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IV. Dissection
Table 22.1. Etiology of iatrogenic aortic dissection in the Inter-
national Registry of Aortic Dissection
Cause Type A Type B
Cardiac surgery 18 (69%) 1 (12%)
Coronarography/
intervention
Renal angioplasty 1 (4%) ±
Complication Iatrogenic (%) Spontaneous (%)
Myocardial ischemia 36 * 5
Myocardial infarction 15* 3
Limb ischemia 14 8
Mortality (30 days) 35 24
* p £ 0.001
7 (27%) 7 (87%)
dromes following invasive vascular procedures or aortic
surgery (Table 22.1).
Finally, pregnancy-related dissection although a dramatic scenario is a rare event as long as the patient is
not affected by any form of connective tissue disease.
The putative association of pregnancy in otherwise
healthy women and acute dissection may largely be an
artifact of selective reporting. Pregnancy is a common
condition and may coincidentally occur only with concomitant existence of other risk factors such as longstanding or pregnancy-associated hypertension, or Marfan's syndrome. Preliminary data from the International
Registry of Aortic Dissection (IRAD) show that pregnancy in Marfan's syndrome is not associated with aortic tears, unless root size exceeds 40 mm.
22.2.1 Marfan's Syndrome
Among hereditary diseases, Marfan's syndrome is the
most prevalent connective tissue disorder with an estimated incidence of 1/7,000 and an autosomal dominant
inheritance with variable penetrance. More than 150
mutations on the fibrillin-1 (FBN-1) gene have been
identified encoding for a defective fibrillin in the extracellular matrix, which may affect the ocular, cardiovascular, skeletal and pulmonary systems, as well as skin
and dura mater. The diagnosis of Marfan's syndrome is
currently based on revised clinical criteria of the Gent
nosology [15]. The Gent criteria pay particular attention to genetic information like Marfan's syndrome in
kindred of an unequivocally affected individual. Moreover, both skeletal and cardiovascular features are major
(e.g., diagnostic) criteria if four or more of eight typical
manifestations are present. Considering, however, borderline manifestations such as the MASS phenotype
(mitral valve, aorta, skeleton, and skin), or subtle phenotypic features (ªforme frusteº), the molecular analysis
of suspected Marfan's syndrome and the delineation of
criteria for differentiating other inherited conditions
(genotypes) from a Marfan phenotype are attracting interest [16±20]. The clinical variety of Marfan's syn-
drome is only partially explained by the number of mutations on the FBN-1 gene. Genetic heterogeneity and
the involvement of a second gene (Marfan syndrome
type 2, MFS2) may further add to the broad spectrum
of symptoms [21].
A common denominator of all phenotypic forms of
aortic wall disease is the dedifferentiation of vascular
smooth muscle cells not only with classic aneurysm formation, but also from enhanced elastolysis of aortic
wall components [22], as shown in a fibrillin-q-deficient
animal model [23]. Moreover, enhanced expression of
metalloproteinases in vascular smooth muscle cells of
the aorta of Marfan patients may promote both fragmentation of medial elastic layers and elastolysis, thus
initiating an activated phenotype of smooth muscle
cells [24]. In parallel, expression of peroxisome proliferator-activated receptor-c (PPAR-c) is upregulated in
smooth muscle cells of the aorta of Marfan patients and
with cystic medial degeneration, and correlates with
clinical severity, while vascular smooth muscle cell
apoptosis is likely to be related to progression of aortic
dilatation. Thus, PPAR-c expression might reflect the
pathogenesis of cystic medial degeneration and disease
progression in the aorta of Marfan and non-Marfan patients without any vascular inflammatory response [25].
22.2.2 Ehlers-Danlos Syndrome
Ehlers-Danlos syndrome (EDS) is a heterogeneous
group of hereditable connective tissue disorders characterized by articular hypermobility, skin hyperextensibility and tissue fragility. Eleven types of EDS have been
characterized; the true prevalence of EDS is unknown.
An aggregate incidence of 1/5,000 births is often cited
with no racial or ethnic predisposition. Aortic involvement is seen primarily in autosomal dominant EDS
type IV [26].
