HEART BLOCK

HEART BLOCK

  1. 1
    Current Diagnosis

    • Assess risk for heart block in the absence of symptoms or heart block on electrocardiogram (ECG).

    •   Review cardiac or systemic disorders associated with cardiac conduction disease (CCD), ECG pattern, family history, maternal antibodies, cardiac interventions, and surgery.

    •   Evaluate documented asystole or bradycardia due to heart block.

    •   Classify heart block: transient, recurrent, progressive, permanent.

    •   Grade signs and symptoms: none, mild, severe.

    • Evaluate signs or symptoms of possible transient heart block with no documentation.

    •   Establish temporal pattern: recent versus remote onset, solitary versus recurrent, daily, weekly, monthly, yearly.

    •   Grade signs and symptoms: none, mild, severe.

    •   Document rhythm during symptoms: telemetry monitoring, Holter monitor, external loop recorder, implantable recorder.

  2. 2
    Current Therapy

    •   Methods of heart rate support:

    •   Immediate: intravenous catecholamines, atropine, or aminophylline1; transcutaneous pacing.

    •   Short term: transvenous temporary pacing.

    •   Long term: permanent pacemakers.

    •   Pacemaker configuration:

    •   Number of leads: 1, 2, 3, 4.

    •   Lead locations: right atrial appendage, Bachman’s bundle, right ventricular apex, outflow tract, left ventricle, coronary sinus.

    •   Programming to minimize ventricular pacing: manufacturer dependent.

    1 Not FDA approved for this indication

    Heart block refers to block or delay of electrical propagation between the atria and ventricles. It is a form of cardiac conduction disease (CCD), which applies more generally to disorders of electrical impulse formation or propagation anywhere along the cardiac conduction system from the sinus node to the ventricular myocardium. Heart block or CCD may present as a syndrome, as an electrocardiographic (ECG) pattern, or as a mechanism of serious signs and symptoms such as sudden death or syncope. Pacemaker therapy is an effective treatment, but it is associated with significant short- and long-term complications. This underscores the importance of recognizing preventable and reversible causes of heart block for accurate targeting of permanent pacing. Risk stratification of patients with heart block, assessment of the benefits and risks of the therapeutic options, and patient education and guidance are largely in the domain of heart rhythm specialists. However, heart block may be encountered unexpectedly in any patient during any clinical encounter. Furthermore, some patients may require evaluation in the absence of known cardiac disease because of increased risk of CCD, or increased risk of CCD in family members or future children. A basic understanding of heart block may be useful in order to initiate emergency treatment and to recognize patients who warrant further evaluation or specialist referral.

  3. 3
    Epidemiology

    The prevalence and incidence of heart block are difficult to establish because they are strongly dependent on the demographic and clinical characteristics of the population sample. The prevalence is higher among the elderly and those with cardiovascular disease. First-degree heart block, defined as prolongation of the PR interval > 200 ms on ECG, occurs in the population setting with prevalence of 0.7% to 2% in the young and up to 14% in the elderly. Higher degrees of heart block can be expected to be less common but similarly associated with age and underlying cardiovascular disease. In a study of the Framingham population, the prevalence of first-degree heart block was 1.6% and was associated with an incidence of pacemaker implantation of 59 per 10,000 person-years in persons with a PR interval > 200 ms compared to 6 per 10,000 person-years in persons with a PR interval < 200 ms. Approximately 36% of the pacemakers were for high-grade atrioventricular (AV) block.

  4. 4
    Risk Factors

    Patients with genetic or acquired CCD and patients subject to trauma or surgical procedures that can damage the conduction system are at increased risk for developing symptomatic advanced heart block. In the Framingham population, subjects with first-degree AV block had an increased risk of mortality, atrial fibrillation, and pacemaker implantation. However, the vast majority with risk factors never develop symptomatic heart block and have not been shown to benefit from intense monitoring or prophylactic pacemaker placement. The few possible exceptions are discussed below.

