ROLE OF AUTOIMMUNE REACTIONS IN DEVELOPMENT OF CARDIAC ARRHYTHMIA AND CONDUCTION DISTURBANCES


Cite item

Full Text

Abstract

Cardiac arrhythmias and conduction disturbances are an important cause of morbidity and mortality in many countries all over the world. Etiology of these disorders remains unclear in many patients. Experimental and clinical studies show that autoimmune reactions may be involved in development of arrhythmias and cardiac blocks. Precise identification of an autoantibody-mediated mechanism opens new perspectives in the treatment and prevention of cardiac arrhythmias including use of immunosuppressive agents or removal of autoantibodies by absorption technique. The review focuses on cardiac autoantigens, autoantibodies and their interactions that may be involved in development of cardiac arrhythmias.

About the authors

E S Rodionova

Russian Research Cardiology Center

Email: katramon@gmail.com
аспирант отд. клинической электрофизиологии и рентгенохирургических методов лечения нарушений ритма и проводимости сердца

N A Mironova

Russian Research Cardiology Center

Email: mirona01@mail.ru
канд. мед. наук, науч. сотр. отд. клинической электрофизиологии и рентгенохирургических методов лечения нарушений ритма и проводимости сердца

O P Aparina

Russian Research Cardiology Center

Email: olla_a@mail.ru
ординатор отд. клинической электрофизиологии и рентгенохирургических методов лечения нарушений ритма и проводимости сердца

M M Rogova

Russian Research Cardiology Center

Email: amble@inbox.ru
аспирант отд. клинической электрофизиологии и рентгенохирургических методов лечения нарушений ритма и проводимости сердца

K A Zykov

Russian Research Cardiology Center

Email: kirillaz72@mail.ru
д-р мед. наук, рук. лаб. иммунопатологии сердечно-сосудистых заболеваний

S P Golytsyn

Russian Research Cardiology Center

Email: golitsyn@cardio.ru
д-р мед. наук, проф., рук. отд. клинической электрофизиологии и рентгенохирургических методов лечения нарушений ритма и проводимости сердца