22.2.3 Annuloaortic Ectasia
and Familial Aortic Dissection
More than five mutations in the FBN-1 gene have now
been identified in patients presenting with either sporadic or familial forms of thoracic aortic aneurysms
and dissection [27, 28]. Histological examination of the
aortic wall reveals elastolysis or loss of elastic fibers,
deposits of mucopolysaccharide-like materials and cystic medial degeneration similar to Marfan's syndrome.
However, no abnormalities of types I and III collagen or
any specific fibrillopathy were found in fibroblast cultures.
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22.2.4 Abdominal Aortic Aneurysms and Dissection
Careful examination of family pedigrees often reveals
involvement of both the abdominal aorta and disease in
proximal aortic segments, or other features suggestive
of Marfan's or EDS syndrome. Differentiation of familial
forms of abdominal aortic aneurysm/dissection from
thoracic aortic aneurysms/dissection with an abdominal
component is difficult considering that only one mutation within the COL3A1 gene is known [29]. In fact,
many candidate genes encoding for collagens, fibrillins,
fibrullins, microfibril-associated glycoproteins, matrix
metalloproteinases and their inhibitors have been investigated, but no mutation has been identified. Similar
pathogenetic processes have been described with coarctation [1] and with the bicuspid aortic valve architecture [2].
22.3 Definition and Classification
The Stanford classification of aortic dissection distinguishes between type A and type B (Fig. 22.1) [29, 30].
Type A involves the ascending aorta; a type B dissection
does not involve the ascending aorta. The De Bakey
classification subdivides the dissection process into
type I dissection involving the entire aorta, type II dissection 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 community [31, 32], although the arch region deserves integration into a modern classification system. Recent observations highlight the importance of precursors of
typical aortic dissection such as intramural hematoma,
Fig. 22.1. The commonest classification systems
of thoracic aortic dissection
Fig. 22.2. Schematic representation of aortic dissec-
tion, penetrating ulcer and intramural hematoma
(IMH)
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IV. Dissection
penetrating aortic ulcers or a localized intimal tears as
variants of a wall-dissecting process [33, 34] (Fig. 22.2).
22.3.1 Classic Aortic Dissection
Acute aortic dissection is characterized by the rapid development of an intimal flap separating the true and
the false lumen [35, 36]. In the majority of cases (approximately 90%) intimal tears are identified as sites of
communication between the true and the false lumen.
The dissection can spread in an antegrade or retrograde
fashion, involving side branches and causing complications such as malperfusion syndrome by dynamic or
static side branch obstruction, tamponade or aortic insufficiency. The arbitrary classification of acute, subacute or chronic dissection appears helpful neither for
didactic nor for differential therapeutic considerations,
but may rather 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 2 weeks after its inception,
although false lumen expansion is likely to develop over
time. Several clinical features may be used to roughly
estimate late risk, including evidence of persistent communication and patent false channel [32, 35, 36].
22.3.2 Intramural Hematoma
Aortic intramural hematoma is considered a precursor
of classic dissection, and originates from ruptured vasa
vasorum in medial wall layers, eventually provoking a
secondary communication with the aortic lumen [34,
37, 38]; this process may be initiated by an ªaortic wall
infarction.º Similar to classic dissection, intramural hematoma may extend along the aorta, may progress, regress or reabsorb. The prevalence of intramural hemorrhage is in the range 10±30% [38±40]. Intramural hematoma can lead to acute aortic dissection in 21±47%
of patients or to regression in about 10%. Involvement
of the ascending aorta is considered an indication for
expeditious surgery owing to the inherent risk of rup-
ture, tamponade or compression of coronary ostia. Distal intramural hematoma may warrant watchful waiting
and potentially stent-graft placement [41±43] (Fig. 22.3).
Studies in Asian patients from Japan and Korea have argued that wall hematoma reflects a more benign condition, in which aggressive medical therapy and serial
imaging allow a watchful waiting strategy [41, 42]. The
reasons for this disparity may relate either to a different gene pool of Asian and white patients or to semantic differences. However, at present the cardiological
and surgical communities have generally concluded that
acute intramural hematoma involving the ascending
aorta should be managed surgically similar to type A
dissection.
