Study of calcium overload in one-dimensional cardiac model. role of spatial distribution of pathology
Matematičeskaâ biologiâ i bioinformatika, Tome 13 (2018) no. 2, pp. 466-479.

Voir la notice de l'article provenant de la source Math-Net.Ru

The premature ventricular contractions are relatively common clinical diagnosis. Ventricular activation initiated from an ectopic focus in the heart ventricles results in the premature contraction. Pathophysiology of this disease is related to calcium overload in cardiomyocytes when delayed after depolarization aroused due to spontaneous calcium release from sarcoplasmic reticulum. This could lead to myocardium activation from an ectopic focus and premature ventricular contraction. In our work, we study calcium overload in cardiomyocytes using one-dimensional monodomain electrophysiological model of the myocardium. Calcium overload in cardiomyocytes is simulated by inhibition of Na$^+$/K$^+$ exchanger and SERCA-pump within the Noble98 cell model. We propose an algorithm to automatically detect premature activation in the one-dimensional model. The main goal of our study is to evaluate the effect of a spatial distribution of pathology on the frequency of premature myocardium excitations. Model simulation showed that an ectopic activation is usually initiated in a region of the maximum pathology. However, if the function of a spatial distribution of pathology had a discontinuity, then an ectopic activation initiated from the region of discontinuity of a function. Also, we study changes in action potential generation in the pathology region. We obtained a nonlinear and a nonlocal relationship between spatial distribution of pathology and the degree of sarcoplasmic reticulum overload in the one-dimensional model.
@article{MBB_2018_13_2_a15,
     author = {T. M. Nesterova and K. S. Ushenin and N. A. Balakina-Vikulova and O. Solovyova},
     title = {Study of calcium overload in one-dimensional cardiac model. role of spatial distribution of pathology},
     journal = {Matemati\v{c}eska\^a biologi\^a i bioinformatika},
     pages = {466--479},
     publisher = {mathdoc},
     volume = {13},
     number = {2},
     year = {2018},
     language = {ru},
     url = {http://geodesic.mathdoc.fr/item/MBB_2018_13_2_a15/}
}
TY  - JOUR
AU  - T. M. Nesterova
AU  - K. S. Ushenin
AU  - N. A. Balakina-Vikulova
AU  - O. Solovyova
TI  - Study of calcium overload in one-dimensional cardiac model. role of spatial distribution of pathology
JO  - Matematičeskaâ biologiâ i bioinformatika
PY  - 2018
SP  - 466
EP  - 479
VL  - 13
IS  - 2
PB  - mathdoc
UR  - http://geodesic.mathdoc.fr/item/MBB_2018_13_2_a15/
LA  - ru
ID  - MBB_2018_13_2_a15
ER  - 
%0 Journal Article
%A T. M. Nesterova
%A K. S. Ushenin
%A N. A. Balakina-Vikulova
%A O. Solovyova
%T Study of calcium overload in one-dimensional cardiac model. role of spatial distribution of pathology
%J Matematičeskaâ biologiâ i bioinformatika
%D 2018
%P 466-479
%V 13
%N 2
%I mathdoc
%U http://geodesic.mathdoc.fr/item/MBB_2018_13_2_a15/
%G ru
%F MBB_2018_13_2_a15
T. M. Nesterova; K. S. Ushenin; N. A. Balakina-Vikulova; O. Solovyova. Study of calcium overload in one-dimensional cardiac model. role of spatial distribution of pathology. Matematičeskaâ biologiâ i bioinformatika, Tome 13 (2018) no. 2, pp. 466-479. http://geodesic.mathdoc.fr/item/MBB_2018_13_2_a15/

[1] O. L. Bokeriya, A. A. Akhobekov, “Zheludochkovaya ekstrasistoliya”, Annaly aritmologii, 12:1 (2015)

[2] J. B. Kostis, K. McCrone, A. E. Moreyra, M. Hosler, N. Cosgrove, Kuo P. T., “The effect of age, blood pressure and gender on the incidence of premature ventricular contractions”, Angiology, 33:7 (1982), 464–473 | DOI

[3] P. W. Kelleher, E. S. Imperial, P. Burnett, R. Mitchell, “Ventricular ectopy during prolonged ambulatory electrocardiographic monitoring in elderly hypertensive subjects”, Journal of the American Geriatrics Society, 38:3 (1990), 201–204 | DOI

[4] Y. Kihara, J. P. Morgan, “Intracellular calcium and ventricular fibrillation. Studies in the aequorin-loaded isovolumic ferret heart”, Circulation research, 68:5 (1991), 1378–1389 | DOI

[5] E. G. Lakatta, T. Guarnieri, “Spontaneous myocardial calcium oscillations”, Journal of cardiovascular electrophysiology, 4:4 (1993), 473–489 | DOI

