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Figure 7.22 Branched arch endograft for exclusion of arch
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aneurysms.
CHAPTER 7 Hybrid endovascular aortic arch surgery 71
the need for a sternotomy. Cook has subsequently
developed several second and third generation
arch grafts, with the latest iteration containing
several internal branches designed to support
covered stents that extend into the innominate
and left carotid arteries and do not require
extensive extra-anatomic bypasses, with the
exception of a left carotid–subclavian bypass.
Conclusions
Since the deployment of the first endovascular
stent-graft in 1994, the field of hybrid thoracic
aortic surgery has made great strides forward and is
rapidly becoming part of the surgical mainstream
[5]. Pioneering endovascular teams around the
world have advanced the application of this technology beyond the initial indications to an array of
thoracic aortic pathologies. Several clinical series
demonstrate impressive support of the therapeutic
promise of hybrid TEVAR. These encouraging
early results, as well as advances in stent-graft
design, promise to expand the application of complex hybrid endovascular therapies for patients
with challenging aortic arch pathology.
(a)
Figure 7.23 (a) Fluoroscopic image demonstrating the
proximal portion of a branched ascending and arch graft
with a wire from the innominate artery through the
innominate limb of the graft (heavy arrow), as well as
from the femoral artery through the short, wide mid-arch
(b)
limb of the graft (thin arrow). (b) Postoperative 3D
reconstruction demonstrating the ascending and arch
graft with a limb into the innominate artery, as well as a
carotid–carotid bypass (arrow).
72 PAR T I Aorta
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36 Estrera AL, Miller CC, 3rd, Porat EE, et al. Staged
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43 Usui A, Tajima K, Nishikimi N, et al. Implantation of an
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44 Hughes GC, Daneshmand MA, Balsara KR, et al. “Hybrid”
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47 Greenberg RK, Haddad F, Svensson L, et al. Hybrid
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51 Pamler RS, Kotsis T, Gorich J, et al. Complications after
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8
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CHAPTER 8
Acute aortic dissection
Ricardo Aun
Universidade de São Paulo, Hospital Albert Einstein, São Paulo, Brazil
Introduction
Acute aortic dissection, aortic intramural
hematoma, and penetrating aortic ulcer are
components of acute aortic syndrome. These events
have similar clinical and epidemiologic aspects, and
may also represent different stages of the same
pathologic process [1].
Aortic dissection results from a tear in the
intimal lining of the aortic wall, followed by blood
entering between the intima and the media, usually
taking a distal course resulting in a new lumen in
the aorta. The true lumen is circumscribed by the
intimal layer. The false lumen is circumscribed by
both the intima and the media layers. Ordinarily,
the blood flow is slower in the false lumen than in
the true lumen [2,3].
Usually, aortic dissection extends until it reaches an
important arterial branch, whether it affects it or not.
As the blood flows, another intimal tear can occur
and communicate within the two lumen (“re-entry”).
Aortic dissection generally starts at certain points:
t
Ascending aorta
t
2–3 cm above coronary artery ostia (65% of all
cases).
t
Descending aorta
t
immediately after the left subclavian artery
emergence (25%).
t
Aortic arch and abdominal aorta (5–10% of all
cases).
Aortic dissection frequently assumes a spiral aspect
and the false lumen is wider than the true lumen.
Classification
Acute aortic dissections are defined as dissections
that have been diagnosed up to 2 weeks after onset
of symptoms. When diagnosed after a 2-weeks
period they are called chronic dissections. Despite
being arbitrary, this is the period when immediate
and life-threatening complications happen [2–4].
The two most accepted classifications are those of
De Bakey and Stanford [3,4].
According to De Bakey’s system, aortic dissections
are separated in to:
t
Type I: originates in the ascending aorta, and
propagates to the aortic arch and descending
aorta.
t
Type II: confined to the ascending aorta.
t
Type III: originates in and is confined to the
descending aorta.
Stanford’s classification is easier and more
popular. It is divided in two groups:
t
Type A: affects the ascending aorta, and may or
not affect the rest of the aorta.
t
Type B: does not affect the ascending aorta
(Fig.8.1).
Epidemiology
Aortic dissections are the most common emergencies related to the aorta. It occurs two or three
times more frequently than aortic aneurysm rupture. Actual incidence of aortic dissections is hard
to predict, mainly because of high mortality before
patients could get to a hospital. Some population
Endovascular and Hybrid Therapies for Structural Heart and Aortic Disease, First Edition.
