Mechanical impairment of the aortic media caused by vasa vasorum dysfunction: a potential key element in the pathogenesis of aortic dissection in hypertensive patients

Abstract

We read with great interest the recent paper of Osada et al. [1] regarding the role of the vasa vasorum (VV) in the triggering process of aortic dissection. The authors evaluated the history and histopathology of 21 patients with thoracic aortic dissection and discussed some intriguing findings that we would like to comment upon. Although ‘hypertension and advanced age seem to be major predisposing factors for aortic dissection’ [1], a pertinent plausible pathogenetic mechanism is still lacking. Some years ago, we proposed such a mechanism after we investigated the structural and mechanical alterations of the porcine aortic wall, resulting from impairment of VV flow [2]. That study demonstrated that impaired aortic wall blood supply leads to (a) structural abnormalities of the outer media and (b) increased aortic stiffness. As diffusion from the lumen is inadequate to supply the whole thickness of the aortic wall with oxygen and nutrients, our pathogenetic model suggests that a decreased VV flow reportedly occurring in arterial hypertension [3]would nutritionally disadvantage the outer media with unfavourable implications on its mechanical characteristics. Thus, the aortic media will act, from a mechanical perspective, as a two-phase material, i.e. a sufficiently nourished inner part with normal elasticity and an ischaemic outer part with increased stiffness. We found the borderline between these parts to be quite sharp in pigs, with a microscopical outset of dissection often observed at this point. Accordingly, we speculated that interlaminar shear stresses develop at that borderline in hypertensive patients [4], eventually leading to detachment of the layers and aortic dissection [2]. Our team thanks Osada et al. for referencing our work. We were content to see several of their findings supporting our pathogenetic concept. First, the striking histopathological similarities between their clinical and our experimental specimens sustain the idea of ischaemic outer media in chronic hypertension. They report ‘atrophy of the smooth muscle cells’ along with ‘clear abnormalities in the elastic laminae, including fragmentation, and