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K. Ivancev, B. Koul Chapter 15 Branch Stent-Graft Systems
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159
a
Fig. 15.3. a Schematic drawing showing an open stent-graft placement from the distal aortic arch. b CT showing a stent-graft ana-
stomosed to the aortic arch, thereby excluding the aneurysm in the aortic arch and in the distal thoracic aorta
eurysm in the descending thoracic aorta [8, 9]
(Fig. 15.4). The portion of the stent-graft that is free
from stents is then used for the reconstruction of the
aortic arch. The stented elephant trunk provides an excellent landing zone for a subsequent stent-graft placement through a femoral access. If there is no suitable
landing zone in the diaphragmatic portion of the descending aorta Teflon felt may be placed as a band at
this level by gaining access to the diaphragmatic portion of the descending aorta through the pericardium
(Fig. 15.4). According to the results reported in the literature this open stent-graft placement under hypothermic cardiopulmonary arrest is associated with a risk,
however low, of permanent spinal cord injury, i.e., paraplegia [10]. Although the causes are multifactorial, a
possible way of minimizing the risk for such a complication may be to use a relatively short stented elephant
trunk or stent-graft, i.e., not longer than 10±15 cm. Any
subsequent persistent leaks in a setting of type B dissection or aneurysm can be treated endoluminally with a
distal stent-graft extension later on (Fig. 15.4).
15.4 Branch Stent-Grafts
for the Thoracic Aortic Arch
Inoue et al. [11] published their results with the use of
a branch stent-graft for the thoracic aorta in 1999. Since
then, little has happened in this field, most likely owing
to the obvious problems associated with the deployment
of branch stent-grafts in such a complex area as the
aortic arch. Attempts have been made to create a modular system for the arch by using a standard stent-graft
placed across the subclavian artery and then puncturing
a hole from the subclavian arteries into the aortic stentgraft and placing a modular extension [12]. Chuter et
al. [13] have placed a modular stent-graft from the right
carotid artery into the ascending aorta and then covered the aortic arch with a stent-graft placed via a femoral approach and connected it with the main stent-
b
graft in the ascending aorta. Extraanatomical bypasses
from the right carotid artery to the left carotid artery
and further to the left subclavian artery which were
previously performed guaranteed preserved circulation
to the supraaortic vessels [13]. All of these attempts exemplify the difficulties in achieving a safe branch stentgraft deployment in the complex area of the aortic arch
[14]. The difficulties include the risk for cerebral embolization [11]. There is a risk of failed orientation and
thereby failed preservation of flow to the important supraaortic vessels, with serious consequences as a result.
Nevertheless, continued attempts are made to solve the
inherent problems with this technique, not least because
there are several advantages to be achieved. There is a
large group of patients with type B dissection where the
primary entry is so close to the left subclavian artery
that coverage of this vessel is inevitable. Although this
has been reported to be an innocuous procedure, an
easily deployed branch stent-graft to the left subclavian
artery may not only maintain the circulation to the left
arm and left vertebral artery but may also improve the
stability and fixation of the stent-graft. Similarly, the
next step with a branch stent-graft further to the left
carotid artery may solve the problem of extraanatomical
bypasses, which today are required if the left carotid artery is blocked by a stent-graft. Further development is
anticipated in this field.
15.5 Discussion
With the advances in stent-graft technique and technology EVAR is today applied in more complex anatomy.
This is particularly true for the aortic arch, where a
combination of open surgical repair techniques, including either extraanatomical bypasses or bypasses from
the ascending aorta to the supraaortic vessels, or a total
replacement of the aortic arch, may be necessary in order to find a less traumatic solution when applying
EVAR in this area. It is an evolving field and it has been
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III. Treatment of Thoracic Degenerative Aortic Aneurysms
a
bcd
e
Fig. 15.4. a Schematic drawing demonstrating the various steps
for deployment of a ªstented elephant trunk.º The elephant
trunk with its stented portion and invaginated unstented graft
portion is deployed in the descending aorta. The stented portion is then sutured to the aorta and the unstented graft portion is retrieved and used for reconstruction of the aortic arch.
