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Simulation of Eisenmenger syndrome with ventricular septal defect using equivalent electronic system

Published online by Cambridge University Press:  26 September 2011

Mehmet Korurek ,
Mustafa Yildiz ,
Ayhan Yüksel  and
Alparslan Şahin
Mehmet Korurek
Affiliation:
Department of Biomedical Engineering, Faculty of Electrical and Electronic Engineering, Istanbul Technical University, Istanbul, Turkey
Mustafa Yildiz*
Affiliation:
Department of Cardiology, Kartal Kosuyolu Yuksek Ihtisas Educational and Research Hospital, Istanbul, Turkey
Ayhan Yüksel
Affiliation:
Department of Biomedical Engineering, Faculty of Electrical and Electronic Engineering, Istanbul Technical University, Istanbul, Turkey
Alparslan Şahin
Affiliation:
Department of Cardiology, Bakırköy Dr. Sadi Konuk Educational and Research Hospital, Istanbul, Turkey
*
Correspondence to: Dr M. Yildiz, MD, PhD, Assoc. Prof., Cardiologist, Internal Medicine Specialist and Physiologist, Department of Cardiology, Kartal Kosuyolu Yuksek Ihtisas Educational and Research Hospital, Istanbul, Turkey. Tel: +90 532 371 17 01; Fax: +90 0216 459 63 21; E-mail: [email protected]
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Abstract

Background: In this study, we aim to investigate the simulation of the cardiovascular system using an electronic circuit model under normal and pathological conditions, especially the Eisenmenger syndrome. Methods and Results: The Eisenmenger syndrome includes a congenital communication between the systemic and pulmonary circulation, with resultant pulmonary arterial hypertension and right-to-left reversal of flow through the defect. When pulmonary vascular resistance exceeds systemic vascular resistance, it results in hypoxaemia and cyanosis. The Westkessel model including Resistor-Inductance-Capacitance pi-segments was chosen in order to simulate both systemic and pulmonary circulation. The left and right heart are represented by trapezoidal shape stiffness for better simulation results. The Eisenmenger syndrome is simulated using a resistance (septal resistance) connected between the left ventricle and right ventricle points of the model. Matlab® is used for the model implementation. In this model, although there is a remarkable increase in the pulmonary artery pressure and right ventricle pressure, left ventricle pressure, aortic pressure, aortic flow, and pulmonary compliance decrease in the Eisenmenger syndrome. In addition, left-to-right septal flow reversed in these diseases. Conclusion: Our model is effective and available for simulating normal cardiac conditions and cardiovascular diseases, especially the Eisenmenger syndrome.

Keywords

Cardiovascular physiologysimulationmodellingEisenmenger syndromeventricular septal defectelectronic circuits
Type
Original Article
Information
Cardiology in the Young , Volume 22 , Issue 3 , June 2012 , pp. 301 - 306
Copyright
Copyright © Cambridge University Press 2012