Edited by Jacques Kpodonu and Raoul Bonan.
© 2013 John Wiley & Sons, Ltd. Published 2013 by John Wiley & Sons, Ltd.
74
Fig. 8.1 Acute dissection with thrombosis of a proximal
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false lumen with sternosis of the true lumen causing
abdominal distention, pain, and renal failure.
studies estimate the incidence at 0.5–3.5 cases per
100,000 individuals per year [2,5,6].
Aortic dissections occur more frequently in
people of African descent than in Caucasians and
are much rarer in Asians; 75% of cases are in
people aged between 40 and 70 years. There is a
peak of incidence of type A dissections from 50
to60 years, and for type B dissections from 60 to
70 years of age. It is also more common in men
(2–5 times). Affected men are usually younger
than women (median age of 63 for men and 69
forwomen). Type A dissections represent 60% of
allcases [6].
Morbidity and mortality
Aortic dissection has an extremely high lethality
rate. According to population studies, 21% of
patients with aortic dissection died before being
admitted to a hospital. When admitted to a hospital,
without treatment, the mortality rate is 22.7% in
the first 6 hours, 50% in 24 hours, and 68% during
the first week [1,6,7].
Once the ascending aorta is involved the
mortality is related to complications like cardiac
CHAPTER 8 Acute aortic dissection 75
tamponade, acute aortic insufficiency, and
involvement of the ostia of coronary arteries. If
there is no involvement of the ascending aorta, the
main causes of death are visceral artery obstruction,
iliac artery obstruction, and aortic rupture [8].
An analysis of the results of current therapy has
been given in the International Registry of Acute
Aortic Dissection (IRAD) study. Looking at 464
patients in 12 centers between 1996 and 1998,
global mortality was 27.4%. In patients with type A
dissections, submitted to surgical treatment, the
mortality rate was 26% against 58% in clinically
treated patients, and aortic rupture was the main
cause of death (41.5%). Patients with type B
dissections and clinical treatment had a mortality
rate of 10.7%. A mortality rate of 31.4% was found
in complicated type B dissections when surgical
treatment was needed [6].
Pathogenesis
Despite the extensive literature on aortic dissection,
its etiology, for various reasons, remains poorly
understood [9]. Histologic changes found in
dissected aortas show a correlation with age and
may represent the normal aging process for
theaorta. The same histologic pattern found in the
aorta of normal elderly subjects showed that none
of the histologic changes observed can be considered as a specific structural change responsible for
the development of aortic dissection [10]. These
changes are: fragmentation of elastin, fibrosis,
defined as an increase in collagen, and necrosis of
the middle layer, defined as areas with apparent loss
of nuclei. They are identified in histologic studies of
the dilated aorta, in dissected and even in normal
aortas of the elderly [11,12].
All mechanisms of weakening of the aortic
media layer through microapoplexia of the vessel
wall seem to lead to more stress, which can induce
aortic dilation and aneurysm formation or an acute
aortic syndrome. Therefore, it seems to be that
histologic changes are not specific, but are due to
general hemodynamic events occurring within the
aorta [1].
In this context, individuals with a dilated
ascending aorta, with a known altered hemodynamic profile, were compared with aortic
dissection and subjects with Marfan’s syndrome,
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a condition that predisposes to aortic dissection.
Only quantitative histologic differences were found
between the normal aorta of “aging” and the
abnormal aorta. In this reading, the dissection is
understood as part of a spectrum of lesions that
have as a common denominator the process of
wound repair. Thus, histologic characteristics of
the dissected aorta in this context would represent
the morphological substrate of this process [13].
Morphological studies of aortic dissection
provide another etiology mechanism of thoracic
aortic dissection. These studies have noted that
thelocation of points in the aortic intimal injury
match: (i) the entry of the false lumen, (ii) the
arteries affected by the progression of the dissection through their ostia, (iii) the points of
re-entry into the true lumen, (iv) the extent of
dissection, and (v) rupture points of false light and
multiple re-entries [14].
Poullis et al., using mathematical models to
assess the shape of curvature of the aortic arch in
the ascending aorta, demonstrated that the conformation of curvature is an independent risk factor
in the etiology of type A dissection and aneurysm
of the ascending aorta [15]. There are no morphological studies devoted to studying the association
between type B dissection and morphology of the
aortic arch.
