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Enhanced External Counterpulsation Treatment Inhibitting Advanced Atherosclerotic Plaque Progression by Augmenting the Plaque Wall Stress: An in vivo FSI Study Based on Animal Experiment |
DU Jian-hang1,2, HUANG Liang2, WU Gui-fu3,4, ZHENG Zhen-sheng4,
FENG Ming-zhe4, DAI Gang4,WU Fu-jun4 |
1. School of Engineering, Guangdong Ocean University, Guangdong Province Zhanjiang 524088, China; 2. Mathematical Sciences Department, Worcester Polytechnics Institute, MA 01609, USA; 3. The Affiliated Futian Hospital of Guangdong Medical College, Guangdong Province Shenzhen 518000, China; 4. Key Laboratory on Assisted Circulation, Ministry of Health, Guangdong Province Guangzhou 510089, China |
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Abstract Enhance external counterpulsation (EECP) procedure has exhibited itself to be an effective therapy for the management of ischemic cardiovascular diseases. However, considering that EECP significantly increases the acute diastolic pressure, whether it will intervene in the chronic progression of advanced plaque causing great concern in clinical application, but yet remains elusive presently. In the current paper, a fluid-structure interface (FSI) numerical model of artery with plaque component was developed based on in vivo hemodynamic measurement performed in a porcine model, to calculate the mechanical stresses of the plaque before and during EECP, and in turn to assess the potential effects of long-term EECP treatment on plaque progression. The results show that EECP augmented the wall shear stress (WSS) and plaque wall stress (PWS) over the cardiac cycles, as well as the spacial oscillatory of WSS (WSSG). During EECP treatment, the PWS level respectively raised 6.82% and 6.07% in two simulation cases. The current pilot study suggests that EECP treatment may play a positive effect on inhibiting the continued plaque progression by increasing the PWS level over the cardiac cycles. Meanwhile, the plaque morphology should be taken into consideration while making patient-specific plan for long-term EECP treatment in clinic.
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Received: 12 December 2015
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Corresponding Authors:
DU Jian-hang. E-mail: Jianhang.Du@yahoo.com
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[1] Manchanda A, Soran O. Enhanced external counterpulsation and future directions: step beyond medical management for patients with angina and heart failure[J]. Journal of the American College of Cardiology, 2007, 50(16):1523-1531. [2] Braith RW, Conti CR, Nichols WW, et al. Enhanced external counterpulsation improves peripheral artery flow-mediated dilation in patients with chronic angina a randomized sham-controlled study[J]. Circulation, 2010, 122(16):1612-1620. [3] Lin W, Xiong L, Han J, et al. External counterpulsation augments blood pressure and cerebral flow velocities in ischemic stroke patients with cerebral intracranial large artery occlusive disease[J]. Stroke, 2012, 43(11): 3007-3011. [4] Liu LP, Xu AD, Wong KS, et al. Chinese consensus statement on the evaluation and intervention of collateral circula-tion for ischemic stroke[J]. CNS Neuroscience & Theraputics, 2014, 20(3): 202-208. [5] Zhang Y, He XH, Chen XL, et al. Enhanced external counterpulsation inhibits intimal hyperplasia by modifying shear stress responsive gene expression in hypercholesterolemic pigs[J]. Circulation, 2007, 116(5): 526-544. [6] Yang DY, Wu GF. Vasculoprotective properties of enhanced external counterpulsation for coronary artery disease: beyond the hemodynamics[J]. International Journal of Candiology, 2013, 166(1): 38-43. [7] Beck DT, Martin SJ, Casey DP, et al. Enhanced external counterpulsation