A stent-graft placed transfemorally is subsequently used for exclusion of an aneurysm in the distal thoracic aorta using the
stented elephant trunk and the distal banded thoracic aorta as
an implantation site. b CT demonstrating aneurysm in the ascending aorta and descending aorta. c, d Aortogram demonstrating the stented elephant trunk and banded distal thoracic
aorta following open repair of the ascending aorta and the aortic arch.
placed stent-graft with a good exclusion of the aneurysm
e Completion angiography following a transfemorally
shown repeatedly to offer results superior to those from
open surgery alone. Branch stent-grafts are under development and the near future will show when this new
technique may replace conventional open surgical repair
of the aortic arch.
K. Ivancev, B. Koul Chapter 15 Branch Stent-Graft Systems
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161
References
1. Tse LW, MacKenzie KS, Montreuil B, Obrand DI, Steinmetz OK. The proximal landing zone in endovascular repair of the thoracic aorta. Ann Vasc Surg 2004; 18(2):178±
185.
2. Schumacher H, Bockler D, Bardenheuer H, Hansmann J,
Allenberg JR. Endovascular aortic arch reconstruction
with supra-aortic transposition for symptomatic contained rupture and dissection: early experience in 8 highrisk patients. J Endovasc Ther 2003; 10(6):1066±1074.
3. Fajer S, Eyal A, Lubezky N, Karmeli R. Combined surgical
and endovascular repair of type B thoracic aortic dissecting aneurysm after failed endovascular treatment. Eur J
Vasc Endovasc Surg 2004; 27(5):559±562.
4. Kato N, Shimono T, Hirano T, Mizumoto T, Ishida M, Fujii H, Yada I, Takeda K. Aortic arch aneurysms: treatment
with extraanatomical bypass and endovascular stent-grafting. Cardiovasc Intervent Radiol 2002; 25(5):419±422.
5. Kato M, Kuratani T, Kaneko M, Kyo S, Ohnishi K. The results of total arch graft implantation with open stent-graft
placement for type A aortic dissection. J Thorac Cardiovasc Surg 2002; 124(3):531±540.
6. Sueda T, Orihashi K, Okada K, Sugawara Y, Imai K, Hamamoto M. Successful shrinkage of distal arch and proximal descending aortic aneurysm after transaortic endovascular stent-grafting. Eur J Cardiothorac Surg 2004;
25(5):716±721.
7. Fleck T, Hutschala D, Czerny M, Ehrlich MP, Kasimir MT,
Cejna M, Wolner E, Grabenwoger M. Combined surgical
and endovascular treatment of acute aortic dissection
type A: preliminary results. Ann Thorac Surg 2002;
74(3):761±765; discussion 765±766.
8. Mizuno T, Toyama M, Tabuchi N, Wu H, Sunamori M.
Stented elephant trunk procedure combined with ascending aorta and arch replacement for acute type A aortic
dissection. Eur J Cardiothorac Surg 2002; 22(4):504±509.
9. Miyamoto S, Hadama T, Anai H, Sako H, Shigemitsu O.
Stented elephant trunk method for multiple thoracic aneurysms. Ann Thorac Surg 2001; 71(2):705±707.
10. Usui A, Ueda Y, Watanabe T, Kawaguchi O, Ohara Y, Takagi Y, Tajima K, Nishikimi N, Ishiguchi T. Clinical results
of implantation of an endovascular covered stent-graft via
midsternotomy for distal aortic arch aneurysm. Cardiovasc Surg 2000; 8(7):545±549.
11. Inoue K, Hosokawa H, Iwase T, Sato M, Yoshida Y, Ueno
K, Tsubokawa A, Tanaka T, Tamaki S, Suzuki T. Aortic
arch reconstruction by transluminally placed endovascular branched stent graft. Circulation 1999; 100(19 Suppl):
II316±321.
12. McWilliams RG, Murphy M, Hartley D, Lawrence-Brown
MM, Harris PL. In situ stent-graft fenestration to preserve
the left subclavian artery. J Endovasc Ther 2004;
11(2):170±174.
