eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Atrioventricular Block, Third Degree, Acquired

Author: M Silvana Horenstein, MD, Associate in Pediatric and Fetal Cardiac Diagnostic, Diagnostico Gineco-Obstetrico, PC; Associate Director, Legacy Department, Best Doctors, Inc
Coauthor(s): Peter P Karpawich, MD, Professor of Pediatric Medicine, Department of Pediatrics (Cardiology), Wayne State University School of Medicine; Director, Cardiac Electrophysiology and Pacemaker Services, Children's Hospital of Michigan
Contributor Information and Disclosures

Updated: Oct 30, 2008

Introduction

Background

In general, atrioventricular block (AVB) refers to a conduction delay or interruption of the impulses generated in the atrium before they reach the ventricles. AVB may be transient or permanent, and the anatomic level at which it occurs varies. These features determine the clinical significance of AVB, which may range from minimal to severely symptomatic, including Stokes-Adams syncope, congestive heart failure, or sudden death.

Depending on the anatomic level at which the atrial impulse is interrupted prior to reaching the ventricles, the AVB may be classified as first-degree, second-degree, or third-degree AVB. The term first-degree AVB is actually a misnomer because nothing is blocked; instead, the conduction time of impulses from the atrium to the ventricles is prolonged. Second-degree AVB occurs either when successive impulses from the atrium to the ventricles are progressively delayed until conduction failure occurs (ie, Mobitz type I second-degree AVB, Wenckebach periodicity) or when an atrial impulse fails to conduct to the ventricles without any measurable lengthening of the preceding PR intervals (ie, Mobitz type II second-degree AVB). Prolongation of the H-V interval may predispose individuals to complete or third-degree AVB.

In complete or third-degree AVB, the conduction of sinus or atrial impulses is entirely interrupted at the level of the atrioventricular node (AVN), in the bundle of His, or is associated with an aberrantly located anatomical AVN that precludes normal anatomical communication to the distal conduction tissue. Atria and ventricles depolarize independently of each other, and the ventricular rate is typically slower than the atrial rate. The surface ECG may reveal either narrow or wide QRS configurations, depending on the location of the interruption and the foci of the escape pacemaker tissue. For example, the QRS is narrow if the escape rhythm is supra-His bundle or is wide if the escape rhythm is intra-His or infra-His bundle. Escape ventricular rhythms with narrow QRS may be more stable than those with wide QRS morphologies.

Pathophysiology

The AVN is composed of specialized cells arranged in 3 zones: the atrial-transitional junction, the transitional-compact node junction, and the nodal-His junction or penetrating His bundle.1 These regions display different electrical properties, such as slowing of AV conduction with progressively increasing atrial rates until conduction block occurs, which protects the ventricles from dangerously rapid rhythms during atrial tachycardias. Other properties of the AVN cells include their ability to pace the heart by producing "escape rhythms" in case of a block above their anatomic level.2 These specialized cells however, may begin to beat faster than the sinus node and may produce tachycardia.

Complete AVB may occur immediately when the AVN is injured by direct trauma during surgery, by ischemia during a coronary event, and by myocardial inflammation and infiltration during a viral illness. It may also occur years after mediastinal radiation secondary to fibrosis. Certain congenital defects may be inherently associated with AVB because of anatomical alteration in the arrangement of the AVN to the proximal His-Purkinje conduction tissue. These defects include double-outlet right ventricle, L-transposition of the great arteries, AV canal defects in the setting of heterotaxy syndrome, and other congenital heart lesions.

Frequency

United States

The overall prevalence of postsurgical complete AVB has been reduced to 5%.

Age

In children, the most common cause of permanent acquired complete AVB is surgery for congenital heart disease. The second most common cause is congenital heart disease associated with complete AVB. Other etiologies of acquired AVB are often reversible and include digitalis and other drug intoxications, viral myocarditis, acute rheumatic fever, Lyme disease, and infectious mononucleosis.

