Staging Of Aortic Dissection

The Stanford classification of aortic dissection distinguishes between type A and type B (Figure 2.1)36,37. Type A means the dissection involves the ascending aorta; a type B dissection does not involve the ascending aorta. This distinction or description is applied in similar fashion to all acute aortic syndromes, including all variants of dissection such as intramural hematoma and penetrating aortic ulcerations. The De Bakey classification subdivides the dissection process in type I dissection involving the entire aorta, type II dissec-

Aortic Dissection Pau
Figure 2.1. Most common classification systems of thoracic aortic dissection (e.g., the Stanford and DeBakey classification).

tion involving only the ascending aorta, and a type III dissection sparing the ascending aorta and the arch. Various attempts to further subdivide both classification systems have not been established in the medical community38,39, although the arch region deserves integration into a modern classification system40. Recent observational evidence highlights the importance of precursors of typical aortic dissection such as intramural hematoma, penetrating aortic ulcers, or localized intimal tears as variants of a wall dissecting process41-46, and suggests a need to utilize the identical staging and classification system for all variants of aortic dissection.

Classic Aortic Dissection

Typical acute aortic dissection is characterized by the rapid development of an intimal flap separating the true and false lumen47-49. In the majority of cases (~90%) intimal tears are identified as sites of communication between true and false lumen49,50. The dissection can spread from diseased segments of the aortic wall in an antegrade or retrograde fashion, involving side branches and causing complications such as malperfusion syndrome by dynamic or static obstruction (from coronaries to iliac arteries), tamponade or aortic insufficiency48,50-52. The arbitrary classification of acute, subacute, or chronic dissection does not appear helpful for didactic or for differential therapeutic considerations but may be used to describe the individual situation and time span of survival of a given patient. From a pathophysiological point of view, progression of dissection is difficult to predict once a patient with dissection has survived the initial two weeks after its inception, although false lumen expansion is likely to develop over time. Several clinical features may be used to estimate late risk, including spontaneous false lumen thrombosis, evidence of persistent communication, patent false channel, and others39,47,53.

Intramural Hematoma

Acute aortic intramural hematoma is considered a precursor of classic dissection, originating from ruptured vasa vasorum in medial wall layers that may provoke a secondary tear and communication with the aortic lumen45,46. This process may be initiated by an aortic wall infarction or micro-apoplexy of the vessel wall. Similar to classic dissection, intramural hematoma may extend along the aorta, may progress or regress, and may eventually reabsorb43-45,54-56. The prevalence of intramural hemorrhage and hematoma in patients with suspected aortic dissection, as observed by various modern imaging techniques, seems to be in the range of 10-30%42,45-56. Intramural hematoma can lead to acute aortic dissection in 28-47% of the patients and is associated with aortic rupture in 21-47%. Regression of intramural hematoma is seen in about 10% of patients. Involvement of the ascending aorta or proximal type AIMH is generally considered an indication for expeditious surgery due to the inherent risk of rupture, tamponade, or compression of coronary ostia42'43'45-59. Distal intramural hematoma may warrant watchful waiting and potentially elective or emergent interventional stent-graft placement60 (Figure 2.2).

PLAQUE RUPTURE/PENETRATING ATHEROSCLEROTIC ULCER (PAU)

Ulceration of atherosclerotic aortic plaques can lead to aortic dissection or perforation61-65. Noninvasive imaging of aortic ulceration has been improved by tomographic scanning and has shed light on its pathophysiology and etiology. The ulcers seem predominantly to affect the descending thoracic aorta, as well as the abdominal aorta, in localized fashion; branch vessel compromise is rare. However, ulcers may penetrate intimal borders, often appearing in nipplelike projection with an adjacent hematoma62,65. Symptomatic ulcers and those with signs of deep erosion are more likely to rupture than others.

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