Take home message for therapy: intramural hematoma
1. Surgery is advocated in patients with acute intramu-
ral hematoma involving the ascending aorta
2. Aggressive medical therapy is advocated in patients
with acute intramural hematoma involving the des-
cending aorta and regular follow-up imaging; in case
of progression to dissection endovascular therapy
may be considered.
22.3.3 Plaque Rupture/Ulceration
Ulceration of atherosclerotic aortic plaques can lead to
aortic dissection or perforation [44±46]. Noninvasive
imaging of aortic ulceration has been improved by tomographic scanning and has shed light on pathophysiology and etiology. Aortic ulcers occur predominantly
in the descending thoracic and abdominal aorta, penetrate intimal borders and appear in nipplelike projection with an adjacent hematoma [46, 47]; symptomatic
ulcers and/or with signs of deep erosion are more likely
to rupture than others.
22.4 Clinical Symptoms
The challenge in managing acute aortic syndrome ±
and especially dissection ± is appropriate clinical suspicion and action in pursuing diagnosis and therapy [48,
Fig. 22.3. Evolutions of acute IMH of the descending
aorta (left) to growing local dissection and formation of an aneurysm on spiral contrast-enhanced
computed tomography scans within 4 months; reconstruction of the dissected aorta and exclusion of aneurysm after interventional stent-graft placement. F/
U follow-up
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Table 22.2. Life-threatening causes of acute chest pain
Acute coronary syndromes
Aortic dissection
Pulmonary embolus
Tension pneumothorax
Esophageal rupture
incompetence or loss of blood and imminent exsanguinations [6, 9, 11, 49].
Consequently, the differential diagnosis of acute aortic dissection should always be considered in patients
presenting with chest pain, back pain, unexplained syncope, abdominal pain, stroke, acute onset of congestive
heart failure, pulse differentials or malperfusion syndrome of extremities or viscera (Table 22.2). In the
Fig. 22.4. Kaplan±Meier survival curves from patients with and
without pulse deficits; log-rank for curves of patients with one,
two or three or more pulse deficits differ from patients with
no pulse deficits (P = 0.03 and 0.004)
present absence of useful specific biomarkers for aortic
dissection, interpretation of positive cardiac markers
may be even more complex in a scenario of the aortic
dissection compromising coronary ostia.
227
49]. Typical features of dissection are the acute onset of
chest and/or back pain of blunt, radiating and migrating nature. Chronic hypertension is common if obvious
signs of connective tissue disorders are absent. Clinical
manifestations of acute aortic dissection are often explained by specific malperfusion syndrome from dissection-related side branch obstruction. Every fifth patient
with acute aortic dissection may present with syncope
from tamponade, severe hypotension or carotid obstruction [6±8, 50, 51]. Emerging heart failure is usually
related to severe aortic regurgitation or coronary obstruction. Cerebrovascular manifestations, limb ischemia or pulse deficits are caused by involvement of a
side branch orifice in the dissection or obliteration of
the true lumen by an expanding false lumen [9, 52].
Paraplegia may emerge if too many pairs of intercostal
arteries are separated from the aortic lumen.
Recurrent abdominal pain, elevation of acute-phase
proteins and increase of lactate dehydrogenase are indicators of involvement of either the celiac trunk (observed in approximately 8% of patients) or the superior
mesenteric artery (in 8±13% of patients). Involvement
of renal arteries may result in oliguria or anuria and
propagation of dissection is heralded by repetitive bouts
of pain, or a deteriorating clinical picture [16, 17].
Pulse deficits on physical examination occur in approximately 20% of patients and are important clues
heralding complications and bad outcome (Fig. 22.4). A
diastolic murmur indicative of aortic regurgitation is
seen in approximately 50% of patients with proximal
dissection. Signs of pericardial effusion, jugular venous
distension or a paradoxical pulse should confirm the diagnosis. Shock may be a presenting sign, resulting from
tamponade, coronary compression, acute aortic valve
22.5 Diagnostic Procedures
Considering the differential diagnosis of acute aortic
dissection, its etiology and the wide spectrum of symptoms, it is not surprising that 70% of ECG findings
were pathological [11]. ECG findings are nonspecific,
with misleading normal results in type B dissection or
acute ischemic changes with involvement of the coronary arteries in type A dissection.
