Aart Mookhoek1, Kapil Krishnan2, Sam Chitsaz3, Heide Kuang2, Liang Ge2, Paul H Schoof4, Ad J J C Bogers1, Johanna J M Takkenberg1, Elaine E Tseng5. 1. Department of Cardiothoracic Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands. 2. Department of Surgery, University of California San Francisco Medical Center and San Francisco Veterans Affairs Medical Center, San Francisco, California. 3. Division of Cardiology, Department of Medicine, University of Texas at Houston, Houston, Texas. 4. Department of Pediatric Cardiothoracic Surgery, Utrecht University Medical Center, Utrecht, The Netherlands. 5. Department of Surgery, University of California San Francisco Medical Center and San Francisco Veterans Affairs Medical Center, San Francisco, California. Electronic address: elaine.tseng@ucsfmedctr.org.
Abstract
BACKGROUND: Progressive dilatation of pulmonary autografts after the Ross operation may reflect inadequate remodeling of the native pulmonary root to adapt to systemic circulation. Understanding the biomechanics of autograft root dilatation may aid designing strategies to prevent dilatation. We have previously characterized normal human pulmonary root material properties; however, the mechanical properties of failed autografts are unknown. In this study, failed autograft roots explanted during reoperation were acquired, and their material properties were determined. METHODS: Failed pulmonary autograft specimens were obtained from patients undergoing reoperation after the Ross operation. Fresh human native pulmonary roots were obtained from the transplant donor network as controls. Biaxial stretch testing was performed to determine tissue mechanical properties. Tissue stiffness was determined at patient-specific physiologic stresses at pulmonary pressures. RESULTS: Nonlinear stress-strain response was present in both failed autografts and normal pulmonary roots. Explanted pulmonary autografts were less stiff than were their native pulmonary root counterparts at 8 mm Hg (134 ± 42 vs 175 ± 49 kPa, respectively) (p = 0.086) and 25 mm Hg (369 ± 105 vs 919 ± 353 kPa, respectively) (p = 0.006). Autograft wall stiffness at both 8 and 25 mm Hg was not correlated with age at the Ross procedure (p = 0.898 and p = 0.813, respectively) or with time in the systemic circulation (p = 0.609 and p = 0.702, respectively). CONCLUSIONS: Failed pulmonary autografts retained nonlinear response to mechanical loading typical of healthy human arterial tissue. Remodeling increased wall thickness but decreased wall stiffness in failed autografts. Increased compliance may explain progressive autograft root dilatation in autograft failures.
BACKGROUND: Progressive dilatation of pulmonary autografts after the Ross operation may reflect inadequate remodeling of the native pulmonary root to adapt to systemic circulation. Understanding the biomechanics of autograft root dilatation may aid designing strategies to prevent dilatation. We have previously characterized normal human pulmonary root material properties; however, the mechanical properties of failed autografts are unknown. In this study, failed autograft roots explanted during reoperation were acquired, and their material properties were determined. METHODS: Failed pulmonary autograft specimens were obtained from patients undergoing reoperation after the Ross operation. Fresh human native pulmonary roots were obtained from the transplant donor network as controls. Biaxial stretch testing was performed to determine tissue mechanical properties. Tissue stiffness was determined at patient-specific physiologic stresses at pulmonary pressures. RESULTS: Nonlinear stress-strain response was present in both failed autografts and normal pulmonary roots. Explanted pulmonary autografts were less stiff than were their native pulmonary root counterparts at 8 mm Hg (134 ± 42 vs 175 ± 49 kPa, respectively) (p = 0.086) and 25 mm Hg (369 ± 105 vs 919 ± 353 kPa, respectively) (p = 0.006). Autograft wall stiffness at both 8 and 25 mm Hg was not correlated with age at the Ross procedure (p = 0.898 and p = 0.813, respectively) or with time in the systemic circulation (p = 0.609 and p = 0.702, respectively). CONCLUSIONS: Failed pulmonary autografts retained nonlinear response to mechanical loading typical of healthy human arterial tissue. Remodeling increased wall thickness but decreased wall stiffness in failed autografts. Increased compliance may explain progressive autograft root dilatation in autograft failures.
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