Annabel M Imbrie-Moore1, Michael J Paulsen2, Yuanjia Zhu3, Hanjay Wang2, Haley J Lucian2, Justin M Farry2, John W MacArthur2, Michael Ma2, Y Joseph Woo4. 1. Department of Cardiothoracic Surgery, Stanford University, Stanford, Calif; Department of Mechanical Engineering, Stanford University, Stanford, Calif. 2. Department of Cardiothoracic Surgery, Stanford University, Stanford, Calif. 3. Department of Cardiothoracic Surgery, Stanford University, Stanford, Calif; Department of Bioengineering, Stanford University, Stanford, Calif. 4. Department of Cardiothoracic Surgery, Stanford University, Stanford, Calif; Department of Bioengineering, Stanford University, Stanford, Calif. Electronic address: joswoo@stanford.edu.
Abstract
OBJECTIVE: Barlow's disease remains challenging to repair, given the complex valvular morphology and lack of quantitative data to compare techniques. Although there have been recent strides in ex vivo evaluation of cardiac mechanics, to our knowledge, there is no disease model that accurately simulates the morphology and pathophysiology of Barlow's disease. The purpose of this study was to design such a model. METHODS: To simulate Barlow's disease, a cross-species ex vivo model was developed. Bovine mitral valves (n = 4) were sewn into a porcine annulus mount to create excess leaflet tissue and elongated chordae. A heart simulator generated physiologic conditions while hemodynamic data, high-speed videography, and chordal force measurements were collected. The regurgitant valves were repaired using nonresectional repair techniques such as neochord placement. RESULTS: The model successfully imitated the complexities of Barlow's disease, including redundant, billowing bileaflet tissues with notable regurgitation. After repair, hemodynamic data confirmed reduction of mitral leakage volume (25.9 ± 2.9 vs 2.1 ± 1.8 mL, P < .001) and strain gauge analysis revealed lower primary chordae forces (0.51 ± 0.17 vs 0.10 ± 0.05 N, P < .001). In addition, the maximum rate of change of force was significantly lower postrepair for both primary (30.80 ± 11.38 vs 8.59 ± 4.83 N/s, P < .001) and secondary chordae (33.52 ± 10.59 vs 19.07 ± 7.00 N/s, P = .006). CONCLUSIONS: This study provides insight into the biomechanics of Barlow's disease, including sharply fluctuating force profiles experienced by elongated chordae prerepair, as well as restoration of primary chordae forces postrepair. Our disease model facilitates further in-depth analyses to optimize the repair of Barlow's disease.
OBJECTIVE: Barlow's disease remains challenging to repair, given the complex valvular morphology and lack of quantitative data to compare techniques. Although there have been recent strides in ex vivo evaluation of cardiac mechanics, to our knowledge, there is no disease model that accurately simulates the morphology and pathophysiology of Barlow's disease. The purpose of this study was to design such a model. METHODS: To simulate Barlow's disease, a cross-species ex vivo model was developed. Bovine mitral valves (n = 4) were sewn into a porcine annulus mount to create excess leaflet tissue and elongated chordae. A heart simulator generated physiologic conditions while hemodynamic data, high-speed videography, and chordal force measurements were collected. The regurgitant valves were repaired using nonresectional repair techniques such as neochord placement. RESULTS: The model successfully imitated the complexities of Barlow's disease, including redundant, billowing bileaflet tissues with notable regurgitation. After repair, hemodynamic data confirmed reduction of mitral leakage volume (25.9 ± 2.9 vs 2.1 ± 1.8 mL, P < .001) and strain gauge analysis revealed lower primary chordae forces (0.51 ± 0.17 vs 0.10 ± 0.05 N, P < .001). In addition, the maximum rate of change of force was significantly lower postrepair for both primary (30.80 ± 11.38 vs 8.59 ± 4.83 N/s, P < .001) and secondary chordae (33.52 ± 10.59 vs 19.07 ± 7.00 N/s, P = .006). CONCLUSIONS: This study provides insight into the biomechanics of Barlow's disease, including sharply fluctuating force profiles experienced by elongated chordae prerepair, as well as restoration of primary chordae forces postrepair. Our disease model facilitates further in-depth analyses to optimize the repair of Barlow's disease.
Authors: Annabel M Imbrie-Moore; Michael J Paulsen; Akshara D Thakore; Hanjay Wang; Camille E Hironaka; Haley J Lucian; Justin M Farry; Bryan B Edwards; Jung Hwa Bae; Mark R Cutkosky; Y Joseph Woo Journal: Ann Thorac Surg Date: 2019-03-02 Impact factor: 4.330
Authors: Annabel M Imbrie-Moore; Matthew H Park; Michael J Paulsen; Mark Sellke; Rohun Kulkami; Hanjay Wang; Yuanjia Zhu; Justin M Farry; Alexandra T Bourdillon; Christine Callinan; Haley J Lucian; Camille E Hironaka; Daniela Deschamps; Y Joseph Woo Journal: J R Soc Interface Date: 2020-12-02 Impact factor: 4.118
Authors: Matthew H Park; Pearly K Pandya; Yuanjia Zhu; Danielle M Mullis; Hanjay Wang; Annabel M Imbrie-Moore; Robert Wilkerson; Mateo Marin-Cuartas; Y Joseph Woo Journal: Cardiovasc Eng Technol Date: 2022-08-08 Impact factor: 2.305
Authors: Samuel Frishman; Ali Kight; Ileana Pirozzi; Sainiteesh Maddineni; Annabel M Imbrie-Moore; Zulekha Karachiwalla; Michael J Paulsen; Alexander D Kaiser; Y Joseph Woo; Mark R Cutkosky Journal: J Med Device Date: 2022-05-18 Impact factor: 0.743
Authors: Isaac Wamala; Mossab Y Saeed; Peter E Hammer; Daniel Bautista-Salinas; Kimberlee Gauvreau; Sunil J Ghelani; Nikolay V Vasilyev; Pedro J Del Nido Journal: Interact Cardiovasc Thorac Surg Date: 2021-08-12
Authors: Annabel M Imbrie-Moore; Yuanjia Zhu; Tabitha Bandy-Vizcaino; Matthew H Park; Robert J Wilkerson; Y Joseph Woo Journal: Ann Biomed Eng Date: 2021-11-03 Impact factor: 4.219
Authors: Annabel M Imbrie-Moore; Yuanjia Zhu; Matthew H Park; Michael J Paulsen; Hanjay Wang; Y Joseph Woo Journal: J Thorac Cardiovasc Surg Date: 2020-11-30 Impact factor: 6.439
Authors: Jordan E Morningstar; Annah Nieman; Christina Wang; Tyler Beck; Andrew Harvey; Russell A Norris Journal: J Am Heart Assoc Date: 2021-06-22 Impact factor: 5.501