Modeling and Simulation of Growth in Diastolic Heart Failure

علوم کاربردی و محاسباتی در مکانیک

Article 8, Volume 35, Issue 3 - Serial Number 33, October 2023, Pages 101-114   

Document Type: Original Article

DOI: 10.22067/jacsm.2023.81490.1173

Authors

Pezhman Namashiri¹; Akbar Allahverdizadeh^{* 2}; Behnam Dadashzadeh¹

¹Department of Mechatronics Engineering, University of Tabriz, Tabriz, Iran

²University of TabrizDepartment of Mechatronics Engineering, University of Tabriz, Tabriz, Iran

Abstract

Heart failure is one of the cardiovascular diseases that causes changes in the structure of the heart and reduces the output of the heart. This disease can be divided into two categories: diastolic and systolic heart failure. In diastolic heart failure, the thickness of the ventricular walls increased and is associated with concentric hypertrophy. In this study, concentric hypertrophy is considered to be caused by pressure overload, as a result of which, the number of sarcomeres increases in parallel, and as a result, causes a relative increase in the transverse area of the cardiomyocytes. Continuum equations of concentric hypertrophy by using an idealized biventricular geometry have been implemented in COMSOL Multiphysics software, the approach presented for implementing the equations is completely new and has fundamental advantages over the implementation of the previous approach, and does not require coding and can be easily implemented in a finite element software. The results of the simulation showed that the thickness of the ventricular walls increases and the volume of the ventricular chambers decreases. The mentioned results are consistent with the clinical observations of the disease and shows that computational modeling can be used as a powerful tool to increase specialist’s knowledge of diseases that have a high mortality rate.

Keywords

Growth; Heart Diseases; Computational Modeling; Finite Element Method

References

[1] R. Klabunde, Cardiovascular physiology concepts, Lippincott Williams & Wilkins, 2011.

 [2] J. Loscalzo, Harrison's cardiovascular medicine 2/E, McGraw-Hill Education, 2013.

 [3] K. Chatterjee and B. Massie, “Systolic and diastolic heart failure: differences and similarities,” Journal of Cardiac Failure, vol. 13, no. 7, pp. 569-576, (2007). https://doi.org/10.1016/j.cardfail.2007.04.006

[4] Z. A. McCrossan, R. Billeter and E. White, “Transmural changes in size, contractile and electrical properties of SHR left ventricular myocytes during compensated hypertrophy,” Cardiovascular Research, vol. 63, no. 2, pp. 283-292, 2004.

[5] M. Genet, L. C. Lee, B. Baillargeon, J. M. Guccione and E. Kuhl, “Modeling pathologies of diastolic and systolic heart failure,” Annals of Biomedical Engineering, vol. 44, no. 1, pp. 112-127, 2016.

[6] S. Göktepe, O. J. Abilez and E. Kuhl, “A generic approach towards finite growth with examples of athlete's heart, cardiac dilation, and cardiac wall thickening,” Journal of the Mechanics and Physics of Solids, vol. 58, no. 10, pp. 1661-1680, 2010.

[7] S. Göktepe, O. J. Abilez, K. K. Parker and E. Kuhl, “A multiscale model for eccentric and concentric cardiac growth through sarcomerogenesis,” Journal of Theoretical Biology, vol. 265, no. 3, Pp. 433-442, 2010.

 [8] E. K. Rodriguez, A. Hoger and A. D. McCulloch, “Stress-dependent finite growth in soft elastic tissues,” Journal of Biomechanics, vol. 27, no. 4, pp. 455-467, 1994.

[9] M. Rausch, A. Dam, S. Göktepe, O. Abilez and E. Kuhl, “Computational modeling of growth: systemic and pulmonary hypertension in the heart,” Biomechanics and Modeling in Mechanobiology, vol. 10, no. 6, pp. 799-811, 2011.

