Electrophysiological remodeling of the right ventricle in experimental heart failure of different etiologies
https://doi.org/10.20538/1682-0363-2019-2-165-174
Abstract
The aim of the study was to evaluate electrophysiological remodeling of the right ventricle in rats in experimental heart failure of different etiologies.
Materials and methods. Isadrin-, doxorubicin- and monocrotaline-induced heart failure models were developed. Unipolar epicardial electrograms of the ventricles (256 recording sites) were recorded using a 144-channel system. The cardiac output and pressure in both ventricles of the heart were measured. Activation-recovery intervals were used as an index of duration of local repolarization, and the general and local dispersions of activation-recovery intervals were used as an index of heterogeneity of ventricular repolarization.
Results. In all models of heart failure, the following were identified: 1) non-uniform prolongation of repolarization with the greatest elongation at the apex of the right ventricle; 2) an increase in apicobasal differences of repolarization with the greatest change in the right ventricle; 3) an increase in the heterogeneity of the repolarization of the epicardial layer of the ventricles with heterogeneous changes in the local heterogeneity of repolarization and a decrease in the interregional differences in the heterogeneity of the electrophysiological properties of the myocardium; 4) more pronounced changes in the repolarization of the right ventricle than in the repolarization of the left ventricle.
Conclusion. Thus, irrespective of the cause of the heart failure, the following changes occur: 1) prolongation of the right ventricular repolarization occurs non-uniformly (mostly due to the apical area), which results in an increase in the right ventricular repolarization heterogeneity; 2) an increase in the heterogeneity of right ventricular repolarization is observed, which causes an increase in the overall heterogeneity of the ventricular epicardial surface.
Supporting agencies: The study was supported by the Program for Fundamental Research of RAS (project №АААА-А17-117012310154-6, 2017-2020).
About the Authors
A. S. Tsvetkova
Institute of Physiology of the Komi Scientific Centre of the Ural Branch of the Russian Academy of Sciences
Russian Federation
Tsvetkova Alena S., PhD, Senior Researcher, Laboratory
of Cardiac Physiology
50, Pervomayskaya Str., GSP-2, Syktyvkar, Komi Republic, 167982
Russian Federation
Tsvetkova Alena S., PhD, Senior Researcher, Laboratory
of Cardiac Physiology
50, Pervomayskaya Str., GSP-2, Syktyvkar, Komi Republic, 167982
V. V. Krandycheva
Institute of Physiology of the Komi Scientific Centre of the Ural Branch of the Russian Academy of Sciences
Russian Federation
Krandycheva Valeria V., PhD, Associate Professor,
Senior Researcher, Laboratory of Cardiac Physiology
50, Pervomayskaya Str., GSP-2, Syktyvkar, Komi Republic, 167982
Russian Federation
Krandycheva Valeria V., PhD, Associate Professor,
Senior Researcher, Laboratory of Cardiac Physiology
50, Pervomayskaya Str., GSP-2, Syktyvkar, Komi Republic, 167982
S. N. Kharin
Institute of Physiology of the Komi Scientific Centre of the Ural Branch of the Russian Academy of Sciences
Russian Federation
Kharin Sergey N., DBSc, Associate Professor, Vicedirector
50, Pervomayskaya Str., GSP-2, Syktyvkar, Komi Republic, 167982
Russian Federation
Kharin Sergey N., DBSc, Associate Professor, Vicedirector
50, Pervomayskaya Str., GSP-2, Syktyvkar, Komi Republic, 167982
References
1. De Groote P. Right ventricular systolic function in heart failure: a long story but still the same question. Arc. Cardiovasc. Dis. 2016; 109 (4): 227–230. DOI: 10.1016/j.acvd.2016.02.001.
2. Schuijt M.T.U., Blok I.M., Zwinderman A.H., van Riel A.C.M.J., Schuuring M.J., de Winter R.J., Duijnhouwer A.L., van Dijk A.P.J., Mulder B.J.M., Bouma B.J. Mortality in pulmonary arterial hypertension due to congenital heart disease: serial changes improve prognostication. Int. J. Cardiol. 2017; 243: 449–453. DOI: 10.1016/j.ijcard.2017.05.101.
3. Churchill T.W., Baggish A.L. The right heart: acute and chronic issues. Curr. Treat Options Cardio Med. 2017; 19 (11): 83. DOI: 10.1007/s11936-017-0581-z.
4. Tadic M., Pieske-Kraigher E., Cuspidi C., Morris D.A., Burkhardt F., Baudisch A., Habfeld S., Tschope C., Pieske B. Right ventricular strain in heart failure: clinical perspective. Arch. Cardiovasc. Dis. 2017; 110 (10): 562–571. DOI: 10.1016/j.acvd.2017.05.002.
5. Ho S.Y., Nihoyannopoulos P. Anatomy, echocardiography, and normal right ventricular dimensions. Heart. 2006; 92: i2–i13. DOI: 10.1136/hrt.2005.077875.
6. Hayashi Y., Takagi M., Kakihara J., Sakamoto S., Tatsumi H., Doi A., Iwata S., Sugioka K., Yoshiyama M. Impact of simple electrocardiographic markers as predictors for deterioration of left ventricular function in patients with freguent right ventricular apical pacing. Heart Vessels. 2018; 33 (3): 299–308. DOI: 10.1007/s00380-017-1053-x [Epub ahead of print].
