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Chronotropic and inotropic dependence of the myocardium in patients with rheumatic heart disease before and after amiodarone treatment

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Abstract

Characteristic features of the electromechanical coupling of the myocardium were studied in patients with heart failure caused by rheumatic heart disease. Experiments were performed on muscle trabeculae isolated from the right atrial auricle in the course of surgical correction of a valve defect. The trabeculae displayed two types of mechanical responses, recorded in the isometric mode, to the postrest test. In the type I response, the mechanical restitution had an ascending pattern, the interval between electrical stimuli increasing. In type II, the mechanical restitution pattern was descending. Amiodarone (1 μM) treatment of the myocardium with the type I response enhanced the postrest potentiation of the mechanical response of trabeculae by more than 30%, but it had no effect on the muscles with the type II response. All patients whose biopsy material displayed the type II response had long episodes of atrial fibrillation. It is conceivable that the observed differences in the rhythm inotropic dependence of the human myocardium in rheumatic heart disease reflect different degrees of cardiomyocyte remodeling. The direction of this process is determined by the range of adaptive changes in intracellular structures, primarily, the sarcoplasmic reticulum.

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References

  1. Boitsov, S.A. and Podlesov, A.M., Arrhythmias in Chronic Heart Failure, Serd. Nedost., 2001, vol. 2, no. 5, p. 10.

    Google Scholar 

  2. Nikitin, N.P. and Alyavi, A.L., Characteristics of Diastolic Dysfunction during Remodeling of the Left Ventricle in Chronic Heart Failure, Kardiologiya, 1998, no. 3, p. 56.

  3. Tereshchenko, S.N. and Demidova, I.V., Khronicheskaya serdechnaya nedostatochnost’: Diagnostika i lechenie: Metodicheskie rekomendatsii (Chronic Heart Failure: Diagnosis and Treatment: Methodical Recommendations), Moscow, 2000.

  4. Olsson, L.G., Swedberg, K., Ducharme, A., et al., Atrial Fibrillation and Risk of Clinical Events in Chronic Heart Failure with and without Left Ventricular Systolic Dysfunction: Results from the Candesartan in Heart Failure—Assessment of Reduction in Mortality and morbidity (CHARM) Program, J. Am. Coll. Cardiol., 2006, vol. 47, no. 10, p. 1997.

    Article  PubMed  Google Scholar 

  5. Bers, D., Eisner, D., and Valdivia, H., Sarcoplasmic Reticulum Ca2+ and Heart Failure Roles of Diastolic Leak and Ca2+ Transport, Circ. Res., 2003, vol. 93, p. 487.

    Article  CAS  PubMed  Google Scholar 

  6. Lindner, M., Erdmann, E., and Beuckelmann, D.J., Calcium Content of the Sarcoplasmic Reticulum in Isolated Ventricular Myocytes from Patients with Terminal Heart Failure, J. Mol. Cell Cardiol., 1998, vol. 30, p. 743.

    Article  CAS  PubMed  Google Scholar 

  7. Perreault, C.L., Williams, C.P., and Morgan, J.P., Cytoplasmic Calcium Modulation and Systolic vs. Diastolic Dysfunction in Myocardial Hypertrophy and Failure, Circulation, 1993, vol. 87. suppl VII, p. VII31.

    Google Scholar 

  8. Yano, M., Ikeda, Y., and Matsuzaki, M., Altered Intracellular Ca2+ Handling in Heart Failure, J. Clin. Invest., 2005, vol. 115, p. 556.

    CAS  PubMed  Google Scholar 

  9. D’Agnolo, A., Luciani, G.B., Mazzucco, A., et al., Contractile Properties and Ca2+ Release Activity of the Sarcoplasmic Reticulum in Dilated Cardiomyopathy, Circulation, 1992, vol. 85, p. 518.

    PubMed  Google Scholar 

  10. Pieske, B., Kretschmann, B., Meyer, M., et al., Alterations in Intracellular Calcium Handling Associated with the Inverse Force-Frequency Relation in Human Dilated Cardiomyopathy, Circulation, 1995, vol. 92, p. 1169.

    CAS  PubMed  Google Scholar 

  11. Pieske, B., Maier, L., Bers, D., and Hasenfuss, G., Ca2+ Handling and Sarcoplasmic Reticulum Ca2+ Content in Isolated Failing and Nonfailing Human Myocardium, Circ. Res., 1999, vol. 85, p. 38.

    CAS  PubMed  Google Scholar 

  12. Sen, L., Cui, G., Fonarow, G.C., and Laks, H., Differences in Mechanisms of SR Dysfunction in Ischemic vs. Idiopathic Dilated Cardiomyopathy, Am. J. Physiol. Heart Circ. Physiol., 2000, vol. 279, p. H709.

    CAS  PubMed  Google Scholar 

  13. Heerdt, P.M., Klotz, S., and Burkhoff, D., Cardiomyopathic Etiology and SERCA2a Reverse Remodeling during Mechanical Support of the Failing Human Heart, Anesth. Analg., 2006, vol. 102, no. 1, p. 32.

    Article  PubMed  Google Scholar 

  14. Sipido, K.R., Stankovicova, T., Flameng, W., et al., Frequency Dependence of Ca2+ Release from the Sarcoplasmic Reticulum in Human Ventricular Myocytes from End-Stage Heart Failure, Cardiovasc. Res., 1998, vol. 37, no. 2, p. 478.