13. Chuter TA, Schneider DB, Reilly LM, Lobo EP, Messina
LM. Modular branched stent graft for endovascular repair
of aortic arch aneurysm and dissection. J Vasc Surg 2003;
38(4):859±863.
14. Chuter TA, Buck DG, Schneider DB, Reilly LM, Messina
LM. Development of a branched stent-graft for endovascular repair of aortic arch aneurysms. J Endovasc Ther
2003; 10(5):940±945.
Pathophysiology
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of Aortic Dissection
Artur Evangelista, Teresa Gonzlez-Alujas
Chapter
16
Contents
16.1 Introduction ......................
16.2 Dissection Mechanism ................. 165
16.3 Pathogenesis ...................... 166
16.3.1 Aortic Parietal Stress ............ 166
16.3.2 Tunica Media Degeneration ......... 166
16.4 Pathophysiology .................... 167
16.4.1 Mechanical Factors .............. 167
16.4.2 Morphologic Aspects ............. 167
16.4.3 Mechanism of Vascular Complications . . 169
16.4.4 Aortic Dissection Evolution ......... 170
16.4.5 Aortic Dilatation and Complications
inChronicPhase...............
165
170
16.1 Introduction
Aortic dissection is defined as the separation of the aortic media with presence of extraluminal blood within
the layers of the aortic wall. In most patients one tear
or one or more entries are present in the aortic intima,
resulting in an abnormal communication between the
true aortic lumen and the split aortic media. With primary intimal dissection the media is exposed to pulsatile aortic flow, likely to create a false aortic lumen and
propagate a dissection, typically antegrade but sometimes retrograde from the site of the intimal tear. The
vast majority of aortic dissections originate in one of
the two sites where the greatest hydraulic stress is located in the ascending aorta, within several centimetres
above the sinuses of Valsalva, and in the descending
aorta, just distal to the origin of the subclavian artery
at the site of the ligamentum arteriosum. Sixty-five percent of intimal tears occur in the ascending aorta, 20%
in the descending aorta, 10% in the aortic arch and 5%
in the abdominal aorta [17]. Most dissections have a reentry site and some communication sites throughout
the descending aorta. The reentry tear is usually located
in the abdominal aorta, iliac arteries or other aortic
branches. These small communications, less than 2 mm
in diameter, are not reentry tears but the ostia of the
intercostal or lumbar arteries that have been severed by
the dissecting haematoma. Reentry of the dissection is
a predisposition for chronic false lumen perfusion with
no tendency to thrombus formation.
16.2 Dissection Mechanism
The two mechanisms regarding the initial event in aortic dissection are primary intimal tear and initial delamination of the tunica media produced by the formation of an intramural haemorrhage. There are different
lesions which can generate a primary entry tear of dissection, such as atherosclerotic lesions of the aortic intima, penetrating aortic ulcers, or iatrogenic intimal lesions [7, 21]. The second mechanism arises from bleeding of the vasa vasorum of the media (Fig. 16.1). All
mechanisms weakening the aorta's media layers via microapoplexy of the vessel wall lead to higher wall stress,
which can induce aortic dilatation, eventually resulting
in intramural haemorrhage, aortic dissection or rupture
[16]. The evolution of symptomatic intramural haematoma is to reabsorption, aneurysm formation or dissection [5]. Only 12% of intramural haematomas evolve to
Fig. 16.1. Intimal flap (arrow) from an intramural haematoma
which led to a classic dissection. TL true lumen, FL false lumen
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IV. Dissection
classic dissection and 24% present only a localised dissection which eventually progresses to pseudoaneurysm
formation [5].
Deterioration and loss of collagen and elastin in the
media layer appear to be the major predisposing factors
in cases of aortic dissection. Therefore, any disease process undermining the integrity of elastic and muscular
components of the media predisposes to aortic dissection [9, 24].
Different processes may produce rupture of the intima:
1. Weakness of the aorta wall due to connective tissue
disease such as Marfan syndrome, Edler±Danlos dis-
ease and bicuspid aorta [12, 22].
2. Mechanical stress induced from an aortic lesion sec-
ondary to jet impact as in aortic valve disease or
aortic valve prosthesis [12, 22].
