a variety of clinical situations (Table 86–7). Heightened vagal tone in athletes or during sleep may be associated with first-degree or type I second-degree AV block and occasionally even complete heart block. The AV block in these situations is usually preceded by slowing of the heart rate. Increased vagal tone during sleep is often associated with obstructive sleep apnea and may lead to high grade AV block and long pauses (Fig. 86–12). This is a common occurrence and pacemaker therapy is rarely indicated in this situation. Vagally mediated AV block may occur in response to various stimuli, such as carotid sinus hypersensitivity, coughing, swallowing, or micturition. Varying degrees of heart block have been described in a large variety of infectious diseases. Heart block associated with endocarditis may be transient or permanent. In patients with endocarditis and ring abscess, heart block may not resolve and pacing may be required. With Lyme disease, cardiac involvement may occur in 8% to 10% of patients. More than 50% of patients with cardiac involvement may develop advanced heart block requiring temporary pacing.21 Even complete AV block generally resolves in 1 to 2 weeks, and permanent pacing is seldom necessary.21 Chagas cardiomyopathy may be associated with persistent AV block.
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Mutations in the cardiac-specific Na+ channel gene (SCN5A) have been associated with PCCD, also referred to as Lev or Lenegre disease.50 It is a relatively common cardiac conduction disorder characterized by age-dependent progressive delay in the propagation of cardiac impulse through the His-Purkinje system with right bundle branch block (RBBB) or left bundle branch block (LBBB), eventually resulting in complete AV block. Patients with classic Lev disease demonstrate fibrosis within the proximal His bundle, whereas those diagnosed with Lenegre disease often demonstrate fibrosis within the more distal bundle branches and Purkinje fibers. SCN5A mutations can produce a variety of other phenotypes, including Brugada syndrome, congenital type 3 long QT syndrome, idiopathic ventricular fibrillation, congenital sick sinus syndrome, atrial fibrillation, and dilated cardiomyopathy. Dominantly inherited mutations in the transient receptor potential melastatin 4 (TRPM4) gene are associated with isolated cardiac conduction disease (ICCD), giving rise to AV conduction block.51 The TRPM4 channel mediates a Ca2+-activated nonelective cationic current (INSCca) involved in cardiac conduction, pacemaking, and action-potential repolarization. Andersen-Tawil syndrome (LQT7) is caused by mutations in the KCNJ2 gene encoding an inward rectifier potassium channel, Kir2.1. Patients may present with conduction abnormalities, such as AV block, bundle branch block, or intraventricular conduction delay. This syndrome is characterized by potassium-sensitive periodic paralysis, ventricular arrhythmias, and dysmorphic features.52 A variety of inherited heart disease has been recently reported to be associated with dilated cardiomyopathy and conduction system disease, including disorders of the nuclear envelope proteins lamin A and C.35 Lamin A/C is necessary for the structural integrity of the nucleus; in the presence of LMNA mutation, myocardial cells exposed to mechanical stress undergo cell damage. LMNA mutations also are associated with dilated cardiomyopathy, with AV conduction defects referred to as “laminopathy.”53
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Acute Myocardial Infarction
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AV block occurs in 12% to 25% of all patients with acute MI; first-degree AV block occurs in 2% to 12%, second-degree AV block in 3% to 10%, and third-degree AV block in 3% to 7%.54 Ischemic injury can produce conduction block at any level of the AV or intraventricular conduction system. Second-degree type I AV block occurs more commonly in inferior than anterior MIs. Inferior infarctions are often associated early on with increased vagal tone causing sinus bradycardia and AV block. Most patients are asymptomatic, and rarely type I AV block may progress to complete AV block. Second-degree type II AV block occurs in 1% of patients with acute MI and predominantly occurs in patients with anterior infarctions. The risk of progression to complete AV block is high in these patients. Complete AV block can occur in both inferior and anterior infarction. In inferior MI, the block is typically at the level of the AV node and the escape rhythm generally arises from the AV junction, with a narrow QRS and an escape rate of 40 to 60 beats/min. The prognosis in these patients is generally good, as the AV block resolves in almost all patients within a few days and almost always by 1 week. Complete AV block resulting from anterior infarction is usually at the His or infra-Hisian level, and the escape rhythm is from the distal Purkinje fibers or the ventricle, with a wide QRS interval and a rate of 20 to 40 bpm. Because of the coexisting extensive infarction and pump failure, AV block resulting from anterior infarctions are associated with high mortality. In patients with acute MI, temporary pacing is generally indicated in patients with complete AV block at any level, type II second-degree AV block, and in patients with type I second-degree AV block if associated with symptomatic bradycardia. Although the incidence of complete AV block in acute MIs has decreased after thrombolytic therapy, the mortality still remains high. In the current era of percutaneous coronary intervention for acute ST-segment elevation MI, the incidence of second or third-degree AV block is significantly lower (3.2% in a retrospective study of 2073 patients).55 In a recent study using the 2003 to 2012 National Inpatient Sample databases, the incidence of complete heart block complicating acute ST-segment elevation MI was 2.2% and the in-hospital mortality was higher in patients with complete heart block compared to those without complete heart block (20.4% vs 8.7%).56 The indications for permanent pacing in patients with acute MI are listed in Table 86–8. Patients with coronary artery disease and ischemic cardiomyopathy may develop persistent AV block. AV nodal block can occur transiently during episodes of ischemia, especially with Prinzmetal angina.
