Evaluating the Hemodynamical Response of a Cardiovascular System under Support of a Continuous Flow Left Ventricular Assist Device via Numerical Modeling and Simulations
Dilated cardiomyopathy is the most common type of the heart failure which can be characterized by impaired ventricular contractility. Mechanical circulatory support devices were introduced into practice for the heart failure patients to bridge the time between the decision to transplant and the actual transplantation which is not sufficient due to the state of donor organ supply. In this study, the hemodynamic response of a cardiovascular system that includes a dilated cardiomyopathic heart under support of a newly developed continuous flow left ventricular assist device—Heart Turcica Axial—was evaluated employing computer simulations. For the evaluation, a numerical model which describes the pressure-flow rate relations of Heart Turcica Axial, a cardiovascular system model describing the healthy and pathological hemodynamics, and a baroreflex model regulating the heart rate were used. Heart Turcica Axial was operated between 8000？rpm and 11000？rpm speeds with 1000？rpm increments for assessing the pump performance and response of the cardiovascular system. The results also give an insight about the range of the possible operating speeds of Heart Turcica Axial in a clinical application. Based on the findings, operating speed of Heart Turcica Axial should be between 10000？rpm and 11000？rpm. 1. Introduction Dilated cardiomyopathy (DCM) is the most common type of nonischemic cardiomyopathy and a major cause of congestive heart failure [1, 2]. It leads to the weakening and enlargement of the heart and impairs its function to pump blood. It can be caused by genetic, viral, immune, alcoholic-toxic, or unknown factors. It can be associated with a different cardiovascular disease. Symptoms of this disease are fatigue, weakness, and systemic or pulmonary emboli [3]. In a DCM patient, reduced contractile function causes a dilatation in the ventricle cavity volume and a thinning in the wall volume. Left ventricular systolic pressure decreases while diastolic pressure increases. With the reduced contractility and systolic pressure, cardiac output decreases. To maintain the perfusion, the arteries and the veins constrict and the blood volume increases. With progression of the disease, systemic arterial pressure decreases and this leads to an increased workload on the right ventricle. Right ventricular systolic pressure and pulmonary arterial pressure increase accordingly, resulting in pulmonary hypertension [4–13]. DCM is conventionally treated with inotropic support, diuretics, and moderate exercise. When these methods fail, especially towards the final stage of the
References
[1]
C. S. Rihal, R. A. Nishimura, L. K. Hatle, K. R. Bailey, and A. J. Tajik, “Systolic and diastolic dysfunction in patients with clinical diagnosis of dilated cardiomyopathy: relation to symptoms and prognosis,” Circulation, vol. 90, no. 6, pp. 2772–2779, 1994.
[2]
T. A. Manolio, K. L. Baughman, R. Rodeheffer et al., “Prevalence and etiology of idiopathic dilated cardiomyopathy (summary of a National Heart, Lung, and Blood Institute workshop),” American Journal of Cardiology, vol. 69, no. 17, pp. 1458–1466, 1992.
[3]
D. P. Zipes, P. Libby, R. O. Bonow, and E. Braunwald, Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, Elsevier Saunders, Philadelphia, Pa, USA, 2005.
[4]
C. A. Beltrami, N. Finato, M. Rocco et al., “Structural basis of end-stage failure in ischemic cardiomyopathy in humans,” Circulation, vol. 89, no. 1, pp. 151–163, 1994.
[5]
D. Burkhoff, J. T. Flaherty, D. T. Yue et al., “In vitro studies of isolated supported human hearts,” Heart and Vessels, vol. 4, no. 4, pp. 185–196, 1988.
[6]
S. B. Felix, A. Staudt, W. V. D？rffel et al., “Hemodynamic effects of immunoadsorption and subsequent immunoglobulin substitution in dilated cardiomyopathy,” Journal of the American College of Cardiology, vol. 35, no. 6, pp. 1590–1598, 2000.
[7]
R. E. Hobbs, L. W. Miller, C. Bott-Silverman, K. B. James, G. Rincon, and E. B. Crossbard, “Hemodynamic effects of a single intravenous injection of synthetic human brain natriuretic peptide in patients with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy,” American Journal of Cardiology, vol. 78, no. 8, pp. 896–901, 1996.
[8]
C. Leclercq, S. Cazeau, H. Le Breton et al., “Acute hemodynamic effects of biventricular DDD pacing in patients with end-stage heart failure,” Journal of the American College of Cardiology, vol. 32, no. 7, pp. 1825–1831, 1998.
[9]
I. Makarenko, C. A. Opitz, M. C. Leake et al., “Passive stiffness changes caused by upregulation of compliant titin isoforms in human dilated cardiomyopathy hearts,” Circulation Research, vol. 95, no. 7, pp. 708–716, 2004.
[10]
P. H. Pak, W. L. Maughan, K. L. Baughman, and D. A. Kass, “Marked discordance between dynamic and passive diastolic pressure-volume relations in idiopathic hypertrophic cardiomyopathy,” Circulation, vol. 94, no. 1, pp. 52–60, 1996.
[11]
H. Sato, M. Hori, H. Ozaki et al., “Exercise-induced upward shift of diastolic left ventricular pressure-volume relation in patients with dilated cardiomyopathy: effects of β-adrenoceptor blockade,” Circulation, vol. 88, no. 5, pp. 2215–2223, 1993.
[12]
N. A. G. Stolf, L. F. P. Moreira, E. A. Bocchi et al., “Determinants of midterm outcome of partial left ventriculectomy in dilated cardiomyopathy,” Annals of Thoracic Surgery, vol. 66, no. 5, pp. 1585–1591, 1998.