[6] M. Fink, P. J. Noble, D. Noble, “Ca$^{2+}$-induced delayed afterdepolarizations are triggered by dyadic subspace Ca$^{2+}$ affirming that increasing SERCA reduces aftercontractions”, American Journal of Physiology-Heart and Circulatory Physiology, 301:3 (2011), H921–H935 | DOI

[7] A. Kursanov, O. Solovyova, L. Katsnelson, V. S. Markhasin, “Role of Mechanics in Rhythm Disturbances in 1D Mathematical Model of Myocardial Tissue with Local Ca$^{2+}$-Overload”, Computing in Cardiology Conference (CinC) (2015), 549–552 | DOI

[8] T. Sulman, L. B. Katsnelson, O. Solovyova, V. S. Markhasin, “Mathematical modeling of mechanically modulated rhythm disturbances in homogeneous and heterogeneous myocardium with attenuated activity of Na$^+$-K$^+$ pump”, Bulletin of Mathematical Biology, 70:3 (2008), 910–949 | DOI | MR | Zbl

[9] J. Bogaert, F. E. Rademakers, “Regional nonuniformity of normal adult human left ventricle”, American Journal of Physiology-Heart and Circulatory Physiology, 280:2 (2001), H610–H620 | DOI | MR

[10] W. E. Cascio, Myocardial ischemia: what factors determine arrhythmogenesis?, Journal of Cardiovascular Electrophysiology, 12:6 (2001), 726–729 | DOI

[11] R. H. Anderson, J. Yanni, M. R. Boyett, N. J. Chandler, H. Dobrzynski, “The anatomy of the cardiac conduction system”, Clinical Anatomy, 22:1 (2009), 99–113 | DOI

[12] D. Noble, A. Varghese, P. Kohl, P. Noble, “Improved guinea-pig ventricular cell model incorporating a diadic space, ikr and iks, and length-and tension-dependent processes”, The Canadian Journal of Cardiology, 14:1 (1998), 123–134

[13] P. Malmivuo, J. Malmivuo, R. Plonsey, Bioelectromagnetism: principles and applications of bioelectric and biomagnetic fields, Oxford University Press, New York, 1995

[14] G. R. Mirams, C. J. Arthurs, M. O. Bernabeu, R. Bordas, J. Cooper, A. Corrias, Y. Davit, S. J. Dunn, A. G. Fletcher, D. G. Harvey et al., “Chaste: an open source C++ library for computational physiology and biology”, PLoS Computational Biology, 9:3 (2013) | DOI | MR

[15] O. Solovyova, N. Vikulova, L. B. Katsnelson, V. S. Markhasin, P. J. Noble, A. Garny, P. Kohl, D. Noble, “Mechanical interaction of heterogeneous cardiac muscle segments in silico: effects on Ca$^{2+}$ handling and action potential”, International Journal of Bifurcation and Chaos, 13:12 (2003), 3757–3782 | DOI | Zbl

[16] D. Noble, A. Garny, P. J. Noble, “How the Hodgkin-Huxley equations inspired the cardiac physiome project”, The Journal of Physiology, 590:11 (2012), 2613–2628 | DOI

[17] O. L. Bokeriya, A. A. Akhobekov, “Ionnye kanaly i ikh rol v razvitii narushenii ritma serdtsa”, Annaly aritmologii, 11:3 (2014)

[18] O. Bernus, R. Wilders, C. W. Zemlin, H. Verschelde, A. V. Panfilov, “A computationally efficient electrophysiological model of human ventricular cells”, American Journal of Physiology-Heart and Circulatory Physiology, 282:6 (2002), H2296–H2308 | DOI

[19] A. Mattiazzi, M. Argenziano, Y. Aguilar-Sanchez, G. Mazzocchi, A. L. Escobar, “Ca$^{2+}$ Sparks and Ca$^{2+}$ waves are the subcellular events underlying Ca$^{2+}$ overload during ischemia and reperfusion in perfused intact hearts”, Journal of Molecular and Cellular Cardiology, 79 (2015), 69–78 | DOI

[20] A. G. Kleber, Y. Rudy, “Basic mechanisms of cardiac impulse propagation and associated arrhythmias”, Physiological Reviews, 84:2 (2004), 431–488 | DOI

[21] N. A. Vikulova, L. B. Katsnelson, A. G. Kursanov, O. Solovyova, V. S. Markhasin, “Mechano-electric feedback in one-dimensional model of myocardium”, Journal of Mathematical Biology, 73:2 (2016), 335–366 | DOI | MR | Zbl

[22] L. B. Katsnelson, T. Sulman, O. Solovyova, V. S. Markhasin, “Role of myocardial viscoelasticity in disturbances of electrical and mechanical activity in calcium overloaded cardiomyocytes: mathematical modeling”, Journal of Theoretical Biology, 272:1 (2011), 83–95 | DOI | MR | Zbl