Rhythminotropic Reactions of Human Myocardium in Ischemic and Rheumatic Heart Diseases against the Background of Amiodarone
Federal State Budgetary Institution «Research Institute of Cardiology», Siberian Branch of the RAMS, Tomsk, Russian Federation
*Corresponding author: Dina S. Kondratyeva, PhD, Research Associate, Federal State Budgetary Institution «Research Institute of Cardiology», Siberian Branch of the Russian Academy of Medical Sciences, 26111a Kievskaya str, Tomsk, 634012, Russian Federation. Tel/Fax: 7-3822-558396 E-Mail: firstname.lastname@example.org
In human heart failure, Ca2+ homeostasis gets disturbed due to a decrease in the function of the sarcoplasmic reticulum (SR). We studied the differences in the SR function in patients with rheumatic and coronary heart disease, against the background of amiodarone. Cardiac preparations from the atrium of 21 patients with coronary artery disease (CAD) and 14 patients with rheumatic heart disease (RHD) were used in this study. Myocardial strips perfused with oxygenated Krebs-Henzelait solution without and with amiodarone (1 mM/l) at 37°C. The steady state stimulation rate of the muscle strips was 0.5 Hz. The single extraordinary impulse was given as 0.2-1.5 sec after the steady state beat. Then, the first beat after a 4- to 60-sec rest period was evaluated. The extrasystoles of the myocardium in both groups, after long intervals, were decreased after amiodarone treatment. The amplitude of post extrasystoles of amiodarone-treated myocardium showed differences only after long intervals in both groups. Two types of inotropic responses of a failing myocardium after rest periods were observed. Type I post-rest contractions maintained the steady state amplitude after all rests. However, type II was characterized by a reduction in the amplitude of the contractions. Amiodarone treatment of the myocardium showing type I reactions led to an increase in the potentiation after rests, but showed no effect on the reaction of the muscle with the type II response. The results suggested that SR dysfunction was different in CAD and RHD. The realization of the therapeutic effect of amiodarone was found to be dependent on the functional activity of the SR.
1. Babick AP, Dhalla NS. Role of subcellular remodeling in cardiac dysfunction due to congestive heart failure. Med Princ Pract 2007; 16(2):81-9.
2. Helm PA, Younes L, Beg MF, Ennis DB, Leclercq C, Faris OP, McVeigh E, Kass D, Miller MI, Winslow RL. Evidence of structural remodeling in the dyssynchronous failing heart. Circ Res 2006; 98(1):125-32.
3. Sharov VG, Todor AV, Sabbah HN. Left ventricular histomorphometric findings in dogs with heart failure treated with the Acorn Cardiac Support Device. Heart Fail Rev 2005; 10(2):141-7.
4. Zarain-Herzberg A, Fragoso-Medina J, Estrada-Avilés R. Calcium-regulated transcriptional pathways in the normal and pathologic heart. IUBMB Life 2011; 63(10):847-55.
5. Crossman DJ, Ruygrok PN, Soeller C, Cannell MB. Changes in the organization of excitation-contraction coupling structures in failing human heart. PLoS One. 2011; 6(3):e17901.
6. Kubalova Z, Terentyev D, Viatchenko-Karpinski S, Nishijima Y, Györke I, Terentyeva R, da Cuñha DN, Sridhar A, Feldman DS, Hamlin RL, Carnes CA, Györke S. Abnormal intrastore calcium signaling in chronic heart failure. Proc Natl Acad Sci U S A. 2005; 102(39):14104-9.
7. Yano M, Ikeda Y, Matsuzaki M. Altered intracellular Ca2+ handling in heart failure. J Clin Invest 2005; 115:556–564.
8. Lamberts RR, Hamdani N, Soekhoe TW, Boontje NM, Zaremba R, Walker LA, de Tombe PP, van der Velden J, Stienen GJ. Frequency-dependent myofilament Ca2+ desensitization in failing rat myocardium. J Physiol 2007; 582(Pt 2):695-709.
9. Marston SB, de Tombe PP. Troponin phosphorylation and myofilament Ca2+-sensitivity in heart failure: increased or decreased. J Mol Cell Cardiol 2008; 45(5):603-7.
10. Wehrens XHT, Lehnart SE, Reiken S, Vest JA, Wronska A, Marks AR. Ryanodine receptor_calcium release channel PKA phosphorylation: A critical mediator of heart failure progression. PNAS 2006; 103(3б): 511–518.
11. Yeh YH, Wakili R, Qi XY, Chartier D, Boknik P, Kääb S, Ravens U, Coutu P, Dobrev D, Nattel S. Calcium-handling abnormalities underlying atrial arrhythmogenesis and contractile dysfunction in dogs with congestive heart failure. Circ Arrhythm Electrophysio. 2008; 1(2):93-102.
12. Narayan SM, Bayer JD, Lalani G, Trayanova NA. Action potential dynamics explain arrhythmic vulnerability in human heart failure: a clinical and modeling study implicating abnormal calcium handling. J Am Coll Cardiol 2008; 52(22):1782-92.
13. Birkeland JA, Sejersted OM, Taraldsen T, Sjaastad I. EC-coupling in normal and failing hearts. Scand Cardiovasc J 2005; 39(1-2):13-23.