Autopsy studies aiming to describe morphological features of the dissected aorta, due to advances
and improvement in imaging resolution, have been
replaced by studies such as angiotomography [16],
transesophageal echo Doppler [17] and magnetic
resonance imaging (MRI) [18].
Knowing the biomechanical aspects of each
component of the arterial wall is essential for a
better understanding of growth and vascular
remodeling, and for the development of vascular
substitutes (prosthetics, endoprothesis, stents). The
stress in the aortic wall and the structural changes
arising from it are the target of biomechanical
studies of the aorta. The biomechanical analysis of
aortic dissection takes as its premise that changes
related to flow and how this interacts with the wall
of the aorta are the etiology of dissection.
Biomechanical studies from computer models of
the aorta [19] and bovine carotid arteries [20] show
that the variation of stress through the thickness of
the aortic wall is not homogeneous and that stress
is greater in the middle layer. These results could
explain the location of the dissection in the aortic
media. Other biomechanical studies using models
from computed tomography (CT) scans confirm
the control of risk factors traditionally associated
with aortic diseases such as hypertension [21] with
increased blood pressure leading to an increase in
stress in the aortic wall.
Other studies in the aorta of pigs [22,23] and
rats [24] were used to better understand the
biomechanical aspects of the aorta, using
destructive tests. Although rare in human models,
such methods have been employed in some
biomechanical studies of the aorta. The following
tests were performed to determine the strength
ofaortic tissue: uniaxial tension test in the radial
[25], axial and circumferential [26,27] direction,
breaking stress test in circular samples of aorta and
balloon inflation in the intact artery [28]. Only a
few of these techniques have been employed to
investigate the aortic dissection [29]. Sommer et al.
propose a new method for the specific destructive
biomechanical study of aortic dissection, using
segments of infrarenal aorta, a segment where dissection is rare [14], and not affected by atherosclerosis, a risk factor traditionally associated with
aortic dissection [30].
Uniaxial destructive biomechanical tests in
aortic tissue have limitations due to the nature of
the forces acting on the aorta during the cardiac
cycle (radial strain, circumferential and
longitudinal). However, they are easy to understand, are widely used in the field of engineering
material, and allow characterization of the material.
Otherwise the large number of variables makes the
mathematical models and constitutive equations
extremely complex, complicating the interpretation
of results [31].
In a study not yet published in our Biomechanics
Laboratory (Department of Vascular Surgery,
University of São Paulo Medical School), we demonstrated the different behavior between the
thoracic and abdominal aorta in biomechanical
characteristics (Table8.1). A detailed knowledge of
aortic tissue pbtained by analyzing biomechanical,
histologic, and morphological characteristics can
contribute to a better understanding of aortic
dissection and the development and refinement of
possible vascular substitutes.
CHAPTER 8 Acute aortic dissection 77
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Table 8.1 Comparison between the average values of strength, tension and stress needed to break the tissue, maximum
deformation, and thickness of the fragments of the thoracic and abdominal aorta.
Thoracic aorta Abdominal aorta T P P-value
N Media dp N Media dp
Stregth (newtons) 86 6.2746 2.024 59 4.7918 2.0696 4.29 0.000032 0.9807
Tension (newtons/mm) 86 2.0708 0.9316 59 1.4448 0.7360 4.32 0.000029 0.9816
Stress (newtons/mm
Deformation (strain) 86 0.6823 0.3209 59 0.4750 0.2430 4.20 0.000046 0.9768
Thickness (mm) 86 1.6960 0.4824 59 1.4332 0.3571 3.56 0.000495 0.9260
2)
86 1.7731 1.1121 59 1.3584 0.9881 2.31 0.022527 0.6170
While studies help describe the natural history
of aortic dissection, important advances have
occurred in their treatment, especially with the
advent of endovascular surgery. Thus studies with
medium-term follow-up demonstrate that the use
of endoprotheses for the treatment of uncomplicated and complicated diseases of the descending
aorta is safe, less invasive, and low risk when
compared to traditional surgical approach [32–35].
Considering that the fixation of the endoprothesis is based on the graft–aortic wall, with different
aspects of this interaction in early and late implantation, great attention was given to the mechanism
of attachment of the stent, with improving technology of these devices (oversize, self-expanding or
balloon-expandable stents, hooks, free-flow stents)
[36]. The evolution of materials composing the
endografts caused difficulties in understanding the
behavior of a specific device model in the long
term. Issues such as integration between the
prosthesis and the aortic wall, morphological
remodeling of aneurysms, and dissection of the
aorta and endograft migration have always been
highlighted as a limitation of this therapy [37].