  5. 5
    Pathophysiology

    The function of the cardiac conduction system is to initiate and coordinate cardiac contraction in order to circulate blood according to physiologic needs. Electrical activation is initiated by pacemaker cells of the sinus node regulated by the autonomic nervous system. Unlike conduction in common electrical circuits in which electrons flow along a conductor according to the voltage gradient, electrical activity in cardiac cells propagates from segment to segment of the cell membrane in cardiac myocytes (myocardial cells) and in specialized cardiac conduction cells. Energy-requiring ion pumps maintain an electrochemical gradient across the insulating cell membrane.

    Electrical activity opens voltage-sensitive ion channels causing regenerative electrical activity as ions shift along their electrochemical gradient. Electrical activity in a single cell excites several adjacent cells via gap junctions. This cascade effect makes it possible for a single cell impulse to spread rapidly throughout the myocardium to enhance synchronous contraction. This also provides a safety mechanism in that each myocardial cell can be activated by many electrical paths. In addition, specialized conduction cells exhibit automaticity (impulse formation). Although normally latent because normal activation inhibits spontaneous discharge, when the normal impulse is blocked, discharges from these subsidiary physiologic pacemakers provide vital heart rate support.

    Block of electrical activation can occur due to failure of any step in the process, for example, lack of metabolic energy, electrolyte imbalance, inflammatory disruption of the membrane, block of ion channels by drugs, or interference with gap junction function due to infiltration of fibrous tissue (Table 1). Because of the extensive redundancy and interconnectivity and because of the capacity to compensate for injury by electrical and anatomic remodeling, there may be extensive damage before signs or symptoms of heart block occur. Regions of the heart where there are fewer alternative paths for electrical activation, such as proximal portions of the His-Purkinje system where all conducting fibers are confined to a relatively small area, are more vulnerable to complete block. Subsidiary pacemakers sometimes fail to provide adequate rate support when heart block occurs because of preexisting injury. If the patient survives an episode of heart block, there is a possibility for recovery due to remodeling.

    However, remodeling can be maladaptive and result in an adverse long-term outcome by further conduction system damage, by left ventricular dysfunction, and by bradycardia-induced ventricular tachyarrhythmias (VTAs). The mechanisms of bradycardia-induced VTAs are not known, but bradyarrhythmias precipitate torsades de pointes, a specific form of VTA, in the presence of drugs that block potassium channels, electrolyte disturbances, certain genetic abnormalities of ion channel function, heart failure, and myocardial hypertrophy. A comprehensive list of drugs that may account for bradyarrhythmia-related ventricular arrhythmias is available at www.torsades.org.

    Table 1

    Mechanisms of Conduction Disturbances (Examples)

    Although there are many potential causes of heart block, the pathophysiology is not known for the vast majority of cases because there are no tests that allow detailed structural or functional examination in patients. By the time of death, morphologic examination may reveal only nonspecific changes such as fibrosis.

    Instead, most etiologies are inferred by history of recent or past exposures (e.g., trauma or radiation), concomitant disorders (e.g., muscular dystrophy, cardiac sarcoidosis), abnormal test results (e.g., Lyme disease) or family history (e.g., SCN5A sodium channel mutations) (Table 2). Because most etiologies cannot be verified, the clinician must remain open to alternative explanations and accept the likelihood of multiple contributors.

    Table 2

    Etiologies of Heart Block

    Some patients, usually young, otherwise healthy individuals, present with prolonged asystole due to heart block but have no other detectable abnormalities and have excellent outcomes in the absence of intervention beyond counseling. This suggests that autonomic influences alone can cause prolonged heart block and suppression of subsidiary pacemakers. It is not known if such responses result from an abnormality or an exaggerated normal reflex. However, the identification of such patients is important because the majority can be managed without pacemakers.

