Human ex-vivo model of Stanford type B aortic dissection

ObjectiveTo report a new human ex vivo model of type B aortic dissection (TBAD) and to assess if the locations of the primary entry tear determine the patterns of dissection propagation.MethodsTwenty fresh human aortas were harvested. TBADs were surgically initiated 2 cm below the left subclavian artery at four different locations (lateral, n = 5; medial, n = 5; anterior, n = 5; posterior, n = 5). Aortas were thereafter connected to a bench-top pulsatile flow model to induce antegrade propagation of the dissection.ResultsAntegrade propagation of the dissection was achieved and reached at least the celiac trunk (CT) in all the cases. Dissection was propagated to the renal aorta in 16 (80%) and infrarenal aorta in seven cases (35%). Left renal artery with or without the CT originated more often from the false channel when primary entry tear was lateral. Right renal artery and the CT most often originated from the false channel when primary entry tear was medial. When the CT was the only one originating from the false channel, primary entry tear was more often anterior, whereas when it originated from the true channel, it was more often posterior.ConclusionsThis human ex vivo model of TBAD is reproducible, since, in all the aortas, extended dissection was achieved and provides the first model of human aortic dissection with infrarenal aorta extension allowing future assessment of endovascular devices developed for human use. Furthermore, it allows clarification of the patterns of aortic dissection propagation and visceral and renal artery involvement according to the site of the primary entry tear.

Clinical RelevanceThe complexities of type B aortic dissection (TBAD) management remain a challenge. To develop strategies more suitable for this specific disease, several animal models have been reported. However, due to their small aortic diameter, they are not suitable to experiment stent grafts designed for human aortas. Furthermore, in these models, the dissection exceptionally reaches the infraceliac aorta, and does not allow the study of the visceral branch vessel compromise, whereas it is a prominent feature of human TBAD. We report the first human ex vivo model of TBAD, the impact of the primary entry tear location on antegrade dissection propagation, and the patterns of visceral and renal artery involvement.