Critical Pressure of Intramural Delamination in Aortic Dissection

Abstract

Computational models of aortic dissection can provide novel insights into possible mechanisms by which this potentially lethal condition develops and propagates. We present results from a phase-field based finite element simulation of a classical experiment that had not previously been understood. Initial simulations agreed qualitatively and quantitatively with the experimental findings, but because of the complexity of the boundary value problem it was still difficult to build intuition. Hence, simplified analytical models were extended to gain further insight. Together, the simplified models and phase-field simulations revealed a power-law-based relation between the pressure required to initiate an intramural tear and key geometric and mechanical factors - area of the initial insult, stiffness of the wall, and characteristic energy of tearing. The degree of axial stretch and luminal pressure similarly influenced the value of the tearing pressure, which was ~70 kPa for a healthy aorta having a sub-millimeter-sized initial insult but even lower for larger tear sizes. Finally, the simulations showed that the direction a tear propagates can be altered by focal regions of weakening or strengthening, which can drive the tear towards the lumen (re-entry) or adventitia (rupture). Additional data are needed, however, on aortas having different predisposing disease conditions.

Evolving Mural Defects, Dilatation, and Biomechanical Dysfunction in Angiotensin II–Induced Thoracic Aortopathies

“…Again, this suggests that the intramural delaminations may nucleate partial medial ruptures by exposing thin portions of the inner media to higher wall stresses that can contribute to defect propagation under the action of persistent hemodynamic loading in vivo. 46 We submit that ex vivo OCT imaging has the potential to reveal local defects that may otherwise be difficult to visualize in vivo given its higher spatial resolution, noting too that ex vivo pressurization was performed with a physiological saline solution as opposed to whole blood as is the case in vivo. That these isolated portions of the media were under high wall stress and yet retained some elasticity was revealed by the highly retracted appearance of the opposing ends of the failed portions of the wall while maintained under physiological loading ex vivo.…”

“…Indeed, the energy dissipation due to tearing appears to contribute to aortic dilatation associated with Ang II infusion. 46 We emphasize here that the primary goal of this study was to characterize the mechanical environment surrounding macroscopic mural defects in thoracic aortopathy, thus admitting a radially homogenized description of material properties across the remnant wall. 30–32 Future, equally important, characterization of the mechanics of microscopic mural defects (including medial delaminations) will necessarily require discrete modeling approaches, 28,46 which could also aid in modeling defect propagation, which was beyond the present scope.…”