In adults, other causes of complete AVB include myocardial infarction (especially inferior), coronary spasm (usually of the right coronary artery), neoplasms (eg, cardiac mesotheliomas), and the etiologies mentioned for the pediatric group. Almost exclusive to adult patients are 2 degenerative diseases of the specialized conducting system: Lev disease and Lenègre disease (see Causes).

Clinical

History

  • Most pediatric patients with postoperative complete atrioventricular block (AVB) have had intracardiac surgery for atrial septal defect (ASD) repair, ventricular septal defect (VSD) repair, valve repair or replacements, or other complex congenital heart surgery.
    • Some patients with surgical complete AVB develop weakness, syncope, or congestive heart failure; others may be asymptomatic. Most of these patients exhibit complete AVB by the time cardiopulmonary bypass ends, and a few develop block in the first weeks after surgery. Fortunately, many recover atrioventricular (AV) conduction within the first 7-10 postoperative days.
    • Rarely, postsurgical patients develop complete AVB months or years after surgery. Late recovery of AV conduction is less common.
  • Symptoms consist of dizziness, exercise intolerance, syncope, failure to thrive (in infants), and congestive heart failure. Patients with infranodal block tend to be more symptomatic than those with higher block sites because low intrinsic escape pacemakers are slower and less reliable than higher-level intrinsic pacemakers.

Physical

  • Typically, patients with complete AVB have bradycardia. However, if the escape heart rate is rapid enough to maintain adequate cardiac output and cerebral perfusion, patients are asymptomatic. These individuals usually present with heart rates of 50-60 beats per minute (bpm).
  • Conversely, if the heart rate is inadequate to maintain blood flow to the brain (usually <50 bpm in children) patients may have syncopal episodes. If the escape pacemaker rate is inadequate, sudden death may ensue.
  • The clinical presentation of newborns with complete congenital AVB may range from asymptomatic presentation with heart rates increasing to 100 bpm upon stimulation (eg, when feeding, crying) to hydropic presentation due to congestive heart failure, to stillborn and hydropic presentation.