  6. 6
    Prevention

    Prevention of heart block is a challenge for the future. Some instances can be prevented by treatment of inflammatory disorders that cause heart block, such as Lyme disease or cardiac sarcoid. Other individuals who should be identified are those with conditions that place them, their relatives, or their unborn children at risk for heart block. This includes patients and family members with genetic disorders associated with heart block. Genetic testing and counseling may be appropriate in some patients with a family history of CCD. Neonatal lupus syndrome is a rare disorder with a high mortality rate and risk of permanent complete heart block in survivors. This occurs in pregnant women with anti-Ro/SSA and/or anti-La/SSB antibodies. Some such women have autoimmune disorders such as systemic lupus erythematosus and Sjögren’s syndrome, but many are asymptomatic. Members of this group may benefit from counseling and anticipatory evaluation and treatment of offspring. Although controversial, fetal monitoring of pregnant women with anti-Ro/SSA and/or anti-La/SSB antibodies and treatment of those with signs of fetal conduction system involvement have been recommended. It should be recognized that with current methods the vast majority of heart block events cannot be predicted or prevented and the vast majority of persons with risk factors never develop symptomatic heart block.

     

  7. 7
    Clinical Manifestations

    Most of the symptoms experienced by patients with heart block are common and nonspecific, including syncope, lightheadedness, fatigue, and dyspnea. Asystole or profound bradycardia may cause syncope, death, or other manifestations of hypoperfusion. Rarely, first-degree AV block results in significant symptoms (e.g., fatigue, palpitations, chest fullness) probably due to atrial contraction against a partially closed mitral valve.

  8. 8
    Diagnosis

    Because various arrhythmias and other cardiac and noncardiac disorders may be responsible for similar symptoms, it is important to identify the cause. An ECG recording of asystole or bradycardia due to heart block at the time of symptoms strongly suggests a causal relationship, but this is usually difficult to accomplish as the symptoms are often transient and infrequent. Absence of arrhythmias at the time of symptoms is also helpful in excluding heart block as the cause. Asymptomatic heart block is not infrequent. Cardiac conduction disturbances are classified by the pattern of ECG complexes. A normal 12-lead ECG lessens the probability of conduction disturbances due to structural changes but it does not eliminate the possibility of transient third-degree block due to reversible functional effects such as intense vagal activity or ischemia. Significant disease of the His bundle may be electrocardiographically silent, but more often concomitant distal disease is evident in the form of fascicular or bundle branch block or a nonspecific intraventricular conduction delay. In a patient with syncope, the presence of bifascicular block raises the possibility of transient third-degree block as the mechanism and of progression to permanent complete block.

    Most patients with conduction disorders are not symptomatic and do not progress to complete block. However, the combination of right bundle branch block (RBBB) and left posterior fascicle block has a greater tendency to progress to complete block than the more common RBBB and left anterior fascicle block. Nevertheless, conduction disturbances of the His-Purkinje system should not be assumed to be responsible for syncope or cardiac arrest because they are relatively common in patients with cardiovascular disorders that cause syncope or cardiac arrest due to other mechanisms. Conduction disturbances can cause dyssynchronous contraction and result in adverse remodeling. In addition, they can mask or mimic the ECG signs of myocardial infarction. Alternating bundle branch block refers to a changing ECG pattern in which both RBBB and left bundle branch block are observed or when the bifascicular block pattern switches between the anterior and posterior fascicle involvement. This pattern is considered a harbinger of complete block and warrants continuous monitoring and evaluation for permanent pacemaker implantation.

  9. 9
    Differential Diagnosis

    The challenge in second- and transient third-degree AV block is distinguishing between block in the AV node, which is often functional and reversible, and infranodal block, which often progresses to permanent complete heart block. ECG clues that block is in the AV node include normal QRS duration (< 100 ms), type I (Wenckebach) pattern, PR prolongation before blocked impulses and PR shortening after pauses, occurrence during enhanced vagal activity (e.g., sleep), narrow QRS escape complexes, and no factors favoring infranodal block. ECG clues for infranodal block include prolonged QRS duration (≥ 120 ms), type II pattern, and escape QRS complexes broader than intrinsic complexes. Type II second degree AV block is almost always due to block in the His-Purkinje system. Other second- degree AV block ECG patterns have poor sensitivity and specificity for site of block.

