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Bito V, Heinzel FR, Claus P, et al. Alterations in excitation-contraction coupling in chronically ischemic or hibernating myocardium. Exp Clin Cardiol. 2005;10(3):142-5
Bito, V., Heinzel, F. R., Claus, P., Bijnens, B., Verbeken, E., Van der Velden, J., Stienen, G., & Sipido, K. R. (2005). Alterations in excitation-contraction coupling in chronically ischemic or hibernating myocardium. Experimental and clinical cardiology, 10(3), 142-5.
Bito, Virginie, et al. "Alterations in excitation-contraction coupling in chronically ischemic or hibernating myocardium." Experimental and clinical cardiology vol. 10,3 (2005): 142-5.
Bito V, Heinzel FR, Claus P, Bijnens B, Verbeken E, Van der Velden J, Stienen G, Sipido KR. Alterations in excitation-contraction coupling in chronically ischemic or hibernating myocardium. Exp Clin Cardiol. 2005;10(3):142-5. PMID: 19641678; PMCID: PMC2716242.
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Exp Clin Cardiol. 2005;10(3):142-5.

Alterations in excitation-contraction coupling in chronically ischemic or hibernating myocardium.

Experimental and clinical cardiology

Virginie Bito, Frank R Heinzel, Piet Claus, Bart Bijnens, Erik Verbeken, Jolanda Van der Velden, Ger Stienen, Karin R Sipido

Affiliations

  1. Laboratory of Experimental Cardiology.

PMID: 19641678 PMCID: PMC2716242

Abstract

In coronary artery disease, areas subtended by a severely stenotic artery or by collateral vessels can develop chronic contractile dysfunction in the absence of necrosis. This dysfunction is thought to be adaptive to the reduced flow reserve and can be reversible upon revascularization, hence the term 'hibernating' myocardium. In the present report, the underlying cellular mechanisms were studied in a pig with severe stenosis in the left circumflex coronary artery, resulting in hibernation in the distal myocardium.After six weeks, single cardiomyocytes were isolated enzymatically from the hibernating region (HIB) and their properties compared with those of cardiomyocytes from the same area in matched control pigs (CTRL). The amplitude of cell shortening during field stimulation (1 Hz) was reduced in HIB versus CTRL; the accompanying Ca(2+) transients were only modestly reduced. In whole cell recording, prolongation of action potential was observed in HIB. When this difference was excluded by using depolarizing steps of fixed duration in both HIB and CTRL, the Ca(2+) transients in HIB myocytes were reduced compared with CTRL. There was also a decrease in peak L-type Ca(2+) current in HIB. In intact cells, increasing the available Ca(2+) for contraction did not correct the contractile deficit in HIB, suggesting alterations to the myofilaments.In conclusion, in this pig model for hibernating myocardium, intrinsic remodelling of the myocytes with a unique profile of excitation-contraction coupling is demonstrated. Along with the changes observed in myocytes from the border zone of a myocardial infarction, or in the remote area, this specific phenotype adds to the diversity and complexity of the remodelling processes in ischemic cardiomyopathy.

Keywords: Calcium; Cardiac myocytes; Ischemic heart disease

References

  1. Circ Res. 1999 Mar 19;84(5):562-70 - PubMed
  2. Cardiovasc Res. 1998 May;38(2):414-23 - PubMed
  3. Am J Physiol. 1999 Jul;277(1):H417-22 - PubMed
  4. Circ Res. 1997 Mar;80(3):393-9 - PubMed
  5. Circulation. 2002 Apr 30;105(17):2099-106 - PubMed
  6. Circulation. 1985 Dec;72(6 Pt 2):V123-35 - PubMed
  7. J Am Coll Cardiol. 2002 Apr 3;39(7):1151-8 - PubMed
  8. Science. 1997 May 2;276(5313):800-6 - PubMed
  9. Circulation. 1997 Apr 1;95(7):1900-9 - PubMed
  10. Circulation. 1997 Apr 1;95(7):1961-71 - PubMed
  11. Circulation. 2002 May 7;105(18):2223-8 - PubMed
  12. Circulation. 1998 May 12;97(18):1848-67 - PubMed
  13. Circulation. 1996 Aug 1;94(3):507-16 - PubMed
  14. Cardiovasc Res. 2003 Feb;57(2):302-11 - PubMed
  15. Circulation. 1997 Nov 4;96(9):2920-31 - PubMed
  16. Lancet. 2003 Jul 5;362(9377):14-21 - PubMed
  17. Circulation. 2003 Feb 18;107(6):883-8 - PubMed
  18. Circ Res. 2001 Oct 26;89(9):831-7 - PubMed
  19. Circulation. 1997 Nov 4;96(9):3205-14 - PubMed
  20. Am J Physiol Heart Circ Physiol. 2001 May;280(5):H1945-53 - PubMed
  21. Circ Res. 2004 Apr 30;94(8):1142-9 - PubMed
  22. Circ Res. 2004 Apr 2;94(6):794-801 - PubMed
  23. Circulation. 1995 Aug 15;92(4):756-66 - PubMed
  24. Am Heart J. 1989 Jan;117(1):211-21 - PubMed
  25. Am J Physiol. 1999 Oct;277(4):H1418-28 - PubMed
  26. Circ Res. 2003 May 2;92(8):897-903 - PubMed
  27. J Am Coll Cardiol. 1996 Jun;27(7):1577-85 - PubMed
  28. Physiol Rev. 1998 Oct;78(4):1055-85 - PubMed
  29. Circulation. 1994 Aug;90(2):735-45 - PubMed
  30. J Am Coll Cardiol. 1999 Dec;34(7):2126-36 - PubMed
  31. Circulation. 1996 Apr 15;93(8):1556-66 - PubMed
  32. Cardiovasc Res. 2004 Apr 1;62(1):63-73 - PubMed
  33. Int J Cardiovasc Intervent. 2000 Jun;3(2):111-120 - PubMed
  34. J Thorac Cardiovasc Surg. 1998 Dec;116(6):997-1004 - PubMed

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