Causes

  • Postsurgical complete AVB is the most common cause for acquired AVB in children, resulting from trauma to the atrioventricular node (AVN) at the time of surgery (ie, hemorrhage, ischemia, necrosis, inflammation, traumatic disruption). It may occur following repairs, including those for VSD, L-transposition of the great arteries (especially), tetralogy of Fallot (TOF), ASD (especially ostium primum ASD), and atrial baffle procedures for complete transposition of the great arteries (although rare). These patients not only have very slow heart rates but are also prone to asystole, with a high risk for sudden death.
  • Transient and permanent complete AVB has been reported following transcatheter closure of perimembranous VSD.3
  • Complete AVB may occur with systemic infections that cause myocardial inflammation and infiltration, such as diphtheria, Borrelia burgdorferi infection (Lyme disease), Chagas disease, Rocky Mountain spotted fever, Yersinia enterocolitica infection, infectious mononucleosis, bacterial endocarditis, and viral myocarditis.
    • Diphtheria is an infection of mucous membranes or skin caused by Corynebacterium diphtheriae, of which certain strains produce the diphtheria toxin. This protein can cause myocarditis, polyneuritis, and other systemic effects. Myocarditis occurs in 10-25% of patients with diphtheria and may develop during the acute phase or after several weeks. This consists of varying degrees of heart block, including complete AVB and arrhythmias, such as atrial fibrillation, premature ventricular beats, ventricular tachycardia, and ventricular fibrillation.
    • Lyme disease is caused by the tick-transmitted spirochete B burgdorferi. It begins with an expanding skin lesion known as erythema migrans. Within several days or weeks, the spirochete spreads hematogenously, and approximately 8% of patients develop cardiac involvement. The most common abnormality is fluctuating degrees of AVB (ie, first-degree, second-degree, and third-degree AVB). Other more diffuse forms of cardiac involvement include left ventricular dysfunction, cardiomegaly, or pancarditis. Cardiac involvement usually lasts for a few weeks, although it may recur.
    • Chagas disease is an endemic zoonosis in certain regions of Central and South America.
      • It is caused by the protozoan Trypanosoma cruzi and is transmitted by hematophagous triatomae insects (ie, reduviids). These insects become infected after sucking blood that contains parasites from vertebrate hosts (eg, birds, mammals).
      • Parasites reproduce in the guts of reduviids, and infective forms are discharged with feces at the time of subsequent blood meals. Therefore, the second host becomes infected with parasites because of skin abrasions that have been contaminated with infected feces.
      • Symptomatic chronic Chagas disease becomes apparent years or even decades after infection. Right bundle branch block is the most common ECG abnormality, but other types of AVB, including complete AVB, are frequently observed. Other forms of rhythm disturbances include premature ventricular contractions, tachyarrhythmias, and bradyarrhythmias. Cardiomyopathy results in right-sided or biventricular heart failure.
  • Rheumatic fever is an inflammatory disease that occurs from pharyngeal infection with group A streptococci, with multisystemic involvement. In acute rheumatic carditis, all the layers of the heart may be compromised. Although most patients with carditis are asymptomatic, some have valvular damage of the mitral and/or aortic valves that may produce regurgitation and even congestive heart failure. In terms of rhythm disturbance in patients with carditis, tachycardia disproportionate to the degree of fever and varying degrees of heart block may occur. The most common type of AVB is first degree.
  • Reiter syndrome is a seronegative arthropathy that may be accompanied by pancarditis with involvement of the AVN (ie, varying degrees of AVB) and proximal aortitis with valve regurgitation. Both of these features are more common in patients with long-standing disease and peripheral joint involvement.
  • Ischemia from acquired coronary disease (eg, Kawasaki disease), or from inferior wall infarcts can transiently or permanently damage the conduction tissue, leading to variable degrees of AVB.
  • Hypertension and aortic and/or mitral stenosis are believed to accelerate the degeneration of the conducting system through calcification and fibrosis.
  • Myotonic dystrophy forms 1 and 2 are neuromuscular diseases inherited in an autosomal dominant fashion, with genetic anticipation, in which cardiac involvement consists of disorders of impulse formation and, especially, AV conduction. They are typically progressive and are caused by an expanded CTG repeat in the 3-prime untranslated region of the DMPK gene and by an expanded CCTG repeat in intron 1 of the ZNF9 gene, respectively. They begin as asymptomatic PR prolongation and lead to complete AVB. Syncope and sudden death may occur; therefore, symptomatic patients require insertion of a permanent pacemaker. Diagnosis is mainly clinical.
  • Kearns-Sayre syndrome is caused by a mitochondrial DNA deletion. Its characteristic triad includes progressive external ophthalmoplegia, pigmentary degeneration of the retina, and progressive cardiac conduction defects, including complete heart block. Other features may include ataxia, hearing loss, dementia, short stature, delayed secondary sexual characteristics, hypoparathyroidism, hypothyroidism, and peripheral neuropathy. The diagnosis is usually made clinically and by demonstration of ragged red fibers on skeletal muscle biopsy.
  • Tuberous sclerosis is a neurocutaneous disorder caused by mutations in any of 4 separate genetic loci in which cutaneous lesions of multiple types are associated with tumors and malformations of the CNS. Mental retardation may be severe, and patients develop intractable seizures. Cardiac rhabdomyomas within the AVN may cause complete AVB and different types of rhythm disturbances, such as ventricular tachycardia when localized in the ventricles. Diagnosis is clinical. The earliest lesions are leaf-shaped hypopigmented spots scattered over the trunk and limbs; they are observed better using a Wood lamp than with the naked eye.
  • Almost exclusive to adult patients are 2 degenerative diseases of the specialized conducting system: Lev disease and Lenègre disease.
    • In Lev disease, calcification and sclerosis of the cardiac skeleton frequently involve the mitral and aortic valves, the central fibrous body, and the summit of the ventricular septum.
    • Lenègre disease is thought to represent a primary sclerodegenerative disease of the conducting system with no involvement of the myocardium or fibrous skeleton of the heart.
  • Intracardiac tumors constitute a very rare cause of acquired complete AV block that occurs through invasion of the conduction system. The term cardiac mesothelioma refers to heterotopic epithelial replacement of the AV node. It is a rare entity and, thus, a rare cause for complete AVB. Cases of congenital complete AVB and complete AVB in adults secondary to cardiac mesotheliomas have been reported. Definitive diagnosis is made only at autopsy, upon which necropsy may reveal extensive infiltration of the AV node and proximal bundle by mesothelioma tissue. Metastatic melanoma has also been described to cause sudden complete AVB and sudden death.4,5
  • Amyloidosis is a systemic disease in which abnormal production of immunoglobulins leads to their deposit in various tissues such as tongue, intestines, skeletal and smooth muscles, nerves, skin, ligaments, heart, liver, spleen, and kidneys. When the heart is affected, cardiomyopathy with marked left ventricular wall thickening, severely decreased systolic and diastolic function, and complete AVB may ensue.
  • Sarcoidosis is an inflammatory systemic disease characterized by formation of granulomas that most frequently affect the lungs, lymph nodes, skin, eyes, and liver. However, it may affect any organ. When it affects the heart, it may cause different types of conduction disturbance, from bundle branch block to complete AVB. Interestingly, AVB may be reversible. Sudden death has been described.
  • Primary cardiac lymphoma has been described to cause complete AVB. Case reports of sinus rhythm restoration after tumor remission have been described.
  • Drugs such as digoxin, beta-blockers, and calcium channel blockers may cause transient complete AVB, which can be fatal if the ventricular escape rhythm is inadequate to maintain brain blood flow or if asystole is prolonged.
  • Clonidine, tricyclic antidepressants, penetrating chest trauma, and radiation may cause complete AVB.
  • Mediastinal radiation for lymphomas such as Hodgkin lymphoma has been described to cause complete AVB.