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A variety of uncommon autoimmune, oncologic, infectious, and iatrogenic disorders can also lead to heart block and are listed in Table 86–7. Certain neuromuscular disorders (myotonic dystrophy, Kearns-Sayre syndrome, peroneal muscular atrophy, Erb limb-girdle dystrophy, Emory-Dreifuss muscular dystrophy, and X-linked muscular dystrophies) may give rise to progressive and insidiously developing conduction disorders of the His-Purkinje system. Myotonic dystrophy and Kearns-Sayre syndrome are associated with high incidence of unpredictable and rapidly progressive conduction system disease.57 Complete heart block may occur after aortic or mitral valve replacement surgery and, rarely, after coronary artery bypass surgery. Preoperative RBBB and multivalve surgery involving the tricuspid valve were shown to be strong independent predictors of postoperative heart block requiring permanent pacemaker implantation. Complete AV block is more common after surgical procedures to correct ventricular septal defects, tetralogy of Fallot, AV canal defects, or myectomy for hypertrophic obstructive cardiomyopathy. Transcatheter aortic valve replacement (TAVR) is a rapidly evolving technology for severe, calcific aortic stenosis. The incidence of complete heart block requiring permanent pacemaker following TAVR is significantly higher than the approximate 5% following surgical aortic valve replacement.58,59 A recent meta-analysis of 41 studies including 11,210 patients undergoing TAVR showed that 17% required permanent pacemaker implantation (Fig. 86–13).60 Two TAVR devices are most currently in clinical use in North America: the Edwards SAPIEN valve (ESV, Edwards Lifesciences Corp., Irvine, CA) and the CoreValve Revalving system (CV, Medtronics, Minneapolis, MN). The rate of permanent pacemaker implantation ranged from 2% to 51% in individual studies (with a median of 28% for the CV and 6% for the ESV). The rate of permanent pacemaker requirement is lower for the ESV compared to CV. The higher rate with CV may be a result of the design (self-expanding as compared to balloon expanding) and lower position in the LV outflow tract.61 Recent changes to the ESV (S3) were noted to be associated with a higher pacemaker implantation rate attributable to lower positioning of the valve in the LV outflow tract.61 Male sex, preexisting conduction abnormalities (first-degree AV block, RBBB, left anterior hemiblock,) and intraprocedural AV block are predictors of need for permanent pacer post-TAVR.62 Recent meta-analysis also suggests that new-onset LBBB post-TAVR is a marker of an increased risk of cardiac death and need for a permanent pacemaker at 1-year follow-up.63
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Complete AV block can also occur in 0.5% to 2% of patients as a complication during radiofrequency catheter ablation of supraventricular arrhythmias, primarily AV node reentrant tachycardias and septal accessory pathways. Radiofrequency catheter ablation is also used to create permanent complete AV block in patients with paroxysmal and chronic atrial tachyarrhythmias (most frequently AF). This treatment option is reserved for the small group of patients in whom AV node–blocking drugs cannot control the heart rate or who are intolerant, unwilling, or unable to take drugs to maintain sinus rhythm or control the ventricular response during AF.
