Angiotensin II-infused mice develop dissecting aneurysms, characterized by intramural rather than intraluminal thrombus, suprarenal rather than infrarenal lesions, medial dissections rather than circumferential elastin degradation and a variability in lesion shape that remained as yet unexplained. In order to provide insight into these intriguing lesions we scanned murine aortas at baseline and after 10, 18 and 29 days of Angiotensin II infusion, both in vivo (ultrasound, micro-CT) and ex vivo (phase-contrast X-ray tomographic microscopy). Dissecting aneurysms of varying severity occurred in 31/34 mice. All of these were characterized by a medial tear near the ostium of thoracic and abdominal aortic side branches, with a predilection for the left and ventral aspects of the ostium of the celiac artery. In 25/31 animals an intramural hematoma was formed. Fully ruptured branch ostia occurred significantly more often in the supraceliac aorta, affecting in particular the left suprarenal artery (the first branch cranial to the celiac artery, 23/25). Animals with a thoracic tear (6/31) had significantly larger intramural hematoma than animals with an abdominal tear (p<0.05), and the length of the hematoma correlated to the number of ruptured side branches (r 2 =0.78). In 11 mice a parallel false channel was formed. The volume of free-flowing intramural blood in the false channel was significantly larger for left than for ventral tears, but was not related to the length of the tear. Our data suggest that (i) medial tears are the primary event in dissecting AAA formation, (ii) an intramural hematoma is formed if the adventitia covering the medial tear dissects and leads to the accumulation of intramural blood from ruptured side branches, (iii) adventitial dissection and hematoma formation progress in the direction of least resistance/smallest side branches (i.e. cranial of the celiac artery) and (iv) a false channel is formed if the radial expansion of the adventitia due to blood flowing out of the medial tear acts in the same (leftward) direction as the expansion due to a ruptured left suprarenal artery. We conclude that Ang II-infused mice can be a valuable model to study the under-researched role of side branches in the formation and progression of aortic dissections.