Moreover, a routine chest X-ray is abnormal in 56%
of cases of suspected aortic dissection. Transthoracic
echocardiography (TTE) has a sensitivity of 60% and a
specificity of 83% for type A dissection and also shows
aortic regurgitation, pleural effusion and pericardial effusion/tamponade. Transesophageal echocardiography
(TEE) with color Doppler interrogation overcomes the
limitations of TTE with a sensitivity of 94±100% for
identifying an intimal flap and 77±87% for identifying
the site of entry; specificity ranges from 77±97% [7, 11
53].
Multislice computed tomography (MCT) scanning is
available in many hospitals and is usually offered on an
emergency basis [54]. MCT provides complete anatomical information of the aorta, including branch vessel involvement, and enables visualization of the ostium and
the proximal part of both coronary arteries. CT scanning has a sensitivity of 83±100% and a specificity of
90±100% for aortic dissection [6, 7, 51]. In randomized
trials, cardiac magnetic resonance was more precise
than TEE and CT and had a precision of nearly 100%
for aortic dissection. For identifying the site of entry,
sensitivity was 85% and specificity 100% [8]. Aortography, an invasive procedure, is no longer required for diagnosing aortic dissection. Coronary angiography adds
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IV. Dissection
little to the decision-making process and should generally be avoided in type A dissection [7].
22.6 Medical Management
Acute aortic dissection of the ascending aorta is highly
lethal, with a mortality rate of 1±2% per hour early
after symptom onset [6, 55]. Acute type A dissection is
a surgical emergency. Medical management alone is associated with a mortality rate of nearly 20% by 24 h
after presentation, 30% by 48 h, 40% by 1 week and
50% by 1 month. Even with surgical repair, the mortality rates are 10% by 24 h, 13% by 7 days and nearly
20% by 30 days, as recently documented in the largest
registry of aortic dissection, although randomized data
are not available [9, 11, 56].
Acute aortic dissection affecting the descending aorta is less lethal than type A dissection. Patients with uncomplicated type B dissection have a 30-day mortality
rate of 10% [6]. Conversely, those who develop an ischemic leg, renal failure, visceral ischemia or contained
rupture often require urgent aortic repair; their mortality rate is 20% by day 2 and 25% by day 30. Not surprisingly, advanced age, rupture, shock and malperfusion are the most important independent predictors of
early mortality [7, 50, 57].
Patients with suspected acute aortic dissection
should be admitted to an intensive care or monitoring
unit and undergo diagnostic evaluation immediately.
Pain and blood pressure control to a target systolic
pressure of 110 mmHg can be achieved using morphine
Table 22.3. Management of patients with suspected aortic dis-
section
Recommendation
a
Class I, II a,
II b, III
sulfate and intravenous beta-blockers (metoprolol, esmolol or labetalol) or in combination with vasodilating
drugs such as sodium nitroprusside or angiotensin-converting enzyme inhibitors. Intravenous verapamil or diltiazem may also be used, if beta-blockers are contraindicated. Monotherapy with beta-blocking agents may be
adequate to control mild hypertension, and in concert
with sodium nitroprusside at an initial dosage of
0.3 lg/kg/min, is often effective in a severe hypertensive
state (Table 22.3). In normotensive or hypotensive patients, careful evaluation for loss of blood, pericardial
effusion or heart failure (by cardiac ultrasound) is mandatory before administering fluids. Patients with profound hemodynamic instability often require intubation,
mechanical ventilation and urgent bedside TEE or rapid
CT for confirmatory imaging. In rare cases, the external
ultrasound diagnosis of cardiac tamponade may justify
immediate sternotomy and surgical access to the ascending aorta to prevent circulatory arrest, shock and
ischemic brain damage. Percutaneous pericardiocentesis
as a temporizing step has often failed, and can accelerate bleeding and shock [58].