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Congenital heart diseases such as corrected transposition of great arteries, ostium primum atrial septal defects, and ventricular septal defects may be associated with complete heart block. Congenital complete AV block is a rare anomaly that results from abnormal embryonic development of the AV node and is not associated with structural heart disease in 50% of cases. Congenital complete heart block is also associated with maternal lupus erythematosus. When congenital complete heart block is detected in utero in a child with a structurally normal heart, the condition is frequently associated with intrauterine exposure to maternal autoantibodies to Ro and La (ie, neonatal lupus); this situation has a better prognosis than when congenital heart disease is present.64 Most children with isolated congenital complete AV block have a stable escape rhythm with a narrow complex. Pacing is generally indicated in children with complete heart block if the heart rate in the awake child is < 50 bpm or if associated with LV systolic dysfunction or ventricular arrhythmias. The indications for pacing in children, adolescents, and patients with congenital heart disease are outlined in Table 86–9.
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Anti-Ro/SSA-associated AV block has been described in adults. Currently available data suggest two possible forms of anti-Ro/SSA-associated AV block in adults: (1) an acquired form and (2) a late progressive congenital form.65 The acquired form is characterized by the presence of anti-Ro/SSA antibody in the affected subject. In these patients immunosuppressive therapy (methylprednisolone plus azathioprine) may normalize rhythm disturbances. By contrast, in the late progressive congenital form, anti-Ro/SSA antibodies are not detectable in the subjects while their mothers are seropositive. Immunosuppressive therapy has no clinical value in these patients. It is estimated that these two forms may represent at least 20% of all cases of isolated complete heart block of unknown origin in adults (10% of each form).
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Cardiac sarcoidosis should be considered in the differential diagnosis in a young patient (20-40 years old) presenting with complete heart block.66 Cardiac manifestations of sarcoidosis are present in at least 25% of patients with systemic sarcoidosis and can include Mobitz II, second-degree AV block, LBBB, RBBB, complete heart block (~30%), ventricular tachyarrhythmias, intracardiac masses, ventricular aneurysms, and dilated cardiomyopathy. Current expert consensus statement on arrhythmias associated with cardiac sarcoidosis recommends that in patients aged < 60 years presenting with unexplained Mobitz II second-degree AV block or complete heart block, further evaluation with high-resolution chest computed tomography and/or cardiac magnetic resonance imaging may be necessary to diagnose cardiac sarcoidosis.67 Patients with conduction system disease and evidence of cardiac or sarcoidosis in other organs should undergo implantation of either a dual-chamber pacemaker or defibrillator.
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Drug-induced bradycardia is a common and important clinical problem.68 Many common drugs, including β-adrenergic blockers, calcium channel antagonists, digoxin, class I and III antiarrhythmic drugs, tricyclic antidepressants, phenothiazines, lithium, and donepezil (a cholinesterase inhibitor used to treat Alzheimer disease), can cause AV conduction disturbances. If the AV block is caused by drug toxicity, is expected to resolve, and is unlikely to recur, pacemaker implantation is generally considered unnecessary, according to current guidelines. However, if AV block occurs in the setting of drug use or toxicity, and the block is expected to recur even after the drug is withdrawn, pacemaker implantation may be considered (class IIb indication). In the majority of patients presenting with presumed drug-induced AV block, discontinuation of the offending medications does not obviate the need for pacemaker implantation.69
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Paroxysmal AV block is defined as the sudden occurrence, during a period of 1:1 AV conduction, of a block of sequential atrial impulses resulting in a transient total interruption of AV conduction.70,71 It is thus the onset of a paroxysm of high-grade AV block associated with a period of ventricular asystole before conduction returns or a subsidiary pacemaker escapes. It may occur in variety of clinical conditions associated with vagal stimulation (eg, coughing, swallowing, vomiting, micturition, during abdominal pain) or in the setting of His-Purkinje conduction system disease. Idiopathic paroxysmal AV block is a distinct form of syncope characterized by a long history of recurrent syncope as a result of idiopathic paroxysmal AV block with long pauses, absence of cardiac and ECG abnormalities, absence of progression to persistent forms of AV block, and efficacy of cardiac pacing therapy.72 These patients show an increased susceptibility to exogenous adenosine. Permanent pacemakers are effective in these patients to prevent symptoms such as syncope.