3. Atherosclerotic disease of the aorta wall [21].
4. Aortic intramural haematoma evolution [5, 18, 26].
5. Iatrogenic lesion by catheters or surgery. Trauma
[10, 16].
6. Aortic inflammatory diseases [16].
Among the predisposing factors, untreated systemic hypertension is encountered in almost 80% of cases of
aortic dissection [8]. Hypertension may not only directly weaken the aortic media, but may also initiate atherosclerosis of the vasa vasorum and thus intramural
haemorrhage due to rupture of nutrient intramural vessels [26]. The causative role of systemic hypertension is
further supported by the finding that coarctation of the
aorta predisposes to aortic dissection [9, 26].
16.3 Pathogenesis
16.3.1 Aortic Parietal Stress
Aortic wall integrity depends mainly on two factors:
contention resistance of its internal and external layers,
determined by their biochemical and anatomical structure, and aortic parietal stress, which is in relation to
arterial tension, luminal diameter and parietal thickness. All this can be expressed by a modified equation
similar to the law of Laplace, where circumferential
stress is directly related to blood pressure and aortic diameter, and inversely to parietal thickness.
As mentioned previously, aortic diameter is the main
determinant of parietal stress. The aorta usually dilates
before dissecting and the geometry of the dilated segment changes from cylindrical to spherical, passing
through ellipsoidal. This change in aortic morphology
causes a slow, progressive increase in circumferential
stress and a rapid increase in longitudinal stress and
accounts for the fact that the majority of intimomedial
tears may be transverse. A further consideration to bear
in mind regarding parietal stress is that its distribution
in aorta wall thickness is not uniform. Since the pressure falls upon the internal arterial surface, parietal
stress is greater on the internal than the external part.
This is, in part, why the internal layers usually tear and
the external layers do not [20, 23].
Arterial hypertension is considered to be a leading
factor in the production of an arterial tear. However,
the frequency of dissection in hypertensive patients is
low and, furthermore, unpredictable. In fact, arterial
pressure is only one of the components of parietal
stress and, in some cases, is not even the most important. An aorta with the same pressure may dissect or
not, depending on the anatomical characteristics (thickness and composition) of its walls and degree of dilatation. Therefore, the factors that may lead to dissection
are as follows: (1) decrease in contention resistance of
the internal layer; (2) increase in arterial pressure; (3)
increase in aortic diameter; and (4) decrease in parietal
thickness.
In the hypertensive type, the internal layer is normal, but there is an increase in parietal stress as a consequence of the increase in arterial pressure. This imbalance will produce a gradual increase in aortic diameter and, with time, a dissection [23].
16.3.2 Tunica Media Degeneration
Degenerative changes produced in the tunica media of
patients who evolve to dissection may affect the elastic
architecture, collagen and muscular component. Loss or
fragmentation of any of these elements diminishes resistance of the aorta wall to haemodynamic stress. This
may lead to aneurysmal dilatation of the aorta wall and
subsequent dissection. In Marfan syndrome, as in other
connective disorders, the dissection is due to medial degeneration. There is enhanced expression of metalloproteinases in vascular smooth muscle cells which may
promote both fragmentation of medial elastic layers and
elastolysis, and may lead to significant medial degeneration. In these circumstances, despite normal aortic pressure, the aorta dilates. When the aortic diameter increases, parietal stress increases and eventually a dissection ensues. In the hypertensive type, circumferential
stress increases linearly with the increase in arterial
pressure. In these cases, an increase of some degree of
dilatation aggravates the circumferential stress even
more. By contrast, in Marfan syndrome, the circumferential stress does not increase linearly, but exponentially. In these patients, a slight rise in arterial pressure
accentuates the circumferential stress even more [23].
In some patients with dissection, rupture or loss of
structural elements of the capa media is evident on optical microscopy; however, in other cases changes are
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167
difficult to perceive or are even absent. These structural
defects do not in themselves explain why some aortas
dilate or rupture, others dissect and many remain free
of any complications despite the presence of capa media
degeneration. It is wrongly assumed that degeneration
of the media is a lesion that diffusely affects the dissected aorta. However, as Prokop et al. [20] pointed out,
once the dissection has begun, it may extend distally,
affecting histologically normal segments, since propagation of the dissection depends basically on the pulse
pressure wave.