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References
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References

  1. Anderson RH, Janse MJ, van Capelle FJ, et al. A combined morphological and electrophysiological study of the atrioventricular node of the rabbit heart. Circ Res. Dec 1974;35(6):909-22. [Medline].

  2. Dobrzynski H, Nikolski VP, Sambelashvili AT, et al. Site of origin and molecular substrate of atrioventricular junctional rhythm in the rabbit heart. Circ Res. Nov 28 2003;93(11):1102-10. [Medline].

  3. Carminati M, Butera G, Chessa M, Drago M, Negura D, Piazza L. Transcatheter closure of congenital ventricular septal defect with Amplatzer septal occluders. Am J Cardiol. Dec 19 2005;96(12A):52L-58L. [Medline].

  4. Ozyuncu N, Sahin M, Altin T, Karaoguz R, Guldal M, Akyurek O. Cardiac metastasis of malignant melanoma: a rare cause of complete atrioventricular block. Europace. Jul 2006;8(7):545-8. [Medline].

  5. Legoux B, Jegou B, Litoux P, Dreno B. [Cardiac metastasis of melanoma disclosed by tamponade]. Ann Dermatol Venereol. 1996;123(6-7):393-4. [Medline].

  6. Bostan OM, Celiker A, Karagoz T, Ozer S, Ozme S. Dual chamber cardiac pacing in children: Single chamber pacing dual chamber sensing cardiac pacemaker or dual chamber pacing and sensing cardiac pacemaker?. Pediatr Int. Dec 2002;44(6):635-40. [Medline].

  7. Vatasescu R, Shalganov T, Paprika D, et al. Evolution of left ventricular function in paediatric patients with permanent right ventricular pacing for isolated congenital heart block: a medium term follow-up. Europace. Apr 2007;9(4):228-32. [Medline].

  8. Thambo JB, Bordachar P, Garrigue S, et al. Detrimental ventricular remodeling in patients with congenital complete heart block and chronic right ventricular apical pacing. Circulation. Dec 21 2004;110(25):3766-72. [Medline].

