J. Rabin1, A. Siddiqui2, J. Gipple2, Z. N. Kon3, B. Taylor3, T. M. Scalea1, H. W. Haslach2 1R Adams Cowley Shock Trauma Center,Surgery,Baltimore, MD, USA 2University Of Maryland,Mechanical Engineering,College Park, MD, USA 3University Of Maryland,Cardiac Surgery,Baltimore, MD, USA
Introduction:
Non-operative management is considered an appropriate treatment strategy for minor aortic injury, while blood pressure control and anti-impulse therapy are routinely utilized to help minimize injury progression. However a universal medical regimen for low grade intimal injuries has not been adopted and risks of injury progression not well described. This study investigates an in-vitro model of minor aortic injury to help identify risks of injury progression and factors associated with the mechanical failure of injured aortic tissue.
Methods:
With IRB approval, ascending aortic tissue was obtained from the operating room after aortic aneurysm repair or heart transplant procurement, stored at 4 degrees Celsius in buffered solution and tested within 48 hours. Minimal aortic injury was modeled by creating a small partial thickness radial notch on the intimal surface of aortic tissue rings. These aortic rings were circumferentially expanded on a custom testing device under video acquisition until maximum diameter or rupture. The test video and aortic tissue were then analyzed to determine point of failure and the crack propagation length & angle.
Results:
A total of 8 rings were obtained from 3 aneurysmal and 2 healthy aortas. Aneurysmal aortic tissue was obtained from a 71 year old female and 68 & 49 year old males. Healthy tissue was obtained from 2 males under the age of 30. All specimens demonstrated circumferential crack propagation from the root of the notch (fig 1) with an average angle 96.3±8.2 degrees between radius and crack. Length of propagation was longer in the aneurysmal tissues (6.60±4.19 mm vs 2.27±1.20 mm). There was no difference in initiation of crack propagation between healthy and aneurysmal tissue which occurred at an average of 1.8 times initial diameter.
Conclusions:
Dilation of minimally damaged or injured aortic rings is associated with crack propagation and injury progression, which contributes to the aortic tissue's mechanical failure. This crack progression is consistent with an applied shear force and deformation within the layers of aortic tissue. Such shear forces are routinely generated through normal circumferential expansion that occurs with each pulsation, as the aortic wall stretches and relaxes, with the magnitude of these aortic shear forces affected by both pulse and blood pressure. The crack propagation demonstrated in this model illustrates the mechanical response to increased levels of applied shear which appears to compromise the structural integrity of the tissue and increases the risk of mechanical failure and aortic rupture. This suggests that strategies to reduce shear stress such as β- blockade, also be implemented in patients with minor aortic injury.