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Electrocardiographic Manifestations
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First-Degree Atrioventricular Block
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Prolongation of the PR interval to > 200 ms constitutes first-degree AV block. It is most commonly caused by conduction delay within the AV node and occasionally caused by intra-atrial or infra-Hisian conduction delay. If the QRS duration is normal, the site of conduction delay is almost always within the AV node. If first-degree AV block occurs in the presence of bundle branch block, the conduction delay can be in the AV node (60% of cases), His-Purkinje system, or both. Patients with first-degree AV block have an excellent prognosis even when associated with chronic bifascicular block, as the rate of progression to third-degree AV block is low, and no specific therapy is indicated (Fig. 86–14).
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Second-Degree Atrioventricular Block
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Second-degree AV block is characterized by intermittent failure of conduction from the atria to the ventricles. If the AV block occurs with the atrial rate in the physiologic range, it is considered a primary arrhythmia. AV block in the setting of atrial tachyarrhythmias is generally a normal response. Based on the electrocardiographic patterns, second-degree AV block is classified into Mobitz types I and II.
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Second-Degree Atrioventricular Block of the Wenckebach Type (Mobitz Type I)
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Second-degree AV block of the Wenckebach type (Mobitz type I) is characterized by the following features: (1) progressive prolongation of the PR interval before a nonconducted P wave, (2) PR interval prolongation at progressively decreasing increments, (3) progressive shortening of R-R intervals, (4) pause encompassing the blocked P wave shorter than the sum of two P-P cycles, and (5) the last conducted PR interval before the blocked P wave longer than the next conducted PR interval (Fig. 86–15). Type I second-degree AV block often occurs with regularity leading to patterns of group beating. When type I second-degree AV block occurs in association with a normal QRS interval, block is almost always in the AV node. In the presence of a prolonged QRS interval, block may be in the AV node, His-Purkinje (rare), or both. Very long PR intervals are usually caused by a block in the AV node. Type I second-degree AV block occurs in a small percentage of normal people and, not uncommonly, in well-trained athletes. Most patients are asymptomatic, whereas some develop symptomatic bradycardia, near syncope, or occasionally syncope caused by progression to complete AV block.
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Mobitz Type II Second-Degree Atrioventricular Block
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Mobitz type II second-degree AV block is characterized by (1) constant P-P intervals and R-R intervals, (2) constant PR intervals before a nonconducted P wave, and (3) pause encompassing the nonconducted P wave equal to two P-P cycles. Type II AV block usually occurs in the presence of bundle-branch block and is almost always caused by a block in the His-Purkinje system (Fig. 86–16). Type II AV block rarely occurs in patients with normal QRS duration. Type II AV block frequently progresses to a complete AV block and may result in syncopal attacks.
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2:1 Atrioventricular Block
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In this form of second-degree AV block, every other P wave is not conducted, making it difficult to diagnose the level of AV block (Fig. 86–17). A 2:1 AV block pattern with normal QRS duration or with a very long PR interval generally suggests block in the AV node. A 2:1 AV block pattern in the presence of bundle branch block especially in the setting of normal PR interval favors block below the AV node, but is not diagnostic (Fig. 86–18). A prolonged electrocardiographic recording may sometimes reveal a transition to varying degrees of AV block (3:2 or 4:3), with type I or type II features that aid in the diagnosis. Rarely, Wenckebach conduction may be noted in the His-Purkinje system. Intracardiac recordings with a His-bundle catheter are sometimes necessary to determine the site of the block (Fig. 86–19). In patients with a 2:1 AV block, vagal maneuvers are helpful in diagnosing the level of AV block. Carotid sinus stimulation may worsen the degree of block if it is in the AV node, whereas slowing of the sinus rate may paradoxically improve the ratio of AV conduction and increase ventricular rate if the block is located in the His-Purkinje system. Similarly, atropine improves AV nodal conduction, but the increased sinus rate may worsen the ratio of AV conduction in patients with His-Purkinje block, resulting in worsened bradycardia. Hence atropine should be used with caution in patients with a 2:1 AV block and bundle branch block where His-Purkinje disease is strongly suspected.
