Abstract 12524: Changes in Pulmonary Autograft Wall Stresses Immediately After the Ross Operation: First Steps Towards Understanding Aneurysmal Remodeling
Introduction: Pulmonary autograft dilatation is the Achilles heel of the Ross operation, often necessitating reoperation. To understand normal and abnormal autograft remodeling, first biomechanical understanding of human autografts after exposure to systemic pressure is required. Our aim was to quantify biomechanical wall stresses on normal autografts after Ross operation prior to remodeling and dilatation.
Hypothesis: Elevated pressure of systemic circulation results in increased autograft wall stress to drive biomechanical remodeling.
Methods: We previously developed a normal human autograft model using micro-computed tomography to obtain zero-pressure luminal geometry. Material properties of normal human autografts (n=9) was obtained by bi-axial stretching. Patient-specific zero-pressure wall thickness was incorporated. Autograft diameter and wall stress were determined at pulmonic and systemic pressures using finite element analyses.
Results: At systemic systole, mean autograft diameter was 35.0±1.7mm at sinuses and 33.4±1.3mm at sinotubular junction (STJ); while at pulmonary systole, they were 32.5±1.9mm and 30.5±1.4mm, respectively. Distensibility, percent change in diameter from diastole to systole, was 1.4% at systemic pressures versus 3.0% at pulmonary pressures. Peak von Mises wall stress was 581±449kPa at systemic systole compared to 89.7±65.3kPa at pulmonic systole. Average wall stress at systemic systole was 223±88.3kPa and at pulmonic systole was 37.4±16.8kPa (Fig 1).
Conclusions: Normal human pulmonary autograft biomechanical responses to systemic pressure were quantified. Nearly 6 fold increase in peak and average wall stress was observed at systemic pressures. Regions of peak stresses were observed in the sinuses. This data will serve as a necessary control for future comparison to aneurysmal pulmonary autografts, and will enable better understanding of patient-specific risk for autograft dilatation.
Author Disclosures: A.D. Wisneski: None. Y. Xuan: None. J.M. Guccione: None. L. Ge: None. E.E. Tseng: None.
- © 2016 by American Heart Association, Inc.