According to Hirst and Gore [9], the capa media lesion in the majority of patients with dissection can be
classified in two groups, depending on whether it predominantly affects the muscle or the elastic architecture. Separation and fragmentation of elastic fibres is
more frequent in young patients (under 40 years) and
particularly in individuals with Marfan syndrome or
other hereditary defects.
Weakening of the aorta wall does not only occur as a
consequence of elastic fibre fragmentation but also because of collagen and mucoid material accumulation.
These changes are more prominent in ascending aorta,
with the segment subjected to greater pulsatile expansion and, therefore, greater stress. As a result of the loss
of elastic tissue, media cohesion is altered, muscle cells
change their usual parallel orientation and cell deterioration is accelerated. Loss of muscle cells is usually focal and more frequent in hypertensive patients and
those over the age of 40. Smooth muscle cells require
oxygen and other nutrients to survive and consequently
depend on adequate blood flow. Thickening of the intima, particularly that due to atherosclerosis, may interfere with its diffusion and permeability and affects the
internal part of the capa media, whereas the external
part may be threatened by atherosclerosis of the vasa
vasorum.
Schlatmann and Becker [24] studied aortas of 100
patients with no known aortic disease and observed
that the degree of elastic fragmentation was greater in
older patients, the changes were more pronounced in
the ascending aorta and the arch than in descending
aorta, and the internal layer of the media was the most
affected.
Larson and Edwards [12] studied 161 necropsies of
patients with dissection. All patients with type A dissection had severe histologic changes. Patients with type B
dissection with and without Marfan syndrome had few
cystic changes in the descending aorta and many atherosclerotic lesions.
The typical histologic findings of tunica media degeneration detected in patients with dissection can also
be observed in elderly patients and hypertensive patients without dissection. In this respect, many authors
consider the changes in the media to result from the
mixture of damage and repair lesions produced by haemodynamic aggressions repeated throughout the pa-
tients' lives [24]. The histologic difference between aortas with and without dissection may be more quantitative than qualitative and aorta wall anomalies in young
patients with Marfan syndrome represented the acceleration in those that appear with ageing.
16.4 Pathophysiology
16.4.1 Mechanical Factors
Several types of mechanical forces that act on the aorta
wall have been described: (1) those related to the vessel
curve in certain sites; (2) those produced by the radial
impact of the pulse pressure wave; and (3) the shearing
longitudinal effect of blood flow.
The heart, ascending aorta and arch form a relatively
mobile complex that hangs from the supraaortic trunks.
In contrast, the descending aorta is more fixed on the
left side of the spinal column. Flexion forces are maximum in the root and aortic isthmus. It is in these sites
where the dissection entry tear is most frequently located. Tears are believed to occur in these areas since
torsion movement of the aortic annulus provokes an additional downward traction of the aortic root and provokes an increase in the longitudinal stress in this segment; and in the isthmus area where the tension is due
to the union of the aortic arch, which is relatively mobile, with the descending thoracic aorta, which is quite
fixed [20]. Several studies have proved that the reduction in pulse pressure wave inhibits dissection progression [27]. The pulsatile nature of aortic flow is one of
the principal causes of dissection progression. The aorta is quite resistant to increases in static pressure. Experimental studies show that the aorta only dissects
when flow is pulsatile [20]. The longitudinal shearing
forces that act on the direction of blood flow are directly related to the pressure gradient between the two aortic lumina, which is small and due to decreased pressure in the true lumen by the Bernoulli effect at high
velocity. In the false lumen, there is not the same decrease in pressure during propagation of the dissection
since it does not carry a net flow.