Studies of the aortic wall in patients with aortic
dissection have failed to point out the interaction
between the histologic, morphological, and biomechanical aspects in etiology of aortic dissection and
its implications for surgical treatment of this
disease.
Risk factors
Hypertension is present in 70–80% of cases of
aortic dissection, being the most prevalent risk
factor for it (Box8.1) [6,7]. Some aortic diseases
are well-established risk factors: the presence of
Box 8.1 Risk factors for acute
aortic dissection.
Hypertension
t
Smoking, dyslipidemia, cocaine/crack
Connective tissue diseases
t
Marfan’s syndrome
t
Ehlers–Danlos syndrome
Hereditary vascular diseases
t
Bicuspid aortic valve
t
Aortic coarctation
Inflammatory diseases
t
Giant cell arteritis
t
Takayasu arteritis
t
Behçet’s disease
t
Syphilis
Blunt chest trauma
Iatrogenic
t
Diagnostic and therapeutic endovascular
procedures
t
After aortic or heart valves surgery
bicuspid aortic valves associated with aortic artery
root dilation (7–14% of all dissections); coarctation;
aortic annulus ectasia; chromosomal abnormalities
(Turner’s and Noonan’s syndromes); hypoplasia
aortic arch; arteritis; and connective tissue diseases
(Marfan’s and Ehlers–Danlos syndromes). Marfan’s
syndrome is responsible for most cases of aortic
dissection in patients younger than 40 years. In
women younger than 40 years, 50% of aortic
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dissections occur during pregnancy, generally
when the diagnosis of Marfan’s syndrome is
established [2–4,6,9].
Intramural hematoma and penetrating
aortic ulcer
The violation of the tunica intima of the aortic wall
is a common feature between the aortic dissection,
intramural hematoma, and penetrating aortic ulcer.
Moreover, they present a similar clinical presentation
to that of sudden chest pain in hypertensive patients.
Both processes can be a precursor of classic dissection. Severe atherosclerotic changes are common in
patients with these diseases, so that patients with a
penetrating aortic ulcer tend to beolder (mean age
77 years) than those with dissection [1,3].
An intramural hematoma of the thoracic aorta is
characterized by an absence of intimal rupture,
identifiable by radiographic means, and by the
column of coagulated blood between the intima
and media layers of the aortic wall, or variable
length. Generally, they are more segmental that
aortic dissections and do not cause occlusion of
aortic branches. It postulates a rupture of the vasa
vasorum or, more likely, the violation of the intima
by an atherosclerotic ulcer, allowing that blood to
penetrate the aortic wall [1,3,37].
Penetrating ulcers in a plaque of the aorta can
cause intramural hematomas, aortic dissections, or
perforation. Symptomatic atherosclerotic ulcers
are deeper and involve a greater risk of rupture (up
to 40% in some series); the prognosis is worse if
they are located in the ascending aorta. The
combination of an ulcer and intramural hematoma
occurs in 90% of cases in the descending aorta.
Despite the overall poor prognosis, the indication
for surgery in aortic ulcers remains related to the
aortic diameter, or clinical and radiologic signs of
deterioration [1,3,38].
Malperfusion syndromes
Involvement of the branches of the aorta in a
framework of aortic dissection can occur by
different mechanisms and with varying severity,
resulting in ischemia of target organs, named the
malperfusion syndrome. Several studies characterize malperfusion syndromes as a complication
of acute aortic dissection in approximately 25–40%
of cases [8]. While carotid artery involvement is
often associated with stroke, obstruction of the
subclavian artery or arteries in the legs are generally well tolerated. In the IRAD study, mesenteric
ischemia was responsible for 15% of deaths related
to acute aortic dissection [6].
Occlusion of a branch can occur by propagation
of the dissection into a branch artery, causing
thrombosis or stenosis, and characterized as static
obstructions. However, the main mechanism of
interruption of flow in a branch artery in aortic
dissection (80% of cases) is called dynamic obstruction, in which the true lumen is collapsed and
unable to provide adequate volume of blood to the
organs, or the flap of intimal dissection suffers prolapse into the ostium of the branch vessel. Generally,
diagnostic tests and imaging are unable to quantify
this type of obstruction, creating doubt and delaying diagnosis, especially in cases of visceral
ischemia. The diagnosis must be established by the
patient’s clinical presentation, laboratory tests, and
indirect signs such as the presence of a slit true
lumen [8,39].