  9. Lewicka-Nowak E, Dabrowska-Kugacka A, Tybura S, et al. Right ventricular apex versus right ventricular outflow tract pacing: prospective, randomised, long-term clinical and echocardiographic evaluation. Kardiol Pol. Oct 2006;64(10):1082-91; discussion 1092-3. [Medline].

  10. [Best Evidence] Occhetta E, Bortnik M, Magnani A, et al. Prevention of ventricular desynchronization by permanent para-Hisian pacing after atrioventricular node ablation in chronic atrial fibrillation: a crossover, blinded, randomized study versus apical right ventricular pacing. J Am Coll Cardiol. May 16 2006;47(10):1938-45. [Medline].

  11. Adams MJ, Lipsitz SR, Colan SD, et al. Cardiovascular status in long-term survivors of Hodgkin's disease treated with chest radiotherapy. J Clin Oncol. Aug 1 2004;22(15):3139-48. [Medline].

  12. Apter S, Shemesh J, Raanani P, et al. Cardiovascular calcifications after radiation therapy for Hodgkin lymphoma: computed tomography detection and clinical correlation. Coron Artery Dis. Mar 2006;17(2):145-51. [Medline].

  13. Belhassen B, Viskin S, Fish R, et al. Catheter-induced mechanical trauma to accessory pathways during radiofrequency ablation: incidence, predictors and clinical implications. J Am Coll Cardiol. Mar 1999;33(3):767-74. [Medline].

  14. Berhouet M, Casset-Senon D, Machet MC, et al. Conduction defects as the presenting feature of sarcoidosis or observed during the course of the disease: regression with corticoid steroid therapy. Arch Mal Coeur Vaiss. Jun 2003;96(6):677-82. [Medline].

  15. Bonatti V, Agnetti A, Squarcia U. Early and late postoperative complete heart block in pediatric patients submitted to open-heart surgery for congenital heart disease. Pediatr Med Chir. May-Jun 1998;20(3):181-6. [Medline].

  16. Boraita Perez A, Serratosa Fernandez L. ["The athlete's heart": most common electrocardiographic findings]. Rev Esp Cardiol. May 1998;51(5):356-68. [Medline].

  17. Bullock A, Finley J, Sharratt G, Ross D. Single lead VDD pacing in children with complete heart block. Can J Cardiol. Jan 1998;14(1):58-62. [Medline].

  18. Cohen SI, Bharati S, Glass J, Lev M. Radiotherapy as a cause of complete atrioventricular block in Hodgkin's disease. An electrophysiological-pathological correlation. Arch Intern Med. Apr 1981;141(5):676-9. [Medline].

  19. Driscoll DJ. Surgical complete atrioventricular block. In: Gillette PC, Garson Jr A, eds. Pediatric Cardiac Dysrhythmias. New York, NY: Grune & Stratton, Inc; 1983:397-419.

  20. Evans DW, Stovin PG. Fatal heart block due to mesothelioma of the atrioventricular node. Br Heart J. Dec 1986;56(6):572-4. [Medline].

  21. Ford SE. Congenital cystic tumors of the atrio-ventricular node: successful demonstration by an abbreviated dissection of the conduction system. Cardiovasc Pathol. Jul-Aug 1999;8(4):233-7. [Medline].

  22. Fujisaki J, Tanaka T, Kato J, et al. Primary cardiac lymphoma presenting clinically as restrictive cardiomyopathy. Circ J. Feb 2005;69(2):249-52. [Medline].

  23. Goldstein DJ, Rabkin D, Spotnitz HM. Unconventional approaches to cardiac pacing in patients with inaccessible cardiac chambers. Ann Thorac Surg. Apr 1999;67(4):952-8. [Medline].

  24. Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee u. Circulation. Oct 15 2002;106(16):2145-61. [Medline]. [Full Text].