16.4.2 Morphologic Aspects
All dissections are characterised by a separation of the
media layer of variable circumferential and longitudinal
extension. Furthermore, a tear of the intima and media
(entry tear) is observed in classic aortic dissection
(Fig. 16.2). In the classic series, an entry tear could not
be identified in less than 5% of necropsies. This intimomedial tear is, in general, perpendicular to the long axis
of the aorta. Blood enters through this orifice, separat-
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IV. Dissection
Fig. 16.2. Transoesophageal echocardiography shows a large en-
try tear (greater than 10 mm) localised distally to the subclavian artery in type B dissection
ing the media into two layers over a distance that varies
in each case. The most internal two thirds of the media
layer form, together with the intima, the internal wall
of the false lumen. This flap is formed not only by the
intima but also by the internal layer of the capa media
and, consequently, should be termed intimomedial flap.
The internal wall of the false lumen is thicker than the
external wall which comprises the external part of the
media and the adventitia.
Once the intimomedial tear has been produced,
blood enters under pressure and a longitudinal dissection of the whole aorta may occur in a few seconds
[21]. The dissecting haematoma can evolve to external
false lumen rupture, reentry tear formation or end in a
cul-de-sac. Thinness of the external wall of the false lumen is the anatomical finding related to aortic rupture.
The thinner it is, the greater the probability of aortic
rupture will be. It may also be assumed that the thicker
it is, the thinner the intimomedial flap will be and, consequently, the greater the probability of a reentry being
produced [21]. Rupture of the false lumen is the most
frequent cause of death. The rupture site is usually near
the entry tear and, therefore, the segment which breaks
most frequently is the right anterolateral wall of the ascending aorta. Blood extravasation usually accumulates
in the pericardial sac (haemopericardium), and death
from cardiac tamponade is therefore frequent. If the
arch ruptures, a haemomediastinum is usually produced; if it is the descending aorta, a left hemithorax;
and if it is the abdominal aorta, a haemoperitoneum.
On occasions, a wide intimomedial tear may serve as
an entry tear and reentry of the false canal. In this case,
flow in the false canal is usually anterograde and retrograde [21]. When the dissecting canal ends in a cul-desac with no exterior rupture of a reentry tear, anterograde and retrograde flow may be observed (Fig. 16.3);
however, in some cases, particularly if the entry tear is
Fig. 16.3. Computed tomography study showing a type A dis-
section with an entry tear in the ascending aorta (black arrow)
and a false lumen ending in a cul-de-sac due to a total thrombosis of the abdominal false lumen (white arrow). TL true lumen, FL false lumen
small, an acute total thrombosis of the false lumen
might be produced. Diagnostic techniques have difficulties in distinguishing the latter from an intramural haematoma. Throughout the aorta, the portion of dissected
aortic circumference is quite predictable since, albeit
variable, the longitudinal course of the dissection has a
determined trend. When the dissection begins in ascending aorta, the dissecting haematoma involves the
larger curve of this arch and affects the right lateral region of the ascending aorta. From the isthmus, the dissection usually adopts a spiral route. The infradiaphragmatic and infrarenal aortas tend to dissect their left
posterior region, leaving the right anterior vessels intact. Further down, the dissection usually affects the
two iliac arteries, though more often the left one. The
common femoral artery rarely dissects. For this reason,
although any of the aorta branches can be affected by
dissection, the right coronary artery, the supraaortic
vessels, the left intercostal arteries, the left renal artery
and the left common iliac artery are more frequently affected. On the other hand, the left coronary artery, the
coeliac trunk, the superior mesenteric artery and the
right renal artery are usually connected to the true lumen. Ambos et al. [1] qualified chronic dissection with
reentry as a ªhealed dissectionº. Nevertheless, the false
lumen is usually larger than the true lumen; with time,
the former dilates and becomes tortuous. Aneurysmal
dilatation of the false lumen is the most frequent late
complication of dissection. The larger the aneurysm,
the more likely rupture of its wall will be (Fig. 16.4).
Some publications suggest that a reentry tear in pa-
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169
Fig. 16.4. Type B dissection by MRI. Large false lumen present-
ing high risk of aortic rupture due to high wall stress of the dilated false lumen (arrows)
tients with chronic dissection does not protect against
rupture of the false lumen.