References

  1. Zheng Z., Croft J., Giles W., Mensah G. Sudden cardiac death in the United States, 1989 to 1998. Circulation 2001; 104: 2158—2163.
  2. Бекбосынова М. С. Показатели иммуновоспалительных процессов и состояние симпатической иннервации миокарда у пациентов с предсердными и желудочковыми нарушениями ритма сердца: Автореф. дис.. д-ра мед. наук. М.: ФГУ РКНПК; 2007.
  3. Kennedy H. L., Underhill S. J. Frequent or complex ventricular ectopy in apparently healthy subjects. Am. J. Cardiol. 1976; 38: 141—148.
  4. Buxton A. E., Waxman H. L., Marchlinsky F.E. Right ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation 1983; 68: 917—927.
  5. Bigger J. T. Identification of patients at high risk for sudden cardiac death. Am. J. Cardiol. 1984; 54: 3D—8D.
  6. Gaita F., Giutetto C., Di Donna P. Long-term follow-up of right ventricular monomorphic extrasystoles. J. Am. Coll. Cardiol. 2001; 38: 364—370.
  7. Ардашев А. В., Склярова Т. Ф., Шаваров А. А. Особенности центральной гемодинамики у пациентов с идиопатическими нарушениями ритма сердца из области выходного тракта правого желудочка до радиочастотной катетерной абляции и в течение года после нее. Кардиология 2009; 3: 4—9.
  8. Chugh S. S., Shen W.-K., Luria D. M. First evidence of premature ventricular complex-induced cardiomyopathy: a potentially reversible cause of heart failure. J. Cardiovasc. Electrophysiol. 2000; 11: 328—329.
  9. Nerheim P., Bigger-Botkin P., Piracha L. Heart failure and sudden death in patients with tachycardia-induced cardiomyopathy and recurrent tachycardia. Circulation 2004; 110: 247—252.
  10. Takemoto M., Yoshimura H., Ohba H. Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves let ventricular dilation and clinical status in patients without structural heart disease. J. Am. Coll. Cardiol. 2005; 45 (8): 1259—1265.
  11. Redfearn D. P., Hill J. D., Keal R. Left ventricular dysfunction resulting from frequent unifocal ventricular ectopics with resolution following radiofrequency ablation. Europace 2003; 5: 247—250.
  12. Yarlagadda R. K., Iwai S., Stein K. M. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation 2005; 112: 1092—1097.
  13. Bikkina M., Larson M. G., Levy D. Prognostic implication of asymptomatic ventricular arrhythmias: the Framingham heart study. Ann. Intern. Med. 1992; 117: 990—996.
  14. Kuhn A., Kottkamp H., Thiele H. Idiopathic right ventricular tachycardia or arrythmogenic right ventricular tachycardia? Dtsch. Med. Wschr. 2000; 25 (22): 692—697.
  15. Пармон Е. В., Трешкур Т. В., Шляхто Е. В. Идиопатические желудочковые нарушения ритма (анализ проблемы). Вестн. арит-мол. 2003; 31: 60—71.
  16. Lazzerini P. E., Capecchi P. L., Guideri F. Autoantibody-mediated cardiac arrhythmias: mechanisms and clinical implications. Basic Res. Cardiol. 2008; 103 (1): 1—11.
  17. Ristic A. D., Maisch B. Cardiac rhythm and conduction disturbances: what is the role of autoimmune mechanisms? Herz 2000; 25 (3): 181—188.
  18. Deubner N., Berliner D. Cardiac b1-adrenoceptor autoantibodies in human heart disease: rationale and design of the Etiology, Titre-Course, and Survival (ETiCS) Study. Eur. J. Heart Fail. 2010; 12: 753—762.
  19. Jahns R., Boivin V., Hein L. et al. Direct evidence for a beta1-adrenergic receptor-directed autoimmune attack as a cause of idiopathic dilated cardiomyopathy. J. Clin. Invest. 2004; 113: 1419—1429.
  20. Tincani A., Biasini-Rebaioli C., Cattaneo R., Riboldi P. Nonorgan specific autoantibodies and heart damage. Lupus 2005; 14: 656—659.
  21. Chiale P. A., Rosenbaum M. B., Elizari M. V. et al. High prevalence of antibodies against beta1and beta2adrenoceptors in patiens with primary electrical cardiac abnormalities. J. Am. Coll. Cardiol. 2005; 26: 864—869.
  22. Smulski C., Labovsky V., Levy G. et al. Structural basis of the crossreaction between an antibody to the Trypanosoma cruzi ribosomal P2b protein and the human b1 adrenergic receptor. FASEB J. 2006; 20: 1396—1406.
  23. Rosenbaum M. B., Chiale P. A., Schejtman D. et al. Antibodies to beta-adrenergic receptors disclosing agonist-like properties in idiopathic dilated cardiomyopathy and Chaga’s heart disease. J. Cardiovasc. Electrophysiol. 1994; 5: 367—375.
  24. Christ T., Wettwer E., Dobrev D. et al. Autoantibodies against the beta1 adrenoceptor from patients with dilated cardiomyopathy prolong action potential duration and enhance contractility in isolated cardiomyocytes. J. Mol. Cell. Cardiol. 2005; 33: 1515—1525.
  25. Baba A., Yoshikawa T., Fukuda Y. et al. Autoantibodies against M2-muscarinic acetylcholine receptors: new upstream targets in atrial fibrillation in patients with dilated cardiomyopathy. Eur. Heart J. 2004; 25: 1108—1115.
  26. Stavrakis S., Kem D. C. Activating autoantibodies to the beta1-adrenergic and M2 muscarinic receptors facilitate atrial fibrillation in patients with Graves’ hyperthyroidism. J. Am. Coll. Cardiol. 2009; 54: 1309—1316.