22.7 Surgical Management
The aim of surgical therapy in proximal type A (types I
and II) aortic dissection is prevention of rupture or development of pericardial effusion which may lead to
cardiac tamponade and death. Similarly, sudden onset
of aortic regurgitation and coronary flow obstruction
requires urgent surgical intervention with the aim to resect the region of intimal tear in dissection limited to
the ascending aorta and replacement by a composite or
interposition graft (if the aortic valves are intact or resuspendable). When the dissection extends to the aortic
arch or the descending aorta, resection of the entire in-
ECG: documentation of ischemia I
Heart rate and blood pressure monitoring I
Pain relief (morphine sulfate) I
Reduction of systolic blood pressure using
beta-blockers (intravenous metoprolol,
esmolol or labetolol)
In patients with severe hypertension despite
beta-blockers, additional vasodilator
(intravenous sodium nitroprusside to titrate
blood pressure to 100±120 mmHg)
In patients with obstructive pulmonary
disease, blood pressure lowering with calcium
channel blockers
Imaging in patients with ECG signs of
ischemia before thrombolysis if aortic
pathology is suspected
Chest X-ray III
Diagnostic imaging (noninvasive) I
a
All recommendations are level of evidence C
Table 22.4. Surgical therapy of acute type A (types I and II)
aortic dissection
I
I
II
II
Recommendation
Emergency surgery to avoid tamponade/aortic
rupture
Valve-preserving surgery ± tubular graft if
normal size aortic root and no pathological
changes of valve cusps
Replacement of aorta and aortic valve
(composite graft) if ecstatic proximal aorta
and/or pathological changes of valve/aortic wall
Valve-sparing operations with aortic root
remodeling for abnormal valves
Valve preservation and aortic root remodeling
in Marfan patients
a
All recommendations are level of evidence C
a
Class I, II a,
II b, III
I
I
I
IIa
IIa
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229
timal flap may not be possible or the patient may require partial or total arch replacement [59]. A recent report highlights the problem of either resecting or leaving unrecognized intimal tears in the arch or descending thoracic aorta, which is seen in 20±30% of patients
and predisposes to later distal aortic reoperation [60].
Considering an operative mortality between 15 and
35% even in centers of excellence, adjunctive measures
such as profound hypothermic circulatory arrest and
selective retrograde perfusion of head vessels have been
used in the surgical management of arch repair or an
open distal anastomosis [61]. Whereas the later recently
gained growing acceptance for improved outcome with
a 5-year survival of 73 Ô 6%, profound hypothermic circulatory arrest failed to improve early complications,
survival and distal reoperation rates in patients with
acute type A dissection; 30-day, 1-year and 5-year survival estimates were 81 Ô 2, 74 Ô 3 and 63 Ô 3%, and thus
were not different from those of other techniques using
propensity-matched retrospective analysis [4]. The key
to success is rapid surgery prior to any hemodynamic
instability or deterioration (Table 22.4).
Once the patient is on extracorporal circulation and
preferably antegrade cerebral perfusion, which is usually established after cannulation of one femoral artery
and the right atrium, the aorta is mobilized to visualize
the innominate artery and the aortic root. If the valve
leaflets are intact, aortic valve reconstruction using David's or Yacoub's resuspension technique is gaining
growing acceptance over valve replacement [62, 63].
The approach to an acute type A (types I and II) dissection (Fig. 22.1) in a previously ectatic proximal aorta
must be different. In such instances, mostly in patients
with Marfan's syndrome, a composite graft (aortic tube
graft with integrated valve) is preferred with coronary
reimplantation [64±66]. Surgical allografts and xenografts are experimental since late postoperative degeneration may require reoperation on the aortic root.
Valve-sparing operations are delicate endeavors in an
emergency and require great surgical competence in
centers with expertise in elective cases. If the dissection
compromises the left or the right ostium without disrupting the coronary vessel, the ostium can usually be
preserved. An ostium completely surrounded by dissected aortic wall may be excised in button form. The
dissected layers around the ostium are conjoined using
tissue adhesive and over-and-over suturing before the
anastomosis to a tube graft is accomplished. Bypass
grafting of coronary arteries using saphenous vein segments is limited to those instances where a small torn
ostium precludes reconstruction.