  25. Hirayama M, Tokuda A, Mutoh T, Kuriyama M. [Coxsackie virus B4 encephalitis in a young female who developed mental symptoms, and consciousness disturbance, and completely recovered]. Rinsho Shinkeigaku. Jan 1998;38(1):60-2. [Medline].

  26. Ho SC, Eng PH, Ding ZP, et al. Thyroid storm presenting as jaundice and complete heart block. Ann Acad Med Singapore. Sep 1998;27(5):748-51. [Medline].

  27. Isselbacher KJ, Harrison TR, eds. Harrison's Principles of Internal Medicine. Vol 2. New York, NY: McGraw-Hill; 1994.

  28. Jimenez Casso S, Benito Bartolome F, Sanchez Fernandez-Bernal C. [Cardiac rhabdomyomas in tuberous sclerosis: clinical symptoms and course in 18 cases diagnosed in childhood]. An Esp Pediatr. Jan 2000;52(1):36-40. [Medline].

  29. Kaplan BM, Miller AJ, Bharati S, Lev M, Martin Grais I. Complete AV block following mediastinal radiation therapy: electrocardiographic and pathologic correlation and review of the world literature. J Interv Card Electrophysiol. Nov 1997;1(3):175-88. [Medline].

  30. Karpawich PP, Rabah R, Haas JE. Altered cardiac histology following apical right ventricular pacing in patients with congenital atrioventricular block. Pacing Clin Electrophysiol. Sep 1999;22(9):1372-7. [Medline].

  31. Kawano H, Okada R, Kawano Y, et al. Mesothelioma in the atrioventricular node. Case report. Jpn Heart J. Mar 1994;35(2):255-61. [Medline].

  32. Kiviniemi MS, Pirnes MA, Eranen HJ, et al. Complications related to permanent pacemaker therapy. Pacing Clin Electrophysiol. May 1999;22(5):711-20. [Medline].

  33. Konno T, Shimizu M, Ino H, et al. A rare type of alternating bundle branch block in a patient with cardiac sarcoidosis--a case report. Angiology. Jan-Feb 2005;56(1):115-7. [Medline].

  34. Lie JT, Lufschanowski R, Erickson EE. Heterotopic epithelial replacement (so-called "mesothelioma") of the atrioventricular node, congenital heart block, and sudden death. Am J Forensic Med Pathol. Jun 1980;1(2):131-7. [Medline].

  35. Lim HE, Pak HN, Kim YH. Acute myocarditis associated with cardiac amyloidosis manifesting as transient complete atrioventricular block and slow ventricular tachycardia. Int J Cardiol. May 24 2006;109(3):395-7. [Medline].

  36. Musso P, Ronzani G, Ravera A, et al. Primary cardiac lymphoma presenting with complete atrioventricular block. Case report and review of the literature. Ital Heart J Suppl. Oct 2002;3(10):1047-50. [Medline].

  37. [Best Evidence] Occhetta E, Bortnik M, Magnani A, et al. Prevention of ventricular desynchronization by permanent para-Hisian pacing after atrioventricular node ablation in chronic atrial fibrillation: a crossover, blinded, randomized study versus apical right ventricular pacing. J Am Coll Cardiol. May 16 2006;47(10):1938-45. [Medline].

  38. Ogano M, Takano H, Fukuma N, et al. Sudden death in a case of cardiac amyloidosis immediately after pacemaker implantation for complete atrioventricular block. J Nippon Med Sch. Oct 2005;72(5):285-9. [Medline].

  39. Okamoto H, Mizuno K, Ohtoshi E. Cutaneous sarcoidosis with cardiac involvement. Eur J Dermatol. Sep 1999;9(6):466-9. [Medline].

  40. Pentz WH. Advanced heart block as a manifestation of a paraneoplastic syndrome from malignant thymoma. Chest. Oct 1999;116(4):1135-6. [Medline].

  41. Rosen KL, Cameron RW, Bigham PJ, Neish SR. Hypertrophic cardiomyopathy presenting with 3rd-degree atrioventricular block. Tex Heart Inst J. 1997;24(4):372-5. [Medline].