  27. Zaho R., Wang W., Wu B. et al. Effects of anti-peptide antibodies against the second extracellular loop of human M2 muscarinic acetylcholine receptors on transmembrane potentials and currents in guinea pig ventricular myocytes. Mol. Cell. Biochem. J. 1994; 163: 185—193.
  28. Oliveira S. F., Pedrosa R. C., Nascimento J. H., Campos de Carvalho A. C. et al. Sera from chronic chagasic patients with complex cardiac arrhythmias depress electrogenesis and conduction in isolated rabbit hearts. Circulation 1997; 96: 2031—2037.
  29. Medei E., Pedrosa R. C., Benchimol Barbosa P. R. et al. Human antibodies with muscarinic activity modulate ventricular repolarization basis for electrical disturbance. Int. J. Cardiol. 2007; 115: 373—380.
  30. Goin J. C., Borda E. S., Auger S., Storino R. Cardiac M2 muscarinic cholinoceptor activation by human chagasic autoantibodies: association with bradycardia. Heart 1999; 82: 273—278.
  31. Hayashi N., Koshiba M., Nishimura K. Prevalence of disease-specific antinuclear antibodies in general population: estimates from annual physical examinations of residents of a small town over 5-year period. Mod. Rheumatol. 2008; 18: 153—160.
  32. Lazzerini P. E., Capecchi P. L., Guideri F. et al. Comparison of frequency of complex ventricular arrhythmias in patients with positive versus negative anti-Ro/SSA and connective tissue disease. Am. J. Cardiol. 2007; 100: 1029—1034.
  33. Li J. M., Horsfall A. C., Maini R. N. Anti-La ((SS-B) but not anti-Ro52 (SS-A) antibodies cross-react with laminin a role in the pathogenesis of congenital heart block? Clin. Exp. Immunol. 1995; 99: 316—324.
  34. Benitah J. P., Gomez A. M., Fauconnier J. et al. Voltage-gated Ca2+ currents in the human pathophysiologic heart: a review. Basic Res. Cardiol. 2002; 97 (Suppl. 1): 111—118.
  35. Xiao G. Q., Hu K., Boutjdir M. Direct inhibition of expressed cardiac Land T-type calcium channels by IgG from mothers whose children have congenital heart block. Circulation 2001; 103: 1599—1604.
  36. Hu K., Qu Y., Boutjdir M. Functional basis of sinus bradycardia in congenital heart block. Circ. Res. 2004; 94: e32—e38.
  37. Brette F., Leroy J., Le Guennec J. Y.l, Salle L. Ca2+ currents in cardiac myocytes: old story, new insights. Progr. Biophys. Mol. Biol. 2006; 91: 1—82.
  38. Qu Y., Baroudi G., Yue Y., Boutjdir M. Novel molecular mechanism involving a1D (Cav 1.3) L-Type calcium channel in autoimmune-associated sinus bradycardia. Circulation 2005; 111: 3034—3041.
  39. Antzelevitch C. Ionic, molecular, and cellular bases of QT-interval prolongation and torsade de pointes. Europace 2007; 9 (Suppl. 4): iv4—iv15.
  40. Lazzerini P. E., Acampa M., Guideri F. et al. Prolongation of the corrected QT interval in adult patients with anti-Ro/SSA-positive connective tissue diseases. Arthr. and Rheum. 2004; 50: 1248— 1252.
  41. Nakamura K., Katayama Y., Kusano K. F. et al. Anti-OCNH2 antibody-induced long QT syndrome: novel acquired form of long QT syndrome. J. Am. Coll. Cardiol. 2007; 50: 1808—1809.
  42. Carapetis J. R., McDonald M., Wilson N. J. Acute rheumatic fever. Lancet 2005; 366: 155—168.
  43. Buyon J. P., Clancy R., Di Donato F. et al. Cardiac 5-HT4 serotoninergic receptors, 52 kD SSA/Ro and autoimmune associated congenital heart block. J. Autoimmun. 2002; 19: 79—86.
  44. Eftgekhari P., Roegel J. C., Lezoualc’h F. et al. Induction of neonatal lupus in pups of mice immunized with synthetic peptides derived from amino acid sequences of the serotoninergic 5-HT4 receptor. Eur. J. Immunol. 2001; 31 (2): 573—579.
  45. Eftekhari P., Salle L., Lezoualc’h F. et al. Anti-SSA/Ro52 autoantibodies blocking the cardiac 5-HT4 serotoninergic receptor could explain neonatal lupus congenital heart block. Eur. J. Immunol. 2000; 30 (10): 2782—2790.
  46. Kamel R., Eftekhari P., Clancy R. et al. Autoantibodies against the serotoningergic 5-HT4 receptor and congenital heart block: a reassessment. J. Autoimmun. 2005; 25: 72—76.
  47. Hariman R. J., Zeiler R. H., Gough W. B., El-Sherif N. Enhancement of triggered activity in ischemic Purkinje fibers by ouabain: a mechanism of increased susceptibility to digitalis toxicity in myocardial infarction. J. Am. Coll. Cardiol. 1985; 5: 672—679.
  48. Baba A., Yoshkawa T., Ogawa S. Autoantibodies produced against sarcolemmal Na-K-ATPase: possible upstream targets of arrhythmias and sudden death in patients with dilated cardiomyopathy. J. Am. Coll. Cardiol. 2002; 40: 1153—1159.
  49. Baba A., Yoshikawa T., Chino M. et al. Autoantibodies: new upstream targets of paroxysmal atrial fibrillation in patients with congestive heart failure. J. Cardiol. 2002; 40: 217—223.
  50. Mandal K., Jahangiri M., Mulhin M. et al. Association of anti-heat shock protein 65 antibodies with development of postoperative atrial fibrillation. Circulation 2004; 110: 2588—2590.

Copyright (c) 2012 Consilium Medicum

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
 
 


This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies