The most effective method for excluding an enlarging and aneurysmal dilated false lumen is the sealing of the proximal entry tear with a customized stent graft; the absence of a distal reentry tear is desirable but not a prerequisite. Besides dissection, however, focal true (or false) aneurysm of the descending thoracic aorta represents another potential target for endovascular repair instead of open surgical repair.
Penetrating aortic ulcers, often originating from a localized intramural hematoma of the aorta, may also benefit from stent-graft patching, both in emergency and elective scenarios (as in posttraumatic aortic lesions such as incomplete aortic rupture after deceleration trauma).
Partial or complete rupture almost always occurs as a result of deceleration trauma (as in a car accident or a fall from a height). Emergent or preferably delayed (but timely) endovascular management by stabilization of the disrupted aorta with stent graft has proven beneficial, with amazing reconstruction of the thoracic aorta by virtue of the inner lining by the endoprothesis that can prevent enlargement, aneurysm formation, and eventual rupture but also allowed self-healing of the transsected aortic tissues.
Conventional treatment of type A (type I, II) dissection consists of surgical reconstruction of the ascending aorta with restoration of antegrade flow into the true lumen. Currently, interventional endovascular strategies have no clinical application in this population except to relieve critical malperfusion prior to surgery by performance of distal fenestration in type B (type III) dissection with ischemic complications. Various scenarios of true lumen compression with resultant malperfusion syndrome are amenable to endovascular management. Typical examples include dynamic malperfusion caused by intima invagination, static collapse of the aortic true lumen, dynamic or static occlusion of one or more vital side branches, or an enlarging false aneurysm due to patent proximal entry tear. Aims of treatment include reconstruction of the thoracic aortic segment by containing the entry tear, initiating thrombosis of the false lumen, remodeling the entire aorta and reestablishing sidebranch flow (Figure 8.1).
With surgical repair of the dissected thoracic aorta, approximately 90% of peripheral pulse deficits can be reversed at the expense, however, of a high mortality; patients with mesenteric or renal ischemia do even worse. Mortality
of patients with renal ischemia is 50-70% and as high as 87% in mesenteric ischemia5-7. The surgical mortality rates in patients with peripheral vascular ischemic complications are similar to those with mesenteric ischemia, with an 89% in-hospital mortality rate8-11. Operative mortality of surgical fenestration varies from 21% to 61%, and thus percutaneous interventional management using endovascular balloon fenestration of a dissecting aortic membrane to treat mesenteric ischemia has emerged as a niche indication in such complicated cases of malperfusion10-12.
The interventional management of aortic dissection and the use of stent grafts evolved slowly in anticipation of the risk of paraplegia from spinal artery occlusion. This complication occurs in up to 18% after surgery11-14.
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