improves endothelial function and exercise capacity in patients with ischaemic left ventricular dysfunction[J]. Clinical and Experimental Pharmacology and Physiology, 2014, 41(9): 628-636. [8] Du JH, Wu GF, Zheng ZS, et al. Enhanced external counterpulsation inducing arterial hemodynamic variations and its chronic effect on endothelial function[J]. Chinese Journal of Biomedical Engineering (English Edition), 2014, 23(1): 127-138. [9] Suresh K, Simandl S, Lawson WE, et al. Maximizing the hemodynamic benefit of enhanced external counterpulsation[J]. Clinical Cardiology, 1998, 21(9): 649-653. [10] Assemat P, Armitage JA, Siu KK, et al. Three-dimensional numerical simulation of blood flow in mouse aortic arch around atherosclerotic plaques[J]. Applied Mathematical Modeling, 2014, 38(17-18): 4175-4185. [11] Gijsen FJH. Plaque mechanics[J]. Journal of Biomechanics, 2014, 47(4):763-764. [12] Tang DL, Kamm RD, Yang C, et al. Image-based modeling for better understanding and assessment of atherosclerotic plaque progression and vulnerability: Data, modeling, validation, uncertainty and predictions[J]. Journal of Biomechanics, 2014, 47(4): 834-846. [13] Peiffer V, Sherwin SJ, Weinberg PD. Does low and oscillatory wall shear stress correlate spatially with early athe-rosclerosis? A systematic review[J]. Cardiovascular Research, 2013, 99(22) :242-250. [14] Chatzizisis YS, Baker AB, Sukhova GK, et al. Augmented expression and activity of extracellular matrix-degrading enzymes in regions of low endothelial shear stress colocalize with coronary atheromata with thin fibrous caps in pigs[J].Circulation, 2011, 123 (6): 621-630. [15] Groen HC, Gijsen FJH, van der Lugt A, et al. Plaque rupture in the carotid artery is localized at the high shear stress region: a case report[J]. Stroke, 2007, 38 (8):2379-2381. [16] Yang C, Canton G, Yuan C, et al. Advanced human carotid plaque progression correlates positively with flow shear stress using follow-up scan data: An in vivo MRI multi-patient 3D FSI study[J]. Journal of Biomechanics, 2010, 43(13): 2530-2538. [17] Gijsen FJH, van der Giessen A, van der Steen A, et al. Shear stress and advanced atherosclerosis in human coronary arteries[J]. Journal of Biomechanics, 2013, 46(2): 240-247. [18] Tang DL, Yang C, Mondal S, et al. A negative correlation between human carotid atherosclerotic plaque progression and plaque wall stress: In vivo MRI-based 2D/3D FSI models[J]. Journal of Biomechanics, 2008, 41(4): 727-736. [19] Tang DL, Teng ZZ, Canton G, et al. Sites of rupture in human atherosclerotic carotid plaques are associated with high structural stresses: an in vivo MRI-based 3D fluid-structure interaction study[J]. Stroke, 2009, 40(10): 3258 -3263. [20] Sadat U, Teng Z, Gillard JH. Biomechanical structural stresses of atherosclerotic plaques[J]. Expert Review of Cardiovascular Therapy, 2010, 8 (10):1469-1481. [21] Teng ZZ, Canton G, Yang C, et al. 3D critical plaque wall stress is a better predictor of carotid plaque rupture sites than flow shear stress: an in vivo MRI-based 3D FSI study[J]. Journal of Biomechanical Engineering, 2010, 132(3): 031007. [22] William SD, Lam Y, Younis HF, et al. On the sensitivity of wall stresses in diseased arteries to variable material properties[J]. Journal of Biomechanical Engineering, 2003, 125(1):147-155. [23] Murphy J, Boyle F. Predicting neointimal hyperplasia in stented arteries using time-dependant computational fluid dy-namics: a review[J]. Computers in Biology & Medicine, 2010, 40(4): 408-418. [24] Buchanan JR, Kleinstreuer C,Truskey CA, et al. Relation between non-uniform hemodynamics and sites of altered permeability and lesion growth at the rabbit aorto-celiac junction[J]. Atherosclerosis, 1999, 143(1): 27-40. |
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