Andrew D. Wisneski1, Peter B. Matthews1, Ali N. Azadani1, Aart Mookhoek2, Sam Chitsaz1, Julius M. Guccione1, Liang Ge1, Elaine E. Tseng1
1Department of Surgery, University of California at San Francisco (UCSF) and San Francisco Veterans Affairs Medical Center (SFVAMC), San Francisco, CA, USA, 2Department of Surgery, Erasmus Medical Center, Rotterdam, Netherlands
Background and aim of the study: Remodelling of the pulmonary autograft upon exposure to systemic pressure can lead to progressive dilatation and aneurysmal pathology. Remodelling is driven by changes in autograft wall stress upon exposure to systemic pressure; however, the magnitude of these changes is unknown. Previously, a porcine autograft finite element model was developed to determine wall stress, but the porcine and human material properties differed significantly. Hence, the study aim was to understand human pulmonary autograft biomechanics that lead to remodelling by determining wall stress magnitudes immediately after the Ross procedure using finite element analysis (FEA).
Methods: Human pulmonary root was scanned by high-resolution microcomputed tomography to construct a realistic three-dimensional geometric mesh. Stress-strain data from biaxial stretch testing was incorporated into an Ogden hyperelastic model to describe autograft mechanical properties for an adult Ross patient. Autograft dilatation and wall stress distribution during pulmonic and systemic pressures prior to remodelling were determined using explicit FEA in LS-DYNA.
Results: Human pulmonary autograft demonstrated non-linear material properties, being highly compliant
in the low-strain region, and stiffening at high strain. The majority of dilatation occurred with <20 mmHg pressurization. From pulmonary to systemic pressures, the increases in autograft diameter were up to 17%. Likewise, the maximal wall stress increased approximately 14.6-fold compared to diastolic pressures (from 13.0 to 190.1kPa), and six-fold compared to systolic pressures (from 48.6 to 289.6kPa).
Conclusion: The first finite element model of the human pulmonary autograft was developed and used to demonstrate how autograft material properties prevent significant dilatation upon initial exposure to systemic pressure. Mild dilatation was noted in the sinuses and sinotubular junction. Autograft wall stress was increased greatly when subjected to systemic pressures, and may trigger biomechanical remodelling of the autograft. Sustained exposure to higher wall stresses, coupled with inadequate remodelling, may lead to future autograft dilatation.
Video 1: Autograft finite element model at systemic systole (120 mmHg) [Click here to view]
Video 2: Autograft finite element model at pulmonary systole (25 mmHg) [Click here to view]
The Journal of Heart Valve Disease 2014;23:377-384
|Human Pulmonary Autograft Wall Stress at Systemic Pressures Prior to Remodelling After the Ross Procedure|
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