[13]
F. Waagstein, K. Caidahl, I. Wallentin, C. H. Bergh, and A. Hjalmarson, “Long-term β-blockade in dilated cardiomyopathy: effects of short- and long-term metoprolol treatment followed by withdrawal and readministration of metoprolol,” Circulation, vol. 80, no. 3, pp. 551–563, 1989.
[14]
M. S. Slaughter, F. D. Pagani, J. G. Rogers et al., “Clinical management of continuous-flow left ventricular assist devices in advanced heart failure,” Journal of Heart and Lung Transplantation, vol. 29, no. 4, pp. S1–S39, 2010.
[15]
K. D. Aaronson, H. Patel, and F. D. Pagani, “Patient selection for left ventricular assist device therapy,” Annals of Thoracic Surgery, vol. 75, no. 6, pp. S29–S35, 2003.
[16]
L. H. Lund, J. Matthews, and K. Aaronson, “Patient selection for left ventricular assist devices,” European Journal of Heart Failure, vol. 12, no. 5, pp. 434–443, 2010.
[17]
E. Sorguven, M. A. Akgun, H. Ahn et al., “Flow simulation and optimization of a left ventricular assist device,” in Proceedings of the ASME International Mechanical Engineering Congress and Exposition (IMECE '07), pp. 1401–1407, Seattle, Wash, USA, November 2007.
[18]
T. Korakianitis and Y. Shi, “A concentrated parameter model for the human cardiovascular system including heart valve dynamics and atrioventricular interaction,” Medical Engineering and Physics, vol. 28, no. 7, pp. 613–628, 2006.
[19]
M. Darowski, C. de Lazzari, G. Ferrari, F. Clemente, and M. Guaragno, “The influence of simultaneous intra-aortic balloon pumping and mechanical ventilation on hemodynamic parameters—numerical simulation,” Frontiers of Medical and Biological Engineering, vol. 9, no. 2, pp. 155–174, 1999.
[20]
C. de Lazzari, M. Darowski, G. Ferrari, F. Clemente, and M. Guaragno, “Computer simulation of haemodynamic parameters changes with left ventricle assist device and mechanical ventilation,” Computers in Biology and Medicine, vol. 30, no. 2, pp. 55–69, 2000.
[21]
A. Ferreira, S. Chen, M. A. Simaan, J. R. Boston, and J. F. Antaki, “A nonlinear state-space model of a combined cardiovascular system and a rotary pump,” in Proceedings of the 44th IEEE Conference on Decision and Control, and the European Control Conference (CDC-ECC '05), pp. 897–902, Sevilla, Spain, December 2005.
[22]
A. S. Hakkoymaz, Optimization of the blood flow through a left ventricular assist device [M.S. thesis], Yeditepe University, Istanbul, Turkey, 2008.
[23]
S. Bozkurt, Dynamic modeling of human cardiovascular system and an axial heart pump [M.S. thesis], Yeditepe University, Istanbul, Turkey, 2009.
[24]
L. de Pater and J. van den Berg, “An electrical analogue of the entire human circulatory system,” Medical Electronics & Biological Engineering, vol. 2, no. 2, pp. 161–166, 1964.
[25]
B. Olshansky, H. N. Sabbah, P. J. Hauptman, and W. S. Colucci, “Parasympathetic nervous system and heart failure pathophysiology and potential implications for therapy,” Circulation, vol. 118, no. 8, pp. 863–871, 2008.
[26]
M. Ursino, “Interaction between carotid baroregulation and the pulsating heart: a mathematical model,” American Journal of Physiology—Heart and Circulatory Physiology, vol. 275, no. 5, pp. H1733–H1747, 1998.
[27]
A. C. Guyton and J. E. Hall, Textbook of Medical Physiology, Elsevier Saunders, Philadelphia, Pa, USA, 2006.
[28]
D. M. Karantonis, N. H. Lovell, P. J. Ayre, D. G. Mason, and S. L. Cloherty, “Identification and classification of physiologically significant pumping states in an implantable rotary blood pump,” Artificial Organs, vol. 30, no. 9, pp. 671–679, 2006.
[29]
D. M. Karantonis, D. G. Mason, R. F. Salamonsen, P. J. Ayre, S. L. Cloherty, and N. H. Lovell, “Classification of physiologically significant pumping states in an implantable rotary blood pump: patient trial results,” ASAIO Journal, vol. 53, no. 5, pp. 617–622, 2007.
[30]
M. Vollkron, H. Schima, L. Huber, R. Benkowski, G. Morello, and G. Wieselthaler, “Advanced suction detection for an axial flow pump,” Artificial Organs, vol. 30, no. 9, pp. 665–670, 2006.
[31]
L. G. E. Cox, S. Loerakker, M. C. M. Rutten, B. A. J. M. de Mol, and F. N. van de Vosse, “A mathematical model to evaluate control strategies for mechanical circulatory support,” Artificial Organs, vol. 33, no. 8, pp. 593–603, 2009.
[32]
V. A. Londhey, U. S. Kamble, C. S. Limaye, S. J. Pednekar, S. H. Kini, and N. E. Borges, “Irreversible dilated cardiomyopathy due to thyrotoxicosis,” Journal of Association of Physicians of India, vol. 54, pp. 575–576, 2006.
[33]
S. Maybaum, D. Mancini, S. Xydas et al., “Cardiac improvement during mechanical circulatory support: a prospective multicenter study of the LVAD working group,” Circulation, vol. 115, no. 19, pp. 2497–2505, 2007.