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High-Grade Atrioventricular Block
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When two or more consecutive atrial impulses do not conduct to the ventricle, it is defined as high-grade AV block. It may be associated with a junctional or ventricular escape rhythm. Occasionally, runs of consecutive atrial impulses may fail to conduct to the ventricles for up to 10 to 20 s with or without an escape rhythm, resulting in ventricular asystole and syncope. The block is usually initiated by a conducted or blocked atrial or ventricular premature beat. The block persists until terminated by an escape beat. Unless a clearly defined reversible etiology is identified, permanent pacing is indicated.
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Third-Degree Atrioventricular Block
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Complete or third-degree AV block is characterized by failure of all P waves to conduct to the ventricle. This results in complete dissociation of P waves and QRS complexes. Complete AV block may occur as a result of block in the AV node or at the His-Purkinje level. In patients with block at the AV node level, the escape rhythm is usually junctional, with a narrow QRS complex (unless associated with preexisting bundle branch block), at rates of 40 to 60 bpm (Fig. 86–20). In complete heart block resulting from His-Purkinje disease, the escape rhythm is ventricular in origin, with a wide QRS interval and at rates of 20 to 40 bpm (Fig. 86–21).
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Atrioventricular Dissociation
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This rhythm is characterized by atrial and ventricular activity independent of each other. AV dissociation may be secondary to AV block (complete heart block) or physiologic refractoriness. AV dissociation can occur when the sinus rate is slower than the secondary junctional or ventricular pacemaker as in patients with sinus bradycardia. In contrast, AV dissociation can also occur in the presence of normal sinus rhythm and accelerated junctional (junctional tachycardia) or ventricular (VT) rhythm with retrograde conduction block. In patients with complete heart block, the atrial rate is faster than the ventricular rate, whereas in AV dissociation, the ventricular rate is faster than the atrial rate. Although AV dissociation is present in complete heart block, it is not synonymous. AV dissociation is usually a manifestation of another rhythm abnormality, such as complete heart block, sinus bradycardia, or VT. Treatment is usually directed toward the underlying cause.
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Clinical Presentation
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Symptoms in patients with AV conduction abnormalities are generally caused by bradycardia and loss of AV synchrony. Patients with significantly prolonged PR intervals may behave in a similar fashion to patients with pacemaker syndrome because of loss of AV synchrony. In patients with structural heart disease and LV dysfunction, this may result in worsening of heart failure. Symptoms caused by more advanced AV block may range from exercise intolerance, easy fatigability, dyspnea on exertion, dizzy spells, and near syncope to frank syncope. In patients with paroxysmal or intermittent complete heart block, these symptoms are episodic, and routine ECGs may not be diagnostic. Children and adolescents with isolated complete heart block may be generally asymptomatic, whereas some may develop symptoms later as adults because of chronotropic incompetence. Other late signs and symptoms include the development of congestive heart failure and nonsustained VT. Children with complete heart block associated with structural heart disease are symptomatic very early on and have an increased risk for sudden death.
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Diagnostic Evaluation
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The prognosis and treatment of AV block depends on its association with symptoms and the level of AV block. Routine 12-lead surface ECGs adequately establish the diagnosis of varying degrees of AV block in many patients. Analyzing the PR interval, QRS duration, Wenckebach phenomenon, and ventricular rates on the surface ECG provides important clues to the level of AV block. In certain situations such as 2:1 AV block, additional maneuvers may be necessary to establish the level of AV block. Responses to carotid sinus massage, atropine, and exercise are often very helpful.
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In patients with complete heart block at the level of the AV node, the resultant junctional escape rhythm usually accelerates with exercise in contrast to the ventricular escape rhythm with infranodal block, which usually remains unchanged. Early studies using His bundle recordings have suggested that intra-His block contributes only 15% to 20% of patients with infranodal AV block.73,74 However, recent observations suggest that in the majority of patients with infranodal AV block, the conduction disease is in the main His bundle, suggesting intra-His block.4,75 In a consecutive series of 100 patients, AV nodal block was noted in 46% of the patients and infranodal (HV) block was observed in 54% of the patients.4 Presence of split His potentials, narrow QRS in the setting of HV block, identification of distal His potential, and correction of His-Purkinje conduction by permanent His bundle pacing were used to identify a high (76%) percentage of patients with intra-His block (Fig. 86–22).
