title: Ascending thoracic aortic aneurysm wall stress analysis using patient-specific finite element modeling of in vivo magnetic resonance imaging.
abstract: OBJECTIVE
  Rupture/dissection of ascending thoracic aortic aneurysms (aTAAs) carries high mortality and occurs in many patients who did not meet size criteria for elective surgery. Elevated wall stress may better predict adverse events, but cannot be directly measured in vivo, rather determined from finite element (FE) simulations. Current computational models make assumptions that limit accuracy, most commonly using in vivo imaging geometry to represent zero-pressure state. Accurate patient-specific wall stress requires models with zero-pressure three-dimensional geometry, material properties, wall thickness and residual stress. We hypothesized that wall stress calculated from in vivo imaging geometry at systemic pressure underestimates that using zero-pressure geometry. We developed a novel method to derive zero-pressure geometry from in vivo imaging at systemic pressure. The purpose of this study was to develop the first patient-specific aTAA models using magnetic resonance imaging (MRI) to assess material properties and zero-pressure geometry. Wall stress results from FE models using systemic pressure were compared with those from models using zero-pressure correction.
  
  
  METHODS
  Patients with aTAAs <5 cm underwent ECG-gated computed tomography angiography (CTA) and displacement encoding with stimulated echo (DENSE)-MRI. CTA lumen geometry was used to create surface contour meshes of aTAA geometry. DENSE-MRI measured cyclic aortic wall strain from which wall material property was derived. Zero- and systemic pressure geometries were created. Simulations were loaded to systemic pressure using the ABAQUS FE software. Wall stress analyses were compared between zero-pressure-corrected and systemic pressure geometry FE models.
  
  
  RESULTS
  Peak first principal wall stress (primarily aligned in the circumferential direction) at systolic pressure for the zero-pressure correction models was 430.62 ± 69.69 kPa, whereas that without zero-pressure correction was 312.55 ± 39.65 kPa (P = 0.004). Peak second principal wall stress (primarily aligned in the longitudinal direction) at systolic pressure for the zero-pressure correction models was 200.77 ± 43.13 kPa, whereas that without zero-stress correction was 156.25 ± 25.55 kPa (P = 0.02).
  
  
  CONCLUSIONS
  Previous FE aTAA models from in vivo CT and MRI have not accounted for zero-pressure geometry or patient-specific material property. We demonstrated that zero-pressure correction significantly impacts wall stress results. Future computational models that use wall stress to predict aTAA adverse events must take into account zero-pressure geometry and patient material property for accurate wall stress determination.
authors.affiliation: Department of Surgery, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA.
authors.forename: Kapil
authors.initials: K
authors.lastname: Krishnan
authors.affiliation: Department of Surgery, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA.
authors.forename: Liang
authors.initials: L
authors.lastname: Ge
authors.affiliation: Department of Radiology, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA.
authors.forename: Henrik
authors.initials: H
authors.lastname: Haraldsson
authors.affiliation: Department of Radiology, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA.
authors.forename: Michael D
authors.initials: MD
authors.lastname: Hope
authors.affiliation: Department of Radiology, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA.
authors.forename: David A
authors.initials: DA
authors.lastname: Saloner
authors.affiliation: Department of Surgery, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA.
authors.forename: Julius M
authors.initials: JM
authors.lastname: Guccione
authors.affiliation: Department of Surgery, University of California San Francisco Medical Center and San Francisco VA Medical Center, San Francisco, CA, USA elaine.tseng@ucsfmedctr.org.
authors.forename: Elaine E
authors.initials: EE
authors.lastname: Tseng
mesh_terms: D000792:Angiography; D001011:Aorta / Q000503:physiopathology*; D017545:Aortic Aneurysm, Thoracic / Q000175:diagnosis / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D003198:Computer Simulation; D020342:Finite Element Analysis; D006801:Humans; D021621:Imaging, Three-Dimensional; D008279:Magnetic Resonance Imaging; D008955:Models, Cardiovascular; D011312:Pressure; D013314:Stress, Mechanical; D014057:Tomography, X-Ray Computed
keywords: Ascending thoracic aortic aneurysm; Finite element analysis; Wall stress