    Unsustained polymorphic ventricular tachycardia is an ominous sign in any context and may result from a variety of cardiac, metabolic, and autonomic abnormalities. However, in the presence of heart block it suggests that heart rate support may be necessary to prevent sustained VTA. QT prolongation and post-pause U-wave accentuation should be sought as other harbingers of bradycardia- related VTA.

    The importance and value of ECG documentation of heart block cannot be overemphasized. ECGs are subject to artifact and may be misleading when standards for acquisition and analysis are not followed. Multiple tracings of suspicious events should be obtained in multiple leads when possible. A 12-lead simultaneous rhythm recording mode is available on most modern ECG machines and should be used when continuous recordings are obtained to document arrhythmias.

    Clinicians encounter heart block in three general contexts. For the patient with documented heart block, the clinician selects therapy based, in part, on whether or not the arrhythmia is permanent or likely to recur. There are currently no tests that provide direct information about the pathologic state of the AV conduction system. Instead, these outcomes must be inferred from functional assessment, that is, from the ECG or electrophysiologic testing. Other indirect sources such as coronary angiography, magnetic resonance imaging, nuclear imaging, and myocardial biopsy, as well as a large number of specific laboratory tests, are often helpful for identifying disorders that may be causative or associated with heart block and that may affect the choice of treatment.

    Another common context is the patient with symptoms for whom the objective is to verify or exclude heart block as the mechanism by correlating the cardiac rhythm with symptoms. Real-time monitoring (e.g., in-patient telemetry) is used for patients who might require immediate access to drugs or pacing devices to prevent or terminate asystole or bradycardia-dependent VTA. Holter monitoring is useful for patients who have very frequent events (at least 1 every 24 hours), and they are useful for capturing asymptomatic rhythm disturbances. External recorders are applied for a month or longer and are very helpful to associate rhythm abnormalities with symptoms and to rule out a rhythm disorder as the cause of symptoms in patients with at least one event per month. Patients with infrequent events may be candidates for implantable loop recorders, which monitor for greater than a year. Modern monitors will provide a permanent record of arrhythmias on activation by the patient or by a detection algorithm.

    Electrophysiologic studies allow precise measurements of AV node and His-Purkinje system function and can provide definitive information regarding the site of block if the conduction disturbance occurs during the study. Additional tests have been developed that “stress” the AV conduction system, including rapid atrial and ventricular pacing and administration of drugs such as procainamide and disopyramide (Norpace). The provocation of heart block is assumed to indicate a propensity for spontaneous AV block.

    Unfortunately, the sensitivity is low and a negative test does not imply a low risk of future episodes. Electrophysiologic studies have the additional advantage of providing immediate test results, as well as providing the results of programmed stimulation for provocation of supraventricular and VTAs, which may be included in the differential diagnosis.

  10. 10
    Therapy

    The object of the evaluation and management for heart block is to prevent death and morbidity by (1) heart rate support in patients with poorly tolerated bradycardia; (2) monitoring and standby heart rate support in patients at high risk for asystole or severe bradycardia; (3) identifying and treating reversible causes of heart block; (4) identifying patients at high risk for sudden death, syncope, or recurrent symptoms; and (5) selecting and implanting the appropriate rate support system as soon as safety permits.

    Advanced cardiac life-support guidelines apply to the patient who is unresponsive or severely compromised by heart block. However, heart block is rarely the primary problem. Therefore, evaluation and treatment of other disorders should continue while efforts to obtain the appropriate heart rate are underway.