22.7.1 The Aortic Arch in Acute Type A (Types I and II)
Dissection
Treatment of the acutely dissected aortic arch remains
an unresolved issue. At present there is growing consensus that any dissected arch should be explored during
hypothermic circulatory arrest. In the absence of an
arch tear, an open distal anastomosis of the graft and
the conjoined aortic wall layers at the junction of the
ascending and arch portions is justified. Arch tears occur in up to 30% of patients with acute dissection [67,
68]. Whenever extensive tears are found, which continue beyond the junction of the transverse and descending aortic segments, or with an acute dissection of
a previously aneurysmatic arch, subtotal or total arch
replacement may be required with reconnection of
some or all supraaortic vessels to the graft during hypothermic circulatory arrest and antegrade head perfusion [69].
In dissecting and nondissecting aneurysms extending to the downstream aorta an elephant trunk extension of the arch graft is an option described by Borst et
al. [70]. This technique greatly facilitates later procedures on the downstream aorta. Instead of performing
a conventional anastomosis between the end of the graft
and the descending aorta, the graft is allowed to float
freely in the aortic lumen. In a later procedure, the elephant trunk section of the graft may either be connected surgically to the distal descending aorta directly
Fig. 22.5. a Reconstructed 3D MRI after percutaneous use of a
customized stent-graft to connect a surgically inserted elephant
trunk with the upper abdominal aorta in order to exclude an
aneurysm that had formed at the distal end of the elephant
b); after placement of the customized stent-graft, the
trunk (
thoracic aneurysm was successfully excluded from circulation
with thrombus formation around the stent-graft protheses (
An aneurysm, SG stent-graft
c).
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IV. Dissection
or be extended with another tubular prosthesis, or it
may be connected interventionally by a customized endovascular stent-graft which may then be anastomosed
at any desired downstream level of the aorta (Fig. 22.5).
In summary, surgery is advised without delay in
acute type A (types I and II) dissection both to prevent
aortic rupture, pericardial tamponade and death and to
relieve aortic regurgitation.
Take home message for treatment of type A dissection
1. Surgery provides definitive treatment for patients
with type A acute aortic dissection
2. The aim of surgery is to prevent aortic rupture, peri-
cardial tamponade, and to relieve aortic regurgita-
tion
3. In general, implantation of a composite graft in the
ascending aorta with or without reimplantation of
coronary arteries is performed
4. A large variety of surgical approaches exist.
22.7.2 Surgery in Type B (Type III) Aortic Dissection
In the current era, indications for operative treatment
in patients with acute type B (type III) dissection are
limited to the prevention or relief of life-threatening
complications such as intractable pain, a rapidly expanding aortic diameter or signs of imminent aortic
rupture and can also be managed by interventional
stent-graft placement. The onset of complications such
as malperfusion of vital aortic side branches warrants
interventional therapy by stent-grafting to improve distal true lumen flow or in rare instances catheter-guided
fenestration of an occlusive lamella. When this
approach does not lead to prompt relief of symptoms,
surgical intervention may still be required. At present
uncomplicated type B (type III) aortic dissections are
usually treated conservatively, since surgical repair has
no proven superiority over medical or interventional
treatment in stable patients. In complicated cases the
concept of interventional stent-graft placement is currently being explored [71±73].
22.7.3 Interventional Endovascular Stent-Graft
Treatment
Conventional treatment of Stanford type A (De Bakey
types I and II) dissection consists of surgical reconstruction of the ascending aorta with complete or partial resection of the dissected aortic segment; endovascular strategies have no clinical application except to relieve critical malperfusion prior to surgery of the ascending aorta by distal fenestration in cases of thoracoabdominal extension (De Bakey type I) and peripheral ischemic complications. Endovascular stent-graft
placement was recently introduced to treat type B dissection, however, it has potential to reconstruct the aorta by sealing one or multiple proximal entry tears with
a Dacron-covered scaffold, thus initiating thrombosis of
the false lumen [71±74]. Reconstruction of a collapsed
true lumen might result in reestablishment of side
branch flow (Fig. 22.6). Most scenarios of malperfusion
syndrome are amenable to endovascular management
considering that surgical mortality rates in patients
with acute peripheral vascular ischemic complications
are similar to those with mesenteric ischemia, and
reach 89% in-hospital mortality [75, 76].
Fig. 22.6. Malperfusion of the
distal aorta by occlusive type B
dissection. Stent-graft placement in the true lumen of the
proximal descending aorta reestablