| Abstract
| - Abstract. Objective: Blunt traumatic aortic injury (BTAI) is part of a spectrum of diseases termed acute aortic syndrome that accounts for 20% of road traffic accident related deaths. The injury has a complex aetiology with a number of putative mechanisms accounting for the injury profile, characteristics of which include a transverse primary intimal tear located at the aortic isthmus. We hypothesised that an understanding of regional aortic wall mechanics would contribute to an understanding of the aetiology of BTAI. Methods: Samples of porcine aorta were prepared from ascending (A), descending (D) and peri-isthmus regions (I). A histological analysis of aortic wall architecture was performed at the site of attachment of the ligamentum arteriosum. Samples were mounted in a bubble inflation clamping rig, connected via a solenoid release valve to a compressed air reservoir. Using a pressure transducer and high-speed camera (1000 fps) we collected data on wall thickness, rupture pressure and radial extension, allowing calculation of ultimate tensile stress. Results: Histological analysis at the point of attachment of the ligamentum arteriosum to the isthmus shows some heterogeneity in cellular architecture extending deep into the tunica media. Wall thickness was significantly different between the three sampled regions (A > I > D, p < 0.05). However, we found no difference in absolute rupture pressure between the three regions (kPa), (A, 300 ± 28.9; I, 287 ± 48.3; D, 321 ± 29.6). Radial extension (cm) was significantly greater in A vs I (p < 0.05), (A, 1.85 ± 0.114; I, 1.66 ± 0.109; D, 1.70 ± 0.138). Ultimate tensile stress (kPa), (A, 3699 ± 789; I, 3248 ± 1430; D, 4260 ± 1626) was significantly greater in D than I (p < 0.05). Conclusions: The mechanism of blunt traumatic aortic rupture is not mechanically simple but must correspond to a complex combination of both relative motion of the structures within the thorax and local loading of the tissues, either as a result of their anatomy or due to the nature of the impact. A pressure spike alone is unlikely to be the primary cause of the peri-isthmus injury but may well be a contributory prerequisite.
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