Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2020, vol. 29, nr 6, June, p. 757–767

doi: 10.17219/acem/122130

Publication type: review article

Language: English

License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)

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Large animals as models of atrial fibrillation

Piotr Frydrychowski1,B,D, Marcin Michałek1,B,D, Agnieszka Sławuta2,C,D,E,F, Agnieszka Noszczyk-Nowak1,A,B,C,D,E,F

1 Department of Internal Medicine and Clinic of Diseases of Horses, Dogs and Cats, Faculty of Veterinary Medicine, Wrocław University of Environmental and Life Sciences, Poland

2 Department of Internal and Occupational Diseases, Hypertension and Clinical Oncology, Wroclaw Medical University, Poland

Abstract

In clinical practice, atrial fibrillation (AF) is the most common cardiac arrhythmia in humans and it may lead to numerous complications, including central nervous system embolism. The electrical activity of the heart in AF is rapid and chaotic, while the atrioventricular conduction leads to irregular ventricular contraction. Consequently, the stroke volume is reduced, which may lead to symptoms of heart failure. Heart failure is one of the causes of AF as well. Numerous in vivo and in vitro models are used to study the pathophysiology of AF. Animal models play a key role in understanding the mechanisms of arrhythmias as well as in developing treatment regimens. The models of AF include large animals (goats, sheep, pigs, dogs) as well as small laboratory animals. This study reviews the large animal models of AF, which enhance our understanding of numerous mechanisms responsible for the development of AF, but we must be aware that the pathomechanism of AF in humans is complex and is affected by numerous factors, including environmental and congenital ones.

Key words

arrhythmia, atrial fibrillation, animal models

References (47)