14. Moss RL, Buck HS. Regulation of cardiac contraction by Ca2+. In: Handbook of Physiology. Page E, Fozzard HA, Solaro RJ (eds.). Oxford University Press, 2001.
15. Duan DD. A leakage leads to failure: roles of sarcoplasmic reticulum Ca2+ leak via RyR2 in heart failure progression. Hypertension 2010; 55(4):849-51.
16. Vandecaetsbeek I, Raeymaekers L, Wuytack F, Vangheluwe P. Factors controlling the activity of the SERCA2a pump in the normal and failing heart. Biofactors 2009; 35(6):484-99.
17. Zima AV, Bovo E, Bers DM, Blatter LA. Ca²+ spark-dependent and -independent sarcoplasmic reticulum Ca²+ leak in normal and failing rabbit ventricular myocytes. J Physiol 2010; 588(Pt 23):4743-57.
18. Ai X, Curran JW, Shannon TR, Bers DM, Pogwizd SM. Ca2+/calmodulin-dependent protein kinase modulates cardiac ryanodine receptor phosphorylation and sarcoplasmic reticulum Ca2+ leak in heart failure. Circ Res 2005; 97(12):1314-22.
19. Lehnart SE, Maier LS, Hasenfuss G. Abnormalities of calcium metabolism and myocardial contractility depression in the failing heart. Heart Fail Rev 2009; 14(4):213-24.
20. Mishra S, Sabbah HN, Rastogi S, Imai M, Gupta RC. Reduced sarcoplasmic reticulum Ca2+ uptake and increased Na+-Ca2+ exchanger expression in left ventricle myocardium of dogs with progression of heart failure. Heart Vessels 2005; 20(1):23-32.
21. Kondtratieva DS, Afanasiev SA, Rebrova TY, Tsapko LP, Karpov RS. Rhythmoinotropic myocardial reactions in rats with postinfarction cardiosclerosis against the background of streptozotocin-induced diabetes. Bull Exp Biol Med 2009; 148(2):181-3.
22. Kondrat'eva DS, Afanas'ev SA, Falaleeva LP, Popov SV. Possible role of sarcoplasmatic reticulum in anti-arrhythmic effects of the class III agent amiodarone]. Vestn Ross Akad Med Nauk 2009; (6):43-7.
23. Gomez AM, Guatimosim S, Dilly KW, Vassort G, Lederer WJ. Heart failure after myocardial infarction: altered excitation-contraction coupling. Circulation 2001; 104(6):688-93
24. Wachter R, Schmidt-Schweda S, Westermann D, Post H, Edelmann F, Kasner M, Lüers C, Steendijk P, Hasenfuss G, Tschöpe C, Pieske B. Blunted frequency-dependent up regulation of cardiac output is related to impaired relaxation in diastolic heart failure. Eur Heart J 2009; 30(24):3027-36.
25. Pieske B., Maier L., Bers D., Hasenfuss G. Ca2+ Handling and Sarcoplasmic Reticulum Ca2+ Content in Isolated Failing and Nonfailing Human Myocardium. Circ Res 1999; 85:38-46.Connolly SJ. Evidence-Based Analysis of Amiodarone Efficacy and Safety. Circulation 1999; 100: 2025-34.
26. Connolly SJ. Evidence-Based Analysis of Amiodarone Efficacy and Safety. Circulation 1999; 100: 2025-34.
27. Letelier LM, Udol K, Ena J, et al. Effectiveness of amiodarone for conversion of atrial fibrillation to sinus rhythm: a meta-analysis. Arch Intern Med 2003; 163:777-85.
28. Osaka T, Yokoyama E, Hasebe H, Kodama I. Effects of chronic amiodarone on the electrical restitution in the human ventricle with reference to its antiarrhythmic efficacy. J Cardiovasc Electrophysiol 2011; 22(6):669-76.
29. Bers DM. Ca influx and sarcoplasmic reticulum Ca release in cardiac muscle activation during postrest recovery. Am J Physiol 1985; 248: H366-H381.
30. Bluhm WF, Meyer M, Swanson EA, Dillmann WH. Postrest potentiation of active force in mouse papillary muscles is greatly accelerated by increased stimulus frequency. Ann N Y Acad Sci 1998; 853:304-7.
31. Mill JG, Vassallo DV, Leite CM. Mechanisms underlying the genesis of post-rest contractions in cardiac muscle. Braz J Med Biol Res 1992; 25(4):399-408.
32. Sen L, Cui G., Fonarow G.C. Laks H. Differences in mechanisms of SR dysfunction in ischemic vs. idiopathic dilated cardiomyopathy. Am J Physiol Heart Circ Physiol 2000; 279: H709–H718.
33. Movsesian MA, Karimi M, Green K, and Jones LR. Ca2+- transporting ATPase, phospholamban, and calsequestrin levelsin nonfailing and failing human myocardium. Circulation 90:653–657, 1994.
34. Zhong M; Zhang Y; Zhang W. Molecular mechanism underlying calcium handling in diastolic heart failure. Zhonghua Yi Xue Za Zhi 2001; 81(11):669-72.
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