    Article  CAS  PubMed  Google Scholar 

  15. Afanas’ev, S.A., Naryzhnaya, N.V., and Popov, S.V., Amiodarone-Induced Changes in Intracellular Ca2+ Homeostasis in the Atrial Myocardium of Patients with Chronic Coronary Insufficiency, Fiziol. Chel., 2003, vol. 29, no. 3, p. 62 [Hum. Physiol. (Engl. Transl.), 2003, vol. 29, no. 3, p. 336].

    Google Scholar 

  16. Ugdyzhekova, D.S., Afanas’ev, S.A., Lukavskaya, I.A., and Popov, S.V., Cardiac Effects of the Class III Antiarrhythmic Drugs Amiodarone and Nibentan, Fiziol. Chel., 2005, vol. 31, no. 4, p. 467 [Hum. Physiol. (Engl. Transl.), 2005, vol. 31, no. 4, p. 467].

    CAS  Google Scholar 

  17. Ugdyzhekova, D.S., Afanas’ev, S.A., Antonchenko, I.V., et al., Characteristic Features of the Myocardial Inotropic Response in Patients with Coronary Heart Disease and Rat Myocardium in the Presence of Amiodarone, Kardiologiya, 2005, vol. 45, no. 3, p. 71.

    CAS  PubMed  Google Scholar 

  18. Ravens, U., Mahl, C., Ohler, A., et al., Mechanical Restitution and Recirculation Fraction in Cardiac Myocytes and Left Ventricular Muscle of Adult Rats, Basic Res. Cardiol., 1996, vol. 91, p. 123.

    Article  CAS  PubMed  Google Scholar 

  19. Wu, S.N., Shen, A.Y., and Hwang, T.L., Analysis of Mechanical Restitution and Post-Rest Potentiation in Isolated Rat Atrium, Chin. J. Physiol., 1996, vol. 39, p. 23.

    CAS  PubMed  Google Scholar 

  20. Maier, L.S., Bers, D.M., and Pieske, B., Differences in Ca2+-Handling and Sarcoplasmic Reticulum Ca2+-Content in Isolated Rat and Rabbit Myocardium, J. Mol. Cell Cardiol., 2000, vol. 32, no. 12, p. 2249.

    Article  CAS  PubMed  Google Scholar 

  21. Bers, D., Lederer, W.J., and Berlin, J.R., Intracellular Ca Transients in Rat Cardiac Myocytes: Role of Na-Ca Exchange in Excitation-Contraction Coupling, Am. J. Physiol., 1990, vol. 258, p. C944.

    CAS  PubMed  Google Scholar 

  22. Kodama, I., Kamiya, K., and Toyama, J., Amiodarone: Ionic and Cellular Mechanisms of Action of the Most Promising Class III Agent, Am. J. Cardiol., 1999, vol. 84, no. 9, p. 20R.

    Article  CAS  PubMed  Google Scholar 

  23. Kodama, I., Kamiya, K., and Toyama, J., Cellular Electropharmacology of Amiodarone, Cardiovasc. Res., 1997, vol. 35, no. 1, p. 13.

    Article  CAS  PubMed  Google Scholar 

  24. Helm, P.A., Younes, L., Beg, M.F., et al., Evidence of Structural Remodeling in the Dyssynchronous Failing Heart, Circ. Res., 2006, vol. 98, no. 21, p. 125.

    CAS  PubMed  Google Scholar 

  25. Rubtsov, A.M., Ca ATPase of the Sarcoplasmic Reticulum: Molecular Organization, Mechanism of Functioning, and Characteristics of Activity Regulation, Usp. Biol. Khim., 2005, vol. 45, p. 235.

    CAS  Google Scholar 

  26. Brillantes, A.M., Allen, P.D., Takahashi, T., et al., Differences in Cardiac Calcium Release Channel (Ryanodine Receptor) Expression in Myocardium from Patients with Endstage Heart Failure Caused by Ischemic vs. Dilated Cardiomyopathy, Circ. Res., 1992, vol. 71, p. 18.

    CAS  PubMed  Google Scholar 

  27. Ono, K., Yano, M., Ohkusa, T., et al., Altered Interaction of FKBP12.6 with Ryanodine Receptor as a Cause of Abnormal Ca2+ Release in Heart Failure, Cardiovasc. Res., 2000, vol. 48, p. 323.

    Article  CAS  PubMed  Google Scholar 

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Authors and Affiliations

  1. Research Institute of Cardiology, Tomsk Research Center, Siberian Branch, Russian Academy of Medical Sciences, Tomsk, 634012, Russia

    D. S. Kondrat’eva, S. A. Afanas’ev, A. V. Evtushenko, V. V. Evtushenko & V. M. Shipulin

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  1. D. S. Kondrat’eva
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  2. S. A. Afanas’ev
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  3. A. V. Evtushenko
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  4. V. V. Evtushenko
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  5. V. M. Shipulin
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Original Russian Text © D.S. Kondrat’eva, S.A. Afanas’ev, A.V. Evtushenko, V.V. Evtushenko, V.M. Shipulin, 2008, published in Fiziologiya Cheloveka, 2008, Vol. 34, No. 1, pp. 52–56.

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Kondrat’eva, D.S., Afanas’ev, S.A., Evtushenko, A.V. et al. Chronotropic and inotropic dependence of the myocardium in patients with rheumatic heart disease before and after amiodarone treatment. Hum Physiol 34, 45–49 (2008). https://doi.org/10.1134/S0362119708010064

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  • DOI: https://doi.org/10.1134/S0362119708010064

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