Clinical findings
The clinical manifestations of acute aortic
dissections are diverse and overlap with a broad
differential diagnosis, requiring a high index
of suspicion to diagnose. The prevalence of
coronary artery disease is 100–200 times more
common then aortic dissection and its incidence in
the emergency room is 0.3% in patients with chest
pain [37,39]. Diagnosis of acute aortic dissections
is missed on initial exam in up 38% of patients [37].
Severe chest pain is the commonest symptom in
acute aortic dissection, and the majority of patients
recall abrupt onset. Pain is described as “sharp,”
“tearing,” or “ripping“. Patients with type B dissection more often experience pain in the back or
abdomen, although there is substantial overlap
[2,40]. The localization and irradiation of pain can
suggest extension of the dissection: anterior chest
pain is associated with dissection of the ascending
aorta; pain radiating to the neck is associated with
dissection of the aortic arc; and pain to the shoulders or lumbar region relates to dissection of the
descending aorta [2,40].
Syncope can complicate the clinical presentation of
aortic dissection in 5–13% of cases, often indicating
CHAPTER 8 Acute aortic dissection 79
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the development of complications such as cardiac
tamponade or obstruction of cerebral vessels [6].
Hypertension is present in the initial physical
examination in 70% of patients with type B
dissection and in 25–35% of patients with type A,
being refractory to the initial clinical therapy in
more than 64% of cases [6].
A pulse deficit occurs in 30–50% of patients with
involvement of the aortic arc, thoraco-abdominal
segment, or both. The innominate artery is
involved in 14.5% of patients, the left carotid artery
in 6%, the left subclavian artery in 14.5%, and a
femoral artery in 13% [6].
Symptoms of a malperfusion syndrome for the
occlusion of branches of the aorta can be prominent
in acute aortic dissection, but may also disguise other
diagnoses: chest pain with myocardial ischemia
(occlusion of coronary arteries); focal neurologic
deficit or syncope (for involvement of the supra-aortic
trunks); ischemia of a superior extremity; paraplegia
(for occlusion of the spinal arteries); and abdominal
pain (mesenteric ischemia) [6].
Peripheral nerve compression by the hematoma
can rarely occur, causing Horner’s syndrome, and/
or dysphonia, by paresis of the left vocal cord
related to compression of the recurrent laryngeal
nerve.
The presence of sudden-onset chest pain,
pulse deficits and mediastinal enlargement in an
X-ray increases by 66 times the likelihood ratio
of acute aortic dissection; however, this diagnostic triad is found in only 27% of patients.
Given the polymorphism of symptoms, some
population studies show that in only 28.8% of
cases of aortic dissection was the diagnosis
suspected on initial evaluation. Thus, a high
index of suspicion and rational use of available
diagnostic tests are essential for early diagnosis
of aortic dissection [6].
Diagnostic tests and imaging
studies
The initial evaluation of a patient with acute chest
pain involves performing an electrocardiogram,
which may show acute ischemic changes in about
20% of dissections of the ascending aorta.
Laboratory tests are essential in the evaluation of
malperfusion syndromes and associated organ
dysfunction (myocardial ischemia, renal, mesenteric
and limbs) and the blood loss associated with
serious cases [6].
The diagnosis is confirmed by performing a CT
scan with contrast or transesophageal echocardiography, depending on the ease of completion of
each examination in the emergency room.
Chest X-ray
A chest X-ray can be readily obtained, and can to
show some signs of acute aortic dissection: 60–90%
of cases have an increased aortic silhouette [6]. The
main findings are: mediastinal widening; a sign of
double aortic arch; diffuse enlargement of the aorta
with little definition and irregularity of contour;
medial displacement of the calcified aortic ring of
>10 mm; deviation of the trachea to the right;
pleural effusion; increased cardiac area; and
opacification of the left lung apex. However, these
modifications are non-specific and no chest
radiograph abnormality was noted in 10–15% of
patients.