16.4.3 Mechanism of Vascular Complications
The mechanism by which dissection can affect any of
the branch arteries from the aorta is twofold:
1. Dynamic obstruction. In this case, the obstruction
of the compromised vessel is dynamic, the true lumen is in the form of a ªCº and the intimomedial
flap has a concave arrangement towards the false lumen. This mechanism has been described from aortographic and computed tomography (CT) findings
and, characteristically, at surgery or during necropsy,
there are no data on the previous existence of arterial obstruction. Usually the true lumen is compressed
by the false lumen and this generates an obstruction
of the arterial ostia (Fig. 16.5).
2. Static obstruction. Here, two situations should be
distinguished ± arterial dissection and location of
the origin of the arterial branch in the false lumen.
In the first case, the intraarterial dissecting haematoma may obstruct the vessel lumen or intraarterial
rupture of the haematoma may be produced, with
formation of the dissection reentry tear. In some
cases, the circumferential laceration of the arterial
ostium may be accompanied by a circumferential
dissection of the proximal segment of the artery and,
thus, the intimomedial flap of the arterial branch
Fig. 16.5. Compression of the ostium of the superior mesenteric
artery (SMA) by the intimal flap secondary to severe compression of the true lumen by the false lumen (arrow)
may be distally impacted, affecting arterial flow. In
many cases, obstruction of arterial branches is twofold: static and dynamic.
Ischaemia of the lower limbs as a complication of dissection has been described in up to 26% of patients
with dissection and may occasionally be isolated [19],
with no other clinical data of suspected dissection. Cerebral vascular accident is associated with increased
early mortality in patients with dissection. The most
frequently involved arteries of the supraaortic trunks
are the innominate artery and the left common carotid
artery. The left subclavian artery is less frequently affected than the right subclavian artery. The characteristic pattern of dissection propagation consists of involvement of the left side of the descending aorta which occurs preferably in the branches which originate on this
side of the aorta. The left kidney is the organ at greatest risk of ischaemia. Kidney failure and mesenteric infarct have been identified by different groups as risk
factors of early death in patients with dissection [6]. If
the dissecting haematoma only affects the intercostal arteries on one side (generally the left), the arteries on
the other side perfuse the spinal cord; however, if the
haematoma affects the arteries on both sides, a medullary infarct will be produced.
The inexistence of a reentry tear in the distal aorta
or its branches may jeopardise perfusion through the
true lumen to such an extent that it collapses from the
pressure or thrombosis of the false canal.
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16.4.4 Aortic Dissection Evolution
Despite the significant advances in imaging techniques
and therapeutic procedures in the last decade, dissection mortality in the first month of evolution continues
to be very high: 25±30% for patients with type A dissections and 10±14% for patients with type B dissections
[8]. Acute aortic dissection has a high risk of complications, clearly higher when the ascending aorta is affected than when it occurs distally to the innominate
trunk. Risk factors for complications and mortality for
patients with type A dissection are shock, hypotension
and tamponade [14]. In contrast, in patients with
type B dissection, mortality is related to shock and visceral ischaemia [16].
Once the acute phase has been overcome, the prognosis of dissection is clearly better, but at 10 years the
survival rate averages 44% for patients with type A aortic dissection and 32% for patients with nonoperated
type B dissection [16]. Mid-to-long-term mortality does
not depend on aortic disease alone but also on different
factors such as age, associated diseases and comorbidity.
One of the factors better related to aortic rupture
evolution is aortic dilatation. Juvonen et al. [11] followed 50 type B dissections. At a mean of 3 years, 18%
presented aortic rupture and 20% required elective surgery for rapid expansion of the aneurysm. Variables associated with aortic rupture were age, chronic obstructive pulmonary disease and elevated mean blood pressure. The last median descending aorta diameter before
rupture in the rupture group was 54 mm. This study
suggested that the continued patency of the false lumen
was not an important predictor of rupture. On the other
hand, two further studies showed aortic dilatation predictors to be an aorta diameter over 40 mm during the
acute phase and an entry tear in the thoracic aorta or
the presence of flow in the false lumen [13]. Nevertheless, the absence of flow in the false lumen in 55% of
cases is surprising, and raises the suspicion that many
of these cases were, in fact, intramural haematomas.