[10] R. C. Kerckhoffs, J. H. Omens and A. D. McCulloch, “A single strain-based growth law predicts concentric and eccentric cardiac growth during pressure and volume overload,” Mechanics Research Communications, vol. 42, no. pp. 40-50, 2012.

 [11] E. Berberoğlu, H. O. Solmaz and S. Göktepe, “Computational modeling of coupled cardiac electromechanics incorporating cardiac dysfunctions,” European Journal of Mechanics-A/Solids, vol. 48, no. pp. 60-73, 2014.

[12] F. Del Bianco, P. C. Franzone, S. Scacchi and L. Fassina, “Electromechanical effects of concentric hypertrophy on the left ventricle: A simulation study,” Computers in Biology and Medicine, vol. 99, no. pp. 236-256, 2018.

[13] K. Yoshida, A. D. McCulloch, J. H. Omens and J. W. Holmes, “Predictions of hypertrophy and its regression in response to pressure overload,” Biomechanics and Modeling in Mechanobiology, vol. 19, no. 3, pp. 1079-1089, 2020.

[14] A. Ahmad Bakir, A. Al Abed, M. C. Stevens, N. H. Lovell and S. Dokos, “A multiphysics biventricular cardiac model: Simulations with a left-ventricular assist device,” Frontiers in Physiology, vol. 9, no. pp. 1259, 2018.

[15] I. J. LeGrice, B. Smaill, L. Chai, S. Edgar, J. Gavin and P. J. Hunter, “Laminar structure of the heart: ventricular myocyte arrangement and connective tissue architecture in the dog,” American Journal of Physiology-Heart and Circulatory Physiology, vol. 269, no. 2, pp. H571-H582, 1995.

[16] G. A. Holzapfel and R. W. Ogden, “Constitutive modelling of passive myocardium: a structurally based framework for material characterization,” Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences, vol. 367, no. 1902, pp. 3445-3475, 2009. https://doi.org/10.1098/rsta.2009.0091

[17] B. Cansız, K. Sveric, K. Ibrahim, R. H. Strasser, A. Linke and M. Kaliske, “Towards predictive computer simulations in cardiology: Finite element analysis of personalized heart models,” ZAMM‐Journal of Applied Mathematics and Mechanics/Zeitschrift für Angewandte Mathematik und Mechanik, vol. 98, no. 12, pp. 2155-2176, 2018.

[18] H. S. Hosseini, D. C. Beebe and L. A. Taber, “Mechanical effects of the surface ectoderm on optic vesicle morphogenesis in the chick embryo,” Journal of Biomechanics, vol. 47, no. 16, pp. 3837-3846, 2014.

[19] G. Himpel, E. Kuhl, A. Menzel and P. Steinmann, “Computational modelling of isotropic multiplicative growth,” Computer Mod Engnnering Science, vol. 8, no. Pp. 119-134, 2005.

 [20] L. H. Opie, Heart physiology: from cell to circulation, Lippincott Williams & Wilkins, 2004.

 [21] M. R. Zile, C. F. Baicu and D. D. Bonnema, “Diastolic heart failure: definitions and terminology,” Progress in Cardiovascular Diseases, vol. 47, no. 5, pp. 307-313, 2005.

[22] S. Dokos, B. H. Smaill, A. A. Young and I. J. LeGrice, “Shear properties of passive ventricular myocardium,” American Journal of Physiology-Heart and Circulatory Physiology, vol. 283, no. 6, pp. H2650-H2659, 2002.

[23] A. K. Abbas, N. Fausto and S. L. Robbins, Robbins and Cotran pathologic basis of disease, Elsevier Saunders, 2020.

 [24] K. Chatterjee, “Pathophysiology of systolic and diastolic heart failure,” Medical Clinics, vol. 96, no. 5, pp. 891-899, 2012.

 [25] K. Yoshida and J. W. Holmes, “Computational models of cardiac hypertrophy,” Progress in Biophysics and Molecular Biology, vol. 159, no. pp. 75-85, 2021.