Prefailure and failure mechanics of the porcine ascending thoracic aorta: Experiments and a multiscale model

ATAA are dilatations of the arterial wall that result primarily from a weakening in the middle smooth muscle layer, or media, of the artery [1–3]. Aneurysm dissection and rupture pose serious risk of mortality and are the primary concerns for patients with an ATAA [1–4]. Cystic medial degeneration (which can be caused by disease, injury, or hereditary condition [2,3]), weakens the aortic wall, allowing for the formation of aneurysms and subsequent dissections. Aneurysm growth and dissection is further driven by increased hemodynamic loading within the media [5]. Ascending aortic dissection, the most prominent failure mode, occurs when the hemodynamic stresses within the media exceed the capacity of its collagen and elastin constituents allowing blood to pass into the medial lamella and peel it apart (delaminate) [6]. Ultimately, this tear can propagate axially along the length of the aorta, either proximally or distally, and in the absence of clinical intervention, may lead to further complications such as ischemia, aortic regurgitation, cardiac tamponade, aortic rupture, and death [1]. Ascending aortic aneurysms have an incidence rate of 10.4 per 100,000 person-years [7], with significant risk of dissection or rupture [7]. Clinically, ATAA management balances the risk of aneurysm rupture with the risk of surgery-related complications and death [2,3]. Risk of rupture is correlated with aneurysm diameter [2,7]; aneurysms greater than 6 cm in diameter exhibit a significantly higher risk of rupture [2]. Thus, for patients without valvular disorders, current guidelines indicate surgical intervention for ATAA diameters greater than 5.5 cm and monitoring for those less than 5.5 cm [2]. In spite of clinical guidelines and what is known about the pathogenesis of aneurysms, dissection and rupture occur in a significant number of patients whose aneurysms are less than 5.5 cm in diameter [8], suggesting that a better understanding of the dissection process is needed. Experimental studies have investigated the mechanical failure of aortic media [6,9,10], but only a few theoretical models have attempted to emulate this response [11–13]. The most notable work to date, by Gasser and Holzapfel [12], employs constitutive FE modeling with two independent continuous and cohesive zones to model the fiber network and ground matrix, respectively. While the Gasser–Holzapfel model is capable of describing the mechanical behavior of the aorta, it fails to capture complex fiber-fiber and fiber-matrix interactions or address failure at the microscopic scale. A model employing microscale mechanics and structure to determine the macroscale response would have potential to incorporate greater anatomical detail and could be applied to a broader range of conditions. This work represents an initial attempt to apply such multiscale concepts to the mechanics of the ATA. The objectives of this study were (1) to characterize the prefailure and failure response of healthy porcine ascending aorta tissue under uniaxial and biaxial loading and (2) to describe that response with a multiscale, FE damage model. The model has been shown to be effective for prefailure and failure behavior of collagen gels [14] and has been applied to prefailure behavior of decellularized arterial wall [15].