    The initial evaluation should include a detailed history and physical examination and review of current and previous ECGs and rhythm strips to determine if heart block is present or occurred in the past and if there were symptoms or other evidence of hemodynamic compromise. Basic laboratory tests (electrolytes, metabolic panel, cardiac biomarkers, thyroid function, blood count, and coagulation studies) and basic imaging (chest x-ray and echocardiography) are usually appropriate. The patient should then be stratified for the appropriate level of care: (1) the unstable patient who requires ongoing evaluation and treatment in an intensive care setting, (2) the stable patient at high risk for asystole or complications who needs temporary transvenous pacing or other invasive procedures, (3) the patient at moderate risk who requires continuous monitoring and standby noninvasive heart rate support measures, (4) the patient at low risk who requires rapid but not immediate access to heart rate support measures that hospital monitoring provides, and (5) the patient at low risk who can be evaluated and managed as an outpatient. Additional testing and procedures may be necessary to determine the etiology of heart block and to determine if there is a

    significant risk of future adverse events.

    Determination of the need for long-term heart rate support, as well as other issues that may affect implantable device selection (e.g., risk for VTAs), should be accomplished as soon as possible because the risk of complications and anxiety associated with temporary heart rate support measures increases over time. Major societies have developed guidelines for implantable rhythm management devices (http://www.cardiosource.org/Science-And-Quality/Practice-Guidelines-and-Quality-Standards.aspx; http://www.escardio.org/guidelines-surveys/esc- guidelines/Pages/GuidelinesList.aspx). The reasons for the selected therapy, including the rationale for any deviation from established guidelines, should be documented and provided to the patient. This will reduce future confusion or misunderstanding about the original rationale for implantation that can affect management of patients with device complications, recalls (safety alerts), and those with a compelling need for device upgrade or explanation.

    Patients with acute coronary syndromes require special consideration. The incidence of heart block in patients with myocardial infarction based on creatine phosphokinase as the marker of necrosis is approximately 10%. Although the incidence is probably lower using more sensitive markers such as troponin, heart block is still likely to be associated with increased in-hospital mortality due to larger infarct size. Tachycardia and high blood pressure increase myocardial oxygen consumption. Therefore, overcorrection of heart rate and blood pressure should be avoided and ischemia should be relieved by reperfusion as soon as possible. Studies in the prethrombolytic era did not demonstrate a benefit in mortality with prophylactic temporary transvenous pacing, and complications were frequent. The risks of transvenous insertion may be higher in patients requiring administration of thrombolytics and other anticoagulants.

    Catheter-based revascularization methods should be given strong consideration because of established effectiveness, the possible avoidance of thrombolytic drugs, and because transvenous temporary pacing, if needed, is readily and safely accomplished during the procedure. Suggestions for standby temporary pacing (Table 3) should take into consideration the risks of transvenous pacing based on local circumstances (experience, fluoroscopic guidance, insertion site, use of anticoagulants, etc.). Most conduction disturbances associated with myocardial ischemia or infarction resolve quickly but can persist for days or weeks. The need for permanent pacemaker implantation as a consequence of myocardial infarction is rare, and prophylactic pacemaker implantation in high-risk subsets has not been shown to reduce mortality. Guidelines for temporary and permanent pacing in acute myocardial infarction have been published (http://www.cardiosource.org/Science-And-Quality/Practice- Guidelines-and-Quality-Standards.aspx;http://www.escardio.org/guidelines-surveys/esc- guidelines/Pages/GuidelinesList.aspx).

    Table 3

    Suggestions for Temporary Pacing in Acute Myocardial Infarction

    Abbreviations: AV = atrioventricular; LAFB, LPFB = left anterior, left posterior fascicle block; LBBB, RBBB = left, right bundle branch  block.

