ABSTRACT
Williams et al. (15) reported the mechanisms of visceral malperfusion in acute aortic
dissection. The authors proposed a system that classifies malperfusion as static or dynamic.
Static lesions are analagous to classic atheromatous lesions that narrow the diameter of the
artery with a fixed obstruction. Dynamic lesions result from compression of the true arterial
lumen by a false lumen secondary to high pressure in the latter. However, this classification
system does not describe all possible cases and it is often difficult to link symptoms with
mechanisms. In fact, it is reasonable to argue that all lesions are dynamic. Static lesions result
from an extension of the dissection into a blind ending visceral artery. This extension leads to a
narrowing in the true channel by compression of the false channel, where the blood enters but
cannot exit. This artery then tends to thrombose, giving rise to the diagnosis of a static lesion.