  42. Strauss WE, Asinger RW, Hodges M. Mesothelioma of the AV node: potential utility of pacing. Pacing Clin Electrophysiol. Sep 1988;11(9):1296-8. [Medline].

  43. Suarez-Mier MP, Sanchez-de-Leon S, Cohle SD. An unusual site for the AV node tumor: report of two cases. Cardiovasc Pathol. Nov-Dec 1999;8(6):325-8. [Medline].

  44. Subramanian R, Flygenring B. Mesothelioma of the atrioventricular node and congenital complete heart block. Clin Cardiol. Aug 1989;12(8):469-72. [Medline].

  45. Thorgeirsson G, Liebman J. Mesothelioma of the AV node. Pediatr Cardiol. Jul-Sep 1983;4(3):219-23. [Medline].

  46. Umetani K, Ishihara T, Yamamoto K, et al. Successfully treated complete atrioventricular block with corticosteroid in a patient with cardiac sarcoidosis: usefulness of gallium-67 and thallium-201 scintigraphy. Intern Med. Mar 2000;39(3):245-8. [Medline].

  47. Villain E. Pediatric cardiac pacing: indications, implant techniques, pacing mode. Ann Cardiol Angeiol (Paris). Jan 2005;54(1):2-6. [Medline].

  48. Villain E, Ouarda F, Beyler C, et al. Predictive factors for late complete atrio-ventricular block after surgical treatment for congenital cardiopathy. Arch Mal Coeur Vaiss. May 2003;96(5):495-8. [Medline].

  49. Vinter S, Isaksen C, Vesterby A. Sudden cardiac death in a young woman: tumor of the atrioventricular (AV) node or citalopram intoxication?. Am J Forensic Med Pathol. Dec 2005;26(4):349-51. [Medline].

  50. Weindling SN, Saul JP, Gamble WJ, et al. Duration of complete atrioventricular block after congenital heart disease surgery. Am J Cardiol. Aug 15 1998;82(4):525-7. [Medline].

  51. Wormser GP, Forseter G, Cooper D, et al. Use of a novel technique of cutaneous lavage for diagnosis of Lyme disease associated with erythema migrans. JAMA. Sep 9 1992;268(10):1311-3. [Medline].

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Further Reading

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Keywords

atrioventricular block, third-degree atrioventricular block, complete atrioventricular block, AVB, complete AVB, third-degree AV block, complete heart block, Stokes-Adams syncope, conduction delay, Stokes-Adams syncope, congestive heart failure, CHF, Mobitz type I second-degree AVB, Wenckebach periodicity, Mobitz type II second-degree AVB, double-outlet right ventricle, L-transposition of the great arteries, viral myocarditis, acute rheumatic fever, Lyme disease, infectious mononucleosis, myocardial infarction, coronary spasm, atrial septal defect, ASD, ventricular septal defect, diphtheria, Borrelia burgdorferi infection, Chagas disease, Rocky Mountain spotted fever, Yersinia enterocolitica infection, bacterial endocarditis, Kawasaki disease, Kearns-Sayre syndrome, rhabdomyomas, tuberous sclerosis, Lev disease, Lenègre disease, amyloidosis

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Contributor Information and Disclosures

Author

M Silvana Horenstein, MD, Associate in Pediatric and Fetal Cardiac Diagnostic, Diagnostico Gineco-Obstetrico, PC; Associate Director, Legacy Department, Best Doctors, Inc
M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Peter P Karpawich, MD, Professor of Pediatric Medicine, Department of Pediatrics (Cardiology), Wayne State University School of Medicine; Director, Cardiac Electrophysiology and Pacemaker Services, Children's Hospital of Michigan
Peter P Karpawich, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Alvin J Chin, MD, Professor of Pediatrics, Division of Cardiology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine
Alvin J Chin, MD is a member of the following medical societies: American Association for the Advancement of Science and American Heart Association
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

 
 
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