Patient-specific finite element modeling of the Cardiokinetix Parachute? device: effects on left ventricular wall stress and function
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- 作者：Lik Chuan Lee (1) (2) (4)
Liang Ge (1) (2) (4)
Zhihong Zhang (4)
Matthew Pease (5)
Serjan D. Nikolic (5)
Rakesh Mishra (3) (4)
Mark B. Ratcliffe (1) (2) (4)
Julius M. Guccione (1) (2) (4) - 关键词：Myocardial infarction ; Remodeling ; Finite element method ; Surgical ventricular restoration
- 刊名：Medical and Biological Engineering and Computing
- 出版年：2014
- 出版时间：June 2014
- 年：2014
- 卷：52
- 期：6
- 页码：557-566
- 全文大小：
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Liang Ge (1) (2) (4)
Zhihong Zhang (4)
Matthew Pease (5)
Serjan D. Nikolic (5)
Rakesh Mishra (3) (4)
Mark B. Ratcliffe (1) (2) (4)
Julius M. Guccione (1) (2) (4)
1. Departments of Surgery, University of California, San Francisco, CA, USA
2. Department of Bioengineering, University of California, San Francisco, CA, USA
4. Division of Surgical Services (112), San Francisco Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA, 94121, USA
5. Cardiokinetix, Inc., Menlo Park, CA, USA
3. Department of Medicine, University of California, San Francisco, CA, USA - ISSN：1741-0444
文摘
The Parachute? (Cardiokinetix, Inc., Menlo Park, California) is a catheter-based device intended to reverse left ventricular (LV) remodeling after antero-apical myocardial infarction. When deployed, the device partitions the LV into upper and lower chambers. To simulate its mechanical effects, we created a finite element LV model based on computed tomography (CT) images from a patient before and 6?months after Parachute? implantation. Acute mechanical effects were determined by in silico device implantation (VIRTUAL-Parachute). Chronic effects of the device were determined by adjusting the diastolic and systolic material parameters to better match the 6-month post-implantation CT data and LV pressure data at end-diastole (ED) (POST-OP). Regional myofiber stress and pump function were calculated in each case. The principal finding is that VIRTUAL-Parachute was associated with a 61.2?% reduction in the lower chamber myofiber stress at ED. The POST-OP model was associated with a decrease in LV diastolic stiffness and a larger reduction in myofiber stress at the upper (27.1?%) and lower chamber (78.4?%) at ED. Myofiber stress at end-systole and stroke volume was little changed in the POST-OP case. These results suggest that the primary mechanism of Parachute? is a reduction in ED myofiber stress, which may reverse eccentric post-infarct LV hypertrophy.