Computed tomography
6
Used for three decades, this is the most commonly used imaging procedure for the detection
and evaluation of aortic dissection, with a sensitivity of 83–95% and specificity of 87–100%, and
showing some limitation in the evaluation of
ascending aorta. With helical CT, the study can
be done in less time, with high accuracy and a
low amount of iodine contrast. It identifies the
two lumens and the flap of intimal dissection,
and, in 90% of cases, the false lumen is larger
than the true. CT can determine the initial and
final sites, visceral branches compromised, and
possible points of re-entry of the false to true
lumen. The CT scan also shows possible points
of rupture and contrast extravasation to the
pleura, or to the hollow viscera (esophagus, duodenum). The orientation of the concavity of the
flap dissection toward the false lumen or the
presence of a collapsed true lumen suggests low
pressure in the true lumen and may correlate to
the malperfusion syndrome of the kidneys, gut,
or lower limb [16,41]. CT is less dependent on
operator skill, and provides useful images
about anatomic correlates to the surgical and
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endovascular procedures, obtaining reliable
information for measurement and analysis.
Transesophageal echocardiography
Transesophageal echocardiography (TEE) has a
sensitivity of 98% and specificity of 63–96%, and
can be performed at the bedside or in an unstable
patient with a suspected diagnosis. TEE has
limitations in assessing the distal part of the
ascending aorta and aortic arch because the
trachea and left bronchus interfere in visualization
of the infradiaphragmatic extent of dissection.
Despite these limitations, it is extremely useful in
assessing the ascending aorta, complementing the
information provided by CT for planning surgical
treatment [17].
Nuclear magnetic resonance
Although accurate (sensitivity and specificity
95–100%), nuclear magnetic resonance has little
application compared with CT scans because of the
longer time required for the exam and the difficulty
of monitoring a critically ill patient during it [18].
Aortography
Aortography has gradually been replaced by
helical imaging tests. With the need for rapid
diagnosis, its limitation is clearly that of being an
invasive procedure, time consuming, and expensive. It has no advantages in terms of sensitivity
and specificity compared with CT and TEE.
Currently, it is not performed before surgical
repair of proximal dissections, although it can be
performed in treatment of distal dissections as
part of the endovascular repair.
Treatment
Successful treatment of aortic dissection depends
on rapid diagnosis and correct assessment of the
extent of the pathologic process. Clinical treatment
seeks to reduce blood pressure, aiming to stabilize
the extent of dissection and decrease the risk of
rupture [42–44].
Clinical management
t
Monitoring in the intensive care unit, oxygen,
intravenous access, and blood sampling. Quickly
evaluate the possibility of cardiac tamponade,
avoiding pericardial puncture in favor of definitive treatment [42].
t
Beta-blockers: the goal is to let the heart rate reduce
to <60 beats/min, if tolerated. Prescribe metoprolol
(5 mg) IV in 3–5 minutes, in case of dissection; this
is the maximum dose. The reduction in heart rate
and inotropism are essential in the management of
acute dissection (if there is contraindication to
beta-blockers, the patient may be prescribed IV
verapamil or diltiazem) [42].
t
Reduction in blood pressure: reduction to the
lowest tolerated by the patient. If possible, leave
the systolic blood pressure at 100–110 mmHg;
for that, prescribe sodium nitroprusside starting
at 0.3–0.5 mg/kg/min, with increases of 0.5
mg/kg/min every 3–5 minutes. Vasodilators
should always be used in combination with
beta-blockers and never alone, because of the
risk of increasing the stress on the aortic wall
with an increased ejection fraction [42].
t
Morphine: give a dose of 2–4 mg IV to achieve
adequate analgesia [42].
Type A dissection
The risk of rupture and complications related to
aortic insufficiency, cardiac tamponade, or
obstruction of the coronary ostia are associated with
a hospital mortality of 60% with medical therapy,
thus justifying immediate surgical treatment in all
cases of type A aortic dissections [2,6]. In patients
with type A dissection complicated by malperfusion,
clinical treatment followed by endovascular fenestration can reduce risks and create the conditions
needed for definitive surgical intervention [45].
Definitive treatment consists of resection of the
dissected segment with interposition of a Dacron
graft. Reimplantation of the coronary ostia or
correction of aortic valve lesions may be needed. The
mortality rate is 10–35% depending on comorbidities
and associated conditions; the neurologic status at
presentation is the main factor of poor prognosis [6].
High rates of surgical mortality related to visceral
malperfusion (50–80% in patients with renal
ischemia and 87% in those with mesenteric
ischemia) in patients undergoing replacement of
the ascending aorta, make some authors propose
an open or endovascular fenestration of the distal
aorta before definitive surgical repair of the
ascending aorta. This increases the survival rate of
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