    Selection of the correct therapeutic approach balances the risks and benefits of therapy against the risks of heart block for both immediate and long-term management. Catecholamines (dobutamine, dopamine, epinephrine, isoproterenol [Isuprel]) are useful for emergency, temporary, and standby heart rate support. The standby mode is accomplished by a prepared infusion at the bedside. To avoid underdoses or overdoses at the time of sudden symptomatic heart block, the optimal dose can be established in advance by test doses starting at low infusion rates. Atropine (0.5 mg every 3–5 minutes, with a maximum dose of 0.04 mg/kg or total of 3 mg) may be useful for treatment or pretreatment of patients who develop heart block at the level of the AV node in the context of elevated vagal tone (e.g., in association with nausea or endotracheal tube suction). Atropine should be avoided in patients with infranodal AV block because prolonged asystole sometimes occurs due to more frequent His- Purkinje system depolarization from increased sinus rate. Vagal activity inhibits sympathetic activity; therefore, reduction of vagal tone by atropine disinhibits sympathetic activity and may account for the unpredictable effects of atropine on heart rate. Elevations in heart rate after atropine can persist for hours and cannot be readily reversed. Aminophylline1 (2.5–6.3 mg/kg IV) is reported to reverse heart block resistant to atropine and epinephrine by antagonizing adenosine. Stimulation of β-adrenergic receptors increases sinus node and subsidiary pacemaker rates, AV node and His-Purkinje system conduction velocities, and myocardial contractility. The effective refractory period shortens in most tissue but this effect varies with dose and specific tissue type. Dobutamine1 (2–40 mcg/kg/min) is a useful β-receptor agonist because it increases cardiac output and lowers filling pressures without excessive rise or fall of blood pressure. Dopamine1 (2–20 mcg/kg/min IV) stimulates β1-adrenergic receptors and increases heart rate by enhancing impulse formation and conduction, as well as myocardial contractility. At higher doses (10–20 mcg/kg/min) dopamine causes vasoconstriction by α1-receptor stimulation. Isoproterenol (0.02–0.06 mg IV bolus, 0.5–10.0 mcg/min IV infusion) stimulates β1- and β2-adrenergic receptors and enhances

    vasodilation more than the other catecholamines. This can result in unwanted hypotension in some circumstances but it is also less likely to cause a reflex increase in vagal tone than drugs that cause vasoconstriction. Epinephrine (1 mg IV boluses for cardiac arrest, 0.2– 1 mg subcutaneously, 0.5–10 mcg/min IV) stimulates both α- and β- adrenergic receptors. It is recommended for asystolic cardiac arrest in part because it increases myocardial and cerebral flow. However, the increase of systemic vascular resistance may be detrimental by augmenting metabolic acidosis and decreasing cardiac performance in patients with poor left ventricular function. The suggested dose ranges are broad because the response to β-adrenergic stimulants such as improved AV conduction varies widely and may be affected by β- adrenergic receptor down-regulation in patients with chronic elevations in sympathetic activity such as patients with long-standing heart failure.

    Temporary pacing includes primarily transcutaneous and transvenous approaches. Transthoracic, transesophageal, and transgastric approaches are rarely used. Transcutaneous pacing provides noninvasive heart rate support as well as immediate access to countershock, but it is often so painful that most patients require sedation. For these reasons its principal uses are for short-term pacing during cardiopulmonary resuscitation and standby pacing in patients at risk for bradyarrhythmias. Capture is not achieved in some patients. Therefore, users should be ready to continue mechanical cardiopulmonary support and seek alternative methods. If used in standby applications, ventricular capture should be verified in advance. Capture is often difficult to ascertain because transcutaneous stimuli cause large deflections on the ECG and pectoral muscle stimulation can be confused with a pulse. Capture should be verified by careful ECG analysis at subthreshold and suprathreshold stimulus amplitudes and confirmed by appropriately timed femoral artery pulses, Korotkoff sounds, or arterial pressure waveforms.

    Transvenous insertion of an electrode catheter is the method of choice for most patients who require temporary pacing. This approach is reliable and safe when performed by competent staff with strict aseptic technique, fluoroscopic guidance, and appropriate catheters.

    Small studies suggest that long-term (> 5 days) temporary pacing can be accomplished with active-fixation permanent pacemaker leads attached to an external pulse generator (not approved by the U.S. Food and Drug Administration [FDA]). Tunneling the lead may enhance stability and reduce the risk of infection.