Sueyoshi et al. [25] recently reported the follow-up by
CT of 62 type B dissections, 75% of segments increased
in size during a mean follow-up of 4 years. The presence of blood in the false lumen was the only significant risk factor, showing an increase of 3.3 mm/year,
while in the group without flow in the false lumen the
increase was 1.4 mm/year. In this study, total false lumen thrombosis was present in 51 of 176 cases. Another interesting finding was that the growth rate of
aortic dissections in the thoracic aorta was higher than
that of the abdominal aorta: 4.1 and 1.2 mm/year, respectively.
Previous studies revealed that aortic diameter was a
strong predictor of enlargement and rupture. The maximum aortic diameter was considered to be between 40
and 60 mm [13]. These results can be explained by the
law of Laplace, which states that the perpendicular
stress on a cylinder is directly proportional to the pressure exerted by the fluid content and its radius and is
inversely proportional to wall thickness. This means
that the larger the diameter, the faster the growth rate
will be if the pressure is constant.
Some results have shown that age is a significant risk
factor for an increase in diameter in univariate analysis
[11]. Anatomically, elasticity and distensibility of the
aorta decline with age. Such changes occur even in normal healthy adults and, for some reasons, these changes
appear earlier and are more progressive in men than in
women.
Erbel et al. [3] proposed a classification based on
dissection extension and the presence and location of
an entry tear. Patients with aortic dissection types with
absence of communication or with localised retrograde
flow in the descending aorta alone had better survival.
Thrombosis formation in the false lumen was a predictive factor of good prognosis. Although the results of
this European multicentre study contribute very interesting data, they are limited by the single use of monoplane transoesophageal echocardiography (TEE), which
limits visualisation of entry tears located in the distal
ascending aorta and the proximal arch.
Some studies have shown that survival at 6 years is
worse for patients with type B dissections than for patients with operated type A dissections [4]. Ergin et al.
[4] reported the survival rate of patients with operated
type A dissections without false lumen flow to be 85%
versus 62% in the group with false lumen flow. Notably,
in this series, false lumen flow was absent in 53% of
cases [15]. In other studies, total obliteration of the
false lumen in the descending aorta was achieved in
only 10±20% of operated type A dissections [4, 15]. The
better prognosis of operated type A dissections could
be due to a smaller entry tear than for type B dissections.
16.4.5 Aortic Dilatation and Complications
in Chronic Phase
The pathophysiology of aortic dissection in the chronic
phase is essential to foresee possible complications and
to select patients who are candidates for more aggressive treatment. Most complications occur in the acute
phase and mortality continues to be relatively high, owing essentially to comorbidity due to associated diseases, aortic rupture due to progressive dilatation, or
extension of the dissection.
Dilatation of the aorta in the long-term evolution of
aortic dissection has been studied by our group.
Although aortic diameters were determined by CT or
MRI, haemokinetic variables of the aorta were defined
A. Evangelista, T. Gonzlez-Alujas Chapter 16 Pathophysiology of Aortic Dissection
https://t.me/med1917
Fig. 16.6. High-pressure pattern in the false lumen owing to a large entry tear and a small distal reentry tear. Transoesophageal
echocardiography shows how contrast in the false lumen has a low rate of progression compared with that in the true lumen. TL
true lumen, FL false lumen
171
Fig. 16.7. Low-pressure pattern in the false lumen owing to similar-sized entry and reentry tears. By transoesophageal echocardio-
graphy contrast moves with similar velocity in the true lumen and the false lumen. TL true lumen, FL false lumen
by TEE performed prior to discharge. Forty-seven patients had type B dissections and 40 had operated
type A dissections. The maximum aortic diameter presented dilatation between 0.2 and 6 mm/year. Dilatation
of the descending aorta was greater in medically treated
type B dissections than in operated type A dissections.
Variables related to greater aortic dilatation were entry
tear size, maximum descending aorta diameter in the
subacute phase and the high-pressure pattern in the
false lumen. An entry tear size over 10 mm implies
higher risk of false lumen enlargement. Maximum aortic diameter in the subacute phase was a significant predictor of progressive dilatation since, according to the
law of Laplace, maximum aortic diameter is the factor
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