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References

1.Perloff, JK, Rosove, MH, Child, JS, Wright, GB. Adults with cyanotic congenital heart disease: hematologic management. Ann Intern Med 1988; 109: 406–413.CrossRefGoogle ScholarPubMed
2.Ammash, NM, Warnes, CA. Ventricular septal defects in adults. Ann Intern Med 2001; 135: 812–824.CrossRefGoogle ScholarPubMed
3.Perloff, JK (ed.). Ventricular septal defect. In: The Clinical Recognition of Congenital Heart Disease, 4th edn. Philadelphia, W.B. Saunders, 1994: 396–439.Google Scholar
4.Neutze, JM, Ishikawa, T, Clarkson, PM, Calder, AL, Barratt-Boyes, BG, Kerr, AR. Assessment and follow-up of patients with ventricular septal defect and elevated pulmonary vascular resistance. Am J Cardiol 1989; 63: 327–331.CrossRefGoogle ScholarPubMed
5.Clarkson, PM, Frye, RL, DuShane, JW, Burchell, HB, Wood, EH, Weidman, WH. Prognosis for patients with ventricular septal defect and severe pulmonary vascular obstructive disease. Circulation 1968; 38: 129–135.CrossRefGoogle ScholarPubMed
6.Heath, D, Edwards, JE. The pathology of hypertensive pulmonary vascular disease: a description of six grades of structural changes in the pulmonary arteries with special reference to congenital cardiac septal defects. Circulation 1958; 18: 533–547.CrossRefGoogle ScholarPubMed
7.Rupnik, M, Runovc, F, Sket, D, Kordas, M. Cardiovascular physiology: simulation of steady state and transient phenomena by using the equivalent electronic circuit. Comput Methods Programs Biomed 2002; 67: 1–12.CrossRefGoogle ScholarPubMed
8.Li, X, Bai, J, Cui, S, Wang, S. Simulation study of the cardiovascular functional status in hypertensive situation. Comput Biol Med 2002; 32: 345–362.CrossRefGoogle ScholarPubMed
9.Tsalikakis, DG, Fotiadis, DI, Sideris, D. Simulations of cardiovascular diseases using electronic circuits. Comput Cardiol 2003; 30: 445–448.Google Scholar
10.Goldwyn, RM, Watt, TB Jr. Arterial pressure pulse contour analysis via a mathematical model for the clinical quantification of human vascular properties. IEEE Trans Biomed Eng 1967; 14: 11–17.CrossRefGoogle Scholar
11.Korurek, M, Yıldız, M, Yüksel, A. Simulation of normal cardiovascular system and severe aortic stenosis using equivalent electronic model. Anadolu Kardiyol Derg 2010; 10: 471–478.CrossRefGoogle ScholarPubMed
12.Rideout, VC. Mathematical and Computer Modelling of Physiological Systems. Prentice Hall International (ISBN: 0135636930, 9780135636930), 1991: 1–261.Google Scholar
13.Levick, JR. Cardiovascular Parameters. An Introduction to Cardiovascular Physiology, 4th edn. Oxford University Press, New York, 2003.Google Scholar
14.Therrien, J, Dore, A, Gersony, W, et al. Canadian Cardiovascular Society. CCS Consensus Conference 2001 update: recommendations for the management of adults with congenital heart disease, Part I. Can J Cardiol 2001; 17: 940–959.Google Scholar
15.Mukkamala, R, Cohen, RJ. A forward model-based validation of cardiovascular system identification. Am J Physiol Heart Circ Physiol 2001; 281: 2714–2730.CrossRefGoogle ScholarPubMed
16.Sever, M, Podnar, T, Runovc, F, Kordas, M. Analog simulation of two clinical conditions: (1) acute left ventricle failure; (2) exercise in patient with aortic stenosis. Comput Biol Med 2007; 37: 1051–1062.CrossRefGoogle Scholar
17.Maasrani, M, Verhoye, JP, Corbineau, H, Drochon, A. Analog electrical model of the coronary circulation in case of multiple revascularizations. Ann Biomed Eng 2008; 36: 1163–1174.CrossRefGoogle ScholarPubMed
18.Felipini, CL, de Andrade, AJ, Lucchi, JC, da Fonseca, JW, Nicolosi, D. An electro-fluid-dynamic simulator for the cardiovascular system. Artif Organs 2008; 32: 349–354.CrossRefGoogle ScholarPubMed
19.Guler, I, Hardalac, F, Barisci, N. Application of FFT analyzed cardiac Doppler signals to fuzzy algorithm. Comput Biol Med 2002; 32: 435–444.CrossRefGoogle ScholarPubMed
20.Aguilar, JL, Balsera, BM, Bernal, JJ. Simulation of the variable compliance of living systems. Comput Biol Med 1982; 12: 133–141.CrossRefGoogle ScholarPubMed
21.Vongpatanasin, W, Brickner, ME, Hillis, LD, Lange, RA. The Eisenmenger syndrome in adults. Ann Intern Med 1998; 128: 745–755.CrossRefGoogle ScholarPubMed
22.Todorovich-Hunter, L, Dodo, H, Ye, C, McCready, L, Keeley, FW, Rabinovitch, M. Increased pulmonary artery elastolytic activity in adult rats with monocrotaline-induced progressive hypertensive pulmonary vascular disease compared with infant rats with nonprogressive disease. Am Rev Respir Dis 1992; 146: 213–223.CrossRefGoogle ScholarPubMed
23.Perkett, EA, Badesch, DB, Roessler, MK, Stenmark, KR, Meyrick, B. Insulinlike growth factor I and pulmonary hypertension induced by continuous air embolization in sheep. Am J Respir Cell Mol Biol 1992; 6: 82–87.CrossRefGoogle ScholarPubMed
24.Perkett, EA, Lyons, RM, Moses, HL, Brigham, KL, Meyrick, B. Transforming growth factor-β activity in sheep lung lymph during the development of pulmonary hypertension. J Clin Invest 1990; 86: 1459–1464.CrossRefGoogle ScholarPubMed
25.Fuse, S, Kamiya, T. Plasma thromboxane B2 concentration in pulmonary hypertension associated with congenital heart disease. Circulation 1994; 90: 2952–2955.CrossRefGoogle ScholarPubMed
26.de P S Soares, R, Maeda, NY, Bydlowski, SP, Lopes, AA. Markers of endothelial dysfunction and severity of hypoxaemia in the Eisenmenger syndrome. Cardiol Young 2005; 15: 504–513.CrossRefGoogle ScholarPubMed
27.Yoshibayashi, M, Nishioka, K, Nakao, K, et al. Plasma endothelin concentrations in patients with pulmonary hypertension associated with congenital heart defects. Evidence for increased production of endothelin in pulmonary circulation. Circulation 1991; 84: 2280–2285.CrossRefGoogle ScholarPubMed
28.Celermajer, DS, Cullen, S, Deanfiel, JE. Impairment of endothelium-dependent pulmonary artery relaxation in children with congenital heart disease and abnormal pulmonary hemodynamics. Circulation 1993; 87: 440–446.CrossRefGoogle ScholarPubMed
29.Dinh Xuan, AT, Higenbottam, TW, Clelland, C, Pepke-Zaba, J, Cremona, G, Wallwork, J. Impairment of pulmonary endothelium-dependent relaxation in patients with Eisenmenger's syndrome. Br J Pharmacol 1990; 99: 9–10.CrossRefGoogle ScholarPubMed
30.Bouzas, B, Gatzoulis, MA. Pulmonary arterial hypertension in adults with congenital heart disease. Rev Esp Cardiol 2005; 58: 465–469.CrossRefGoogle ScholarPubMed