  1. Allessie MA, Boyden PA, Camm AJ, et al. Pathophysiology and prevention of atrial fibrillation. Circulation. 2001;103(5):769–777.
  2. Noszczyk-Nowak A, Pasławska U, Zyśko D, Gajek J, Nicpoń J, Hebel M. Migotanie przedsionków u psów. Medycyna Wet. 2008;64:686–689.
  3. Saunders A, Gordon S, Miller M. Canine atrial fibrillation. Compend Contin Educ Vet. 2009;31(11):E1–9.
  4. Ninio DM, Saint DA. Passive pericardial constraint protects against stretch-induced vulnerability to atrial fibrillation in rabbits. Am J Physiol Heart Circ Physiol. 2006;291(5):H2547–2549.
  5. Henry BL, Gabris B, Li Q, et al. Relaxin suppresses atrial fibrillation in aged rats by reversing fibrosis and upregulating Na+ channels. Heart Rhythm. 2016;13(4):983–991.
  6. Wijffels MC, Kirchhof CJ, Dorland R, Allessie MA. Atrial fibrillation begets atrial fibrillation: A study in awake chronically instrumented goats. Circulation. 1995;92(7):1954–1968.
  7. Neuberger HR, Schotten U, Verheule S, et al. Development of a substrate of atrial fibrillation during chronic atrioventricular block in the goat. Circulation. 2005;111(1):30–37.
  8. Greiser M, Neuberger HR, Harks E, et al. Distinct contractile and molecular differences between two goat models of atrial dysfunction: AV block-induced atrial dilatation and atrial fibrillation. J Mol Cell Cardiol. 2009;46(3):385–394.
  9. van der Velden HM, Ausma J, Rook MB, et al. Gap junctional remodeling in relation to stabilization of atrial fibrillation in the goat. Cardiovasc Res. 2000;46(3):476–486.
  10. Ausma J, Wijffels M, Thoné F, Wouters L, Allessie M, Borgers M. Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat. Circulation. 1997;96(9):3157–3163.
  11. Ausma J, Litjens N, Lenders MH, et al. Time course of atrial fibrillation-induced cellular structural remodeling in atria of the goat. J Mol Cell Cardiol. 2001;33(12):2083–2094.
  12. Ausma J, van der Velden HM, Lenders MH, et al. Reverse structural and gap-junctional remodeling after prolonged atrial fibrillation in the goat. Circulation. 2003;107(15):2051–2058.
  13. Neuberger HR, Schotten U, Blaauw Y, et al. Chronic atrial dilation, electrical remodeling, and atrial fibrillation in the goat. J Am Coll Cardiol. 2006;47(3):644–653.
  14. Remes J, van Brakel TJ, Bolotin G, et al. Persistent atrial fibrillation in a goat model of chronic left atrial overload. J Thorac Cardiovasc Surg. 2008;136(4):1005–1011.
  15. Anné W, Willems R, Holemans P, et al. Self-terminating AF depends on electrical remodeling while persistent AF depends on additional structural changes in a rapid atrially paced sheep model. J Mol Cell Cardiol. 2007;43(2):148–158.
  16. Deroubaix E, Folliguet T, Rücker-Martin C, et al. Moderate and chronic hemodynamic overload of sheep atria induces reversible cellular electrophysiologic abnormalities and atrial vulnerability. J Am Coll Cardiol. 2004;44(9):1918–1926.
  17. Kistler PM, Sanders P, Dodic M, et al. Atrial electrical and structural abnormalities in an ovine model of chronic blood pressure elevation after prenatal corticosteroid exposure: Implications for development of atrial fibrillation. Eur Heart J. 2006;27(24):3045–3056.
  18. Power JM, Beacom GA, Alferness CA, et al. Susceptibility to atrial fibrillation: A study in an ovine model of pacing-induced early heart failure. J Cardiovasc Electrophysiol. 1998;9(4):423–435.
  19. Mandapati R, Skanes A, Chen J, Berenfeld O, Jalife J. Stable microreentrant sources as a mechanism of atrial fibrillation in the isolated sheep heart. Circulation. 2000;101(2):194–199.
  20. Lee AM, Miller JR, Voeller RK, et al. A simple porcine model of inducible sustained atrial fibrillation. Innovations (Phila). 2016;11(1):76–78.
  21. Schwarzl M, Alogna A, Zweiker D, et al. A porcine model of early atrial fibrillation using a custom-built, radio transmission-controlled pacemaker. J Electrocardiol. 2016;49(2):124–131.
  22. Linz D, Hohl M, Khoshkish S, et al. Low-level but not high-level baroreceptor stimulation inhibits atrial fibrillation in a pig model of sleep apnea. J Cardiovasc Electrophysiol. 2016;27(9):1086–1092.
  23. Diness JG, Skibsbye L, Simó-Vicens R, et al. Termination of vernakalant-resistant atrial fibrillation by inhibition of small-conductance Ca(2+)-activated K(+) channels in pigs. Circ Arrhythm Electrophysiol. 2017;10(10):e005125.
  24. Jones DL, Guiraudon GM, Skanes AC, Guiraudon CM. Anatomical pitfalls during encircling cryoablation of the left atrium for atrial fibrillation therapy in the pig. J Interv Card Electrophysiol. 2008;21(3):187–193.
