4.0 Pathophysiology of Non-A Non-B
dissection
The wall of the aorta comprises three layers, the tunica intima, tunica
media which largely is constituted of structural proteins including
elastin and collagen and adventitia (Levy et al. , 2020; Frederick
and Woo, 2012). These layers form a thick aortic wall able to withstand
high pulsatile pressure and shear stress.
Aortic Dissection is a condition characterised by the separation of
these aortic layers. Classically it involves the breaching of the tunica
intima, resulting in blood being diverted into a newly created channel
within the medial layer of the aorta, known as the false lumen. A tear
in the intimal layer tends to arise in locations where the rise in blood
pressure is the greatest, commonly 2-2.5cm above the aortic root (Levyet al. , 2020). The separation of these layers paves the way for
the formation of a false lumen. Increase in size of the false lumen can
lead to an aortic rupture which has a high mortality rate or a second
intimal tear which allows blood to re-enter the intima to form a
double-barrelled aorta (Gawinecka, Schönrath and von Eckardstein, 2017).
This tear can occur in any part of the aorta including the ascending,
arch and descending aorta.
Other origins of an aortic dissection include an intramural haematoma
and aortic ulceration. The former occurs due to the formation of a
haematoma in the media, as a result of bleeding into the aortic wall
from the vasa vasorum (Alomari et al. , 2014; Nienaber et
al. , 2016). The latter, also referred to as a penetrating aortic ulcer
and linked to atherosclerotic disease, is a penetration of the elastic
lamina and can result in a haematoma forming in the tunica media
(Hayashi et al. , 2000). Such haematomas can contribute to an
aneurysm forming prior to aortic dissection.
The formation of an aortic aneurysm is thought to be more likely as a
consequence of weakening of the tunica media, through the degeneration
of collagen and elastin, which in turn increases higher wall stress.
This is explained by Laplace’s Law which states that ‘wall stress is
directly proportional to pressure (i.e. hypertension) and radius, and
inversely proportional to vessel wall thickness (Patel and Arora, 2008).
Compromising the integrity of the aortic wall raises the risk of an
aortic dissection. This is key to the risk factors associated with the
condition.
Should an aortic dissection progress, through the passage of blood
further down the false lumen of the tunica media, it has potential to
stretch past the aorta and into the major blood vessels, leading to
ischaemia. Dissections can progress in an anterograde or retrograde
fashion. This progression of the dissection can result in pressure
differences which may lead to the compression or obstruction of the true
lumen by the false lumen. Following this, fenestration may
re-communicate the false with the true lumen or there is a risk the
dissection may rupture into the surrounding cavities (Patel and Arora,
2008).
Carino et al. in their systematic review demonstrated in their analysis
that 88% of non-A non-B aortic dissection patients had a complicated
disease course and that 29% of these patients had signs of
malperfusion; defined as a loss of blood supply to vital organs
resulting in end-organ ischaemia (Carino et al. , 2019; Deeb,
Patel and Williams, 2010). This percentage formed a considerably larger
proportion than observed in type B aortic dissections (Pape et
al. , 2015; Estrera et al. , 2007; Ziganshin, Dumfarth and
Elefteriades, 2014).