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In patients with paroxysmal symptoms of near syncope or syncope and no significant conduction abnormalities on the surface ECG, prolonged electrocardiographic monitoring with 24- to 48-hour Holter recordings or 30-day event monitors may be helpful. Newer event monitors with automatic detection algorithms and cellular technology have increased the yield of these monitors. An ILR may be necessary to establish the diagnosis, particularly in patients with infrequent symptoms. Electrophysiology study is indicated in patients with syncope or near syncope in whom high-grade AV block is suspected as the cause. In patients with structural heart disease, in addition to AV conduction disease, VT can also be a major etiology for syncope, and electrophysiology study can be very useful in establishing the diagnosis.
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Identifying transient or reversible causes for AV conduction disturbances is the first step in management. Withdrawal of any offending drugs, correction of any electrolyte abnormalities, or treatment of any infectious processes should be considered before permanent pacing therapy. If the drugs causing AV block are essential for treatment of other medical conditions, permanent pacing may be considered. However, it has become increasingly realized that many patients with AV block believed to be precipitated by drugs may develop recurrent heart block in follow-up even after discontinuation of the offending agent(s).68 In patients with advanced AV block and hemodynamic decompensation unresponsive to drug therapy such as atropine or isoprenaline, as in digitalis toxicity, hyperkalemia, acute anterior MI, or Lyme myocarditis, temporary pacing should be instituted until AV block resolves or permanent pacing can be initiated. Temporary pacing can be accomplished by transcutaneous pacing systems in those patients at low-to-moderate risk for developing complete heart block or in patients with complete heart block and hemodynamically stable escape rhythms. Transcutaneous pacing for prolonged periods is very uncomfortable and transvenous pacing should be performed in patients with need for continuous active pacing.
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Permanent pacemaker implantation is indicated in most patients with advanced heart block associated with symptoms. Permanent pacemakers are also indicated in asymptomatic patients with complete heart block and infra-Hisian second-degree AV block. Permanent pacing has clearly been shown to decrease mortality in patients with advanced heart block and syncope.76 The indications for pacing in children with AV block and in adults with acquired heart block are described in Table 86–9 and Table 86–10, respectively.
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Most patients with AV block require dual-chamber pacemakers, because this mode of pacing maintains AV synchrony and prevents development of pacemaker syndrome. In patients with associated sinus node dysfunction, dual-chamber pacemakers with a rate-responsive function (DDDR) are the preferred mode of choice. In patients with normal sinus node function and AV block, VDD pacing using a single lead with a series of electrodes for atrial sensing and ventricular pacing and sensing is an ideal mode of pacing, because it provides AV synchrony and rate responsiveness and is superior to single-chamber VVI pacing. In patients with chronic atrial fibrillation and bradycardia, rate-responsive single-chamber ventricular pacing (VVIR) is adequate. Early studies of comparison of pacing modes in a small number of patients with AV block had shown that physiologic pacing (DDD or VDD) enhanced survival compared with VVI pacing.75,77 However, prospective, randomized, large-scale trials showed that dual-chamber pacing provided little benefit over ventricular pacing for the prevention of death (see Table 86–4). The incidence of pacemaker syndrome was as high as 26% in patients with ventricular pacing, necessitating cross-over to dual-chamber pacing in the pacemaker selection in the elderly trial.35
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Growing recognition of the long-term adverse effects of RV apex pacing has stimulated interest in strategies to promote physiologic pacing and to minimize or eliminate the deleterious effects.78,79 There is controversy, however, regarding the optimal ventricular pacing sites and approach in patients undergoing permanent pacemaker implantation for AV block in whom ventricular pacing cannot be avoided.80 Some investigators advocate LV or biventricular pacing, whereas others suggest a role for selective-site RV pacing. Alternative RV pacing sites (ie, non-RV apex), including the His bundle, RV septum, RV outflow tract, and dual-site right ventricle, have been investigated, but the benefits of alternative-site pacing remain unresolved.81,82 In a recently published protect-pace study that randomized 240 patients with high-grade AV block to high septal or RV apical pacing (> 90% RV pacing), there was no significant difference in intrapatient change in LV ejection fraction (LVEF) between the two groups.83