  25. Paslawska U, Gajek J, Kiczak L, et al. Development of porcine model of chronic tachycardia-induced cardiomyopathy. Int J Cardiol. 2011;153(1):36–41.
  26. Shiroshita-Takeshita A, Schram G, Lavoie J, Nattel S. Effect of simvastatin and antioxidant vitamins on atrial fibrillation promotion by atrial-tachycardia remodeling in dogs. Circulation. 2004;110(16):2313–2319.
  27. Shiroshita-Takeshita A, Brundel BJ, Lavoie J, Nattel S. Prednisone prevents atrial fibrillation promotion by atrial tachycardia remodeling in dogs. Cardiovasc Res. 2006;69(4):865–875.
  28. Gaspo R, Bosch RF, Talajic M, Nattel S. Functional mechanisms underlying tachycardia-induced sustained atrial fibrillation in a chronic dog model. Circulation. 1997;96(11):4027–4035.
  29. Doshi RN, Wu TJ, Yashima M, et al. Relation between ligament of Marshall and adrenergic atrial tachyarrhythmia. Circulation. 1999;100(8):876–883.
  30. Wu TJ, Ong JJ, Chang CM, et al. Pulmonary veins and ligament of Marshall as sources of rapid activations in a canine model of sustained atrial fibrillation. Circulation. 2001;103(8):1157–1163.
  31. Zhou S, Chang CM, Wu TJ, et al. Nonreentrant focal activations in pulmonary veins in canine model of sustained atrial fibrillation. Am J Physiol Heart Circ Physiol. 2002;283(3):H1244–H1252.
  32. Kijtawornrat A, Roche BM, Hamlin RL. A canine model of sustained atrial fibrillation induced by rapid atrial pacing and phenylephrine. Comp Med. 2008;58(5):490–493.
  33. Sinno H, Derakhchan K, Libersan D, Merhi Y, Leung TK, Nattel S. Atrial ischemia promotes atrial fibrillation in dogs. Circulation. 2003;107(14):1930–1936.
  34. Rivard L, Sinno H, Shiroshita-Takeshita A, Schram G, Leung TK, Nattel S. The pharmacological response of ischemia-related atrial fibrillation in dogs: Evidence for substrate-specific efficacy. Cardiovasc Res. 2007;74(1):104–113.
  35. Li D, Fareh S, Leung TK, Nattel S. Promotion of atrial fibrillation by heart failure in dogs: Atrial remodeling of a different sort. Circulation. 1999;100(1):87–95.
  36. Li D, Shinagawa K, Pang L, et al. Effects of angiotensin-converting enzyme inhibition on the development of the atrial fibrillation substrate in dogs with ventricular tachypacing-induced congestive heart failure. Circulation. 2001;104(21):2608–2614.
  37. Okuyama Y, Miyauchi Y, Park AM, et al. High resolution mapping of the pulmonary vein and the vein of Marshall during induced atrial fibrillation and atrial tachycardia in a canine model of pacing-induced congestive heart failure. J Am Coll Cardiol. 2003;42(2):348–360.
  38. Ammar EM, Kudrin AN. Comparative antiarrhythmic activity of beta-N-hexamethyleneimino-P-butoxypropiophenone, quinidine and novocaine amide in aconitine auricular fibrillation and flutter in cats. Farmakol Toksikol. 1969;32(4):415–418.
  39. Gendenshteĭn EI, Kostin IV, Simon IB. Anti-arrhythmic activity of the beta2-adrenoblockader alpheprol. Biull Eksp Biol Med. 1976;81(6):694–696.
  40. Byrne JE, Gomoll AW, McKinney GR. Antiarrhythmic properties of MJ 9067 in acute animal models. J Pharmacol Exp Ther. 1977;200(1):147–154.
  41. Winslow E. Hemodynamic and arrhythmogenic effects of aconitine applied to the left atria of anesthetized cats: Effects of amiodarone and atropine. J Cardiovasc Pharmacol. 1981;3(1):87–100.
  42. Gendenshteĭn EI, Kostin IV. Antiarrhythmic activity of trimecaine in experimental arrhythmia and its effect on the heart conduction system. Farmakol Toksikol. 1976;39(4):426–428.
  43. Gendenshteĭn EI, Kostin V, Volkova ND. Antiarrhythmic activity of adrenergic blockaders with different mechanisms of action. Kardio­logiia. 1977;17(4):116–120.
  44. Kaverina NV, Senova ZP, Vikxliàev IuI, Ul’iànova OV. Antiarrhythimic properties of ethmozine. Farmakol Toksikol. 1970;33(6):693–697.
  45. Schmidt C, Wiedmann F, Langer C, et al. Cloning, functional characterization, and remodeling of K2P3.1 (TASK-1) potassium channels in a porcine model of atrial fibrillation and heart failure. Heart Rhythm. 2014;11(10):1798–1805.
  46. Schmidt C, Wiedmann F, Beyersdorf C, et al. Genetic ablation of TASK-1 (tandem of P domains in a weak inward rectifying K(+) Channel-related acid-sensitive K(+) Channel-1) (K(2P)3.1) K(+) channels suppresses atrial fibrillation and prevents electrical remodeling. Circ Arrhythm Electrophysiol. 2019;12(9):e007465.
  47. Wiedmann F, Schulte JS, Gomes B, et al. Atrial fibrillation and heart failure-associated remodeling of two-pore-domain potassium (K(2P)) channels in murine disease models: Focus on TASK-1. Basic Res Cardiol. 2018;113(4):27.
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