  11. 11
    Monitoring

    Patients with high-grade or symptomatic heart block require close monitoring until the process is reversed by treatment or a pacemaker is implanted. All patients who receive pacemakers require lifelong follow-up by a trained team of physicians, nurses, and ancillary personnel using standard procedures guided by practice guidelines and manufacturer recommendations.

     

  12. 12
    Complications

    Catecholamines used to increase heart rate may precipitate tachyarrhythmias by electrophysiologic effects mediated by adrenergic receptors or by myocardial ischemia, and they may worsen hemodynamic status. The adverse effects of catecholamines increase with duration of exposure. Ischemia and receptor-mediated electrophysiologic effects occur immediately after administration; changes in gene expression of ion channels begin as early as several hours; and long-term changes such as myocardial hypertrophy, apoptosis, and fibrosis occur within 24 hours and may progress over much longer periods. This suggests that the duration and dose of catecholamine infusions should be minimized. Complications of temporary transvenous pacing include inadequate pacing or sensing thresholds, vascular complications, pneumothorax, myocardial perforation, infection, and dislodgment. Permanent pacemakers are highly effective, safe, and cost-effective with few contraindications.

    Although the complications are rarely life threatening, they should be carefully considered and acknowledged. Septicemia or endocarditis has been reported in 0.5% of patients. In patients with pacemaker- related endocarditis, the in-hospital mortality rate is reported to be over 7% with a 20-month mortality rate over 25%. The rate of significant complications has been reported to be 3.5%. About 10% of pacemakers will become infected or develop some other type of failure that may require extraction. In a recent series the rate of major complications associated with extraction was 1.4%. There is a long- term continuous risk of infection, thrombosis, and erosion. In young persons there is a periodic need to replace generators and leads.

    Abandoned leads block venous access and extractions are associated with significant risks. Perhaps of greater consequence is the constant inconvenience of lifelong follow-up, electromagnetic interference, and false alarms from electronic surveillance devices, as well as exclusion from important procedures, such as magnetic resonance imaging of the thorax. Conventional pacing, that is, from the right ventricular apex, is now known to be detrimental and may cause adverse ventricular remodeling, atrial fibrillation, heart failure, and premature death. Although it has been shown that patients with reduced left ventricular function are at greater risk for adverse effects, it is not known how to identify other patients at risk. Strategies for reducing the adverse effects of conventional pacing are under study and recommendations are evolving. Because the decision for pacemaker implantation includes selection of lead configuration, lead locations, and pacing mode, patient guidance and education are complex.

  13. 13
    Conclusions

    Heart block remains a challenge because the cellular mechanisms responsible are poorly understood, prediction of symptomatic heart block (who and when) is unreliable, treatments that restore normal conduction do not exist for most conditions, and pacemaker therapy can have significant long-term adverse consequences. Fortunately, current devices and leads are much more reliable than in the past and remote monitoring has enhanced early detection of problems and has substantially reduced the inconvenience of device monitoring. The newest generation of devices will allow many patients with pacemakers to safely undergo magnetic resonance imaging. Ongoing clinical trials will provide guidance in pacemaker configurations and programming that will minimize adverse effects. In the future, achievements in molecular biology will elucidate mechanisms and produce treatments that will relegate artificial pacemakers to museum pieces.

  14. 14
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    Cheng S., Keyes M.J., Larson M.G., et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA. 2009;301:2571.

    Epstein A.E., DiMarco J.P., Ellenbogen K.A., et al.

    ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. J Am Coll Cardiol. 2008;51:e1.

    Hazinski M.F., Samson R., Schexnayder S. Handbook of emergency cardiovascular care for healthcare providers. Dallas, TX: American Heart Association; 2010.

    Smits J.P.P., Velkkamp M.W., Wilde A.A.M. Mechanisms of inherited cardiac conduction disease. Europace. 2005;7:122.

    Vardas P.E., Auriccho A., Blanc J.J., et al. Guidelines for cardiac pacing and cardiac resynchronization therapy. Eur Heart J.

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    1  Not FDA approved for this  indication.

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