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Current guidelines indicate that cardiac resynchronization therapy can be useful for patients with symptomatic heart failure and LVEF ≤ 35% who are expected to require frequent ventricular pacing (> 40%) after device implantation. However, the role of biventricular pacing in patients with AV block and a normal LVEF or only modest depression of LV function remains unsettled. The Biventricular Versus RV Pacing in Heart Failure Patients With Atrioventricular Block (BLOCK HF) study was a prospective trial that randomized 691 patients with mild-to-moderate heart failure (NYHA Class I, II, or III), LV dysfunction (LVEF ≤ 0.50), and AV block to RV pacing versus biventricular pacing with an average follow-up of 37 months.84 Patients randomly assigned to biventricular pacing had a significantly lower incidence of the primary outcome (time to death from any cause, an urgent care visit for heart failure that required intravenous therapy, or a 15% or more increase in the LV end-systolic volume index) over time than did those assigned to RV pacing (hazard ratio, 0.74; 95% credible interval, 0.60 to 0.90). The Biventricular Pacing for Atrioventricular Block to Prevent Cardiac Desynchronization (BioPace) trial85 randomized 1810 patients with AV block (mean age 73.5 years) to either RV pacing (n = 908) or biventricular pacing (n = 902) and after a mean follow-up of 5.6 years, the groups had a similar rate of the composite end point that included time-to-death or first hospitalization as a result of heart failure, with a nonsignificant trend in favor of biventricular (hazard ratio 0.87; P = .08). It is unclear which patients, if any, would benefit from biventricular pacing in the setting of normal LV function.
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The His bundle is an ideal RV stimulation site from a hemodynamic standpoint. However, the technical challenge of long-term implementation of permanent His bundle pacing (HBP) had thus far been a major obstacle to its reliable application in routine clinical practice. By preserving normal electrical activation of the ventricles, HBP prevents ventricular dyssynchrony and its long-term consequences (Fig. 86–23). Recent studies have shown that permanent HBP is technically feasible and may be safe in routine clinical practice.86,87 Preliminary data suggest that permanent HBP is associated with an improvement in exercise capacity, myocardial perfusion, ventricular synchrony, and LVEF compared to RV pacing.88,89
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Conduction disturbances that occur at various levels of the branches of the His-Purkinje system are described as bundle branch block or intraventricular conduction defects. In patients with isolated chronic RBBB or LBBB, the progression to advanced AV block is rare. Patients with bifascicular block (RBBB and left anterior or posterior fascicular block) or LBBB and left axis deviation have a 6% annual incidence of progression to complete heart block.90 In patients with acute MI, the development of new bifascicular block and first-degree AV block is associated with a very high risk (42%) for progression to high-grade AV block. These patients are generally recommended to undergo prophylactic temporary pacing. Alternating bundle branch block, even in asymptomatic patients, is a sign of advanced conduction disturbance in the His-Purkinje system and is considered a class I indication for permanent pacing. In patients with bundle branch block, His-bundle recordings can occasionally be helpful in identifying patients at high risk for progression to high-grade AV block. The incidental findings of markedly prolonged HV interval (> 100 ms) or atrial-pacing–induced infra-Hisian block91 that is not physiologic during an electrophysiology study are considered to indicate high risk for progression to advanced AV block, and prophylactic permanent pacing is recommended (Table 86–11). Intraventricular conduction disturbances are usually associated with significant structural heart disease, especially dilated (ischemic or idiopathic) cardiomyopathies, and are a marker of poor prognosis both in terms of advanced heart failure and increased mortality in these patients. LBBB in patients with cardiomyopathy is associated with significant ventricular dyssynchrony, worsening heart failure, and increased mortality. Biventricular pacing in these patients has been shown to improve heart failure and decrease mortality.92,93 In a subgroup of patients with nonischemic cardiomyopathy, biventricular pacing can normalize LV function (hyperresponders), raising the possibility of LBBB-induced cardiomyopathy.94 Recent evidence also suggests that bundle branch block is often caused by to disease in the proximal His bundle and may be amenable to correction by permanent HBP.95,96
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