7. Kanzaki H., Satomi K., Noda T., Shimizu W., Kamakura S., Kitaura Y., Ishizaka N., Kitakaze M. Comparison of the acute effects of right ventricular apical pacing and biventricular pacing in patients with heart failure. Intern. Med. 2015; 54 (11): 1329–1335. DOI: 10.2169/internalmedicine.54.3081.
8. Sweeney M.O., Prinzen F.W. A new paradigm for physiologic ventricular pacing. J. Am. Coll. Cardiol. 2006; 47 (2): 282–288. DOI: 10.1016/j.jacc.2005.09.029.
9. Tsvetkova A.S., Kibler N.A., Nuzhny V.P., Shmakov D.N., Azarov J.E. Acute effects of pacing site on repolarization and haemodynamics of the canine ventricles. Europace. 2011; 13 (6): 889–896. DOI: 10.1093/europace/eur053.
10. Teerlink J.R., Pfeffer J.M., Pfeffer M.A. Progressive ventricular remodeling in response to diffuse isoproterenol-induced myocardial necrosis in rats. Circ. Res. 1994;75 (1): 105–113. DOI: 10.1161/01.res.75.1.105.
11. Tong J., Ganguly P.K., Singal P.K. Myocardial adrenergic changes at two stages of heart failure due to adriamycin treatment in rats. Am. J. Physiol. 1991; 260 (3): H909–H916.
12. Siveski-Iliskovic N., Kaul N., Singal P.K. Probucol promotes endogenous antioxidants and provides protection against adriamycin-induced cardiomyopathy in rats. Circulation. 1994; 89 (6): 2829–2835. DOI: 10.1161/01.cir.89.6.2829.
13. Kazachenko A.A., Okovityy S.V., Kulikov A.N., Gustaynis K.R., Nagorny M.B., Shulenin S.N., Erokhina I.L., Emel’yanova O.I. Comparative characteristics of some pharmacological models of the chronic heart failure. Experimental and Clinical Pharmacology. 2008; 71 (6):16–19 (in Russ.)].
14. Shipsey S.J., Bryant S.M., Hart G. Effects of hypertrophy on regional action potential characteristics in the rat left ventricle: а сellular basis for T-wave inversion? Circulation. 1997; 96: 2061–2068. DOI: 10.1161/01.cir.96.6.2061.
15. Kharin S.N. Krandycheva V.V., Shmakov D.N. Sequence of repolarization of the epicardial ventricle surface in rats with renovascular hypertension. VI symposium on comparative electrocardiography: abstracts. 2004: 77–78 (in Russ.)].
16. Donohoe P., Hendry B.M., Walgama O.V., Bertaso F., Hopster D.J., Shattock M.J., James A.F. An altered repolarizing potassium current in rat cardiac myocytes after subtotal nephrectomy. J. Am. Soc. Nephrol. 2000; 11 (9): 1589–1599.
17. Hanumanth K. Reddy, Sanjeev Wasson, Santhosh K.G. Koshy, Ravi Komatireddy. Structural correlates of electrical remodeling in ventricular hypertrophy. Cardiovascular Research. 2003; 58 (3): 495–497. DOI: 10.1016/S0008-6363(03)00369-9.
18. Gordon F. Tomaselli, Eduardo Marbán. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovascular Research. 1999; 42 (2): 270–283. DOI:10.1016/s0008-6363(99)00017-6.
19. Bos R., Mougenot N., Médiani O., Vanhoutte P.M., Lechat P. Potassium canrenoate, an aldosterone receptor antagonist, reduces isoprenaline-induced cardiac fibrosis in the rat. J. Pharmacol. Exp. Ther. 2004; 309 (3):1160–1166. DOI: 10.1124/jpet.103.063388.
20. Di Diego J.M., Sun Z.Q., Antzelevitch C. I(to) and action potential notch are smaller in left vs. right canine ventricular epicardium. Am. J. Physiol. 1996; 271 (2/2):H548–H561.
21. Volders P.G., Sipido K.R., Carmeliet E., Spatjens R.L., Wellens H.J., Vos M.A. Repolarizing K currents ITO1 and IKs are larger in right than left canine ventricular midmyocardium. Circulation. 1999; 99 (2): 206–210. DOI: 10.1161/01.cir.99.2.206.
22. Watanabe T., Delbridge L.M., Bustamante J.O., McDonald T.F. Heterogeneity of the action potential in isolated rat ventricular myocytes and tissue. Circ. Res. 1983;52 (3): 280–290. DOI: 10.1161/01.res.52.3.280.
23. Gуmez A.M., Benitah J.P., Henzel D., Vinet A., Lorente P., Delgado C. Modulation of electrical heterogeneity by compensated hypertrophy in rat left ventricle. Am. J. Physiol. 1997; 272 (3): H1078–H1086.
24. Krandycheva V., Kharin S., Strelkova M., Shumikhin K., Sobolev A., Shmakov D. Ventricular repolarization in rat model of global heart failure. Clinical and Experimental Pharmacology and Physiology. 2013; 40 (7): 431–437. DOI: 10.1111/1440-1681.12104.
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Tsvetkova A.S., Krandycheva V.V., Kharin S.N. Electrophysiological remodeling of the right ventricle in experimental heart failure of different etiologies. Bulletin of Siberian Medicine. 2019;18(2):165-174. https://doi.org/10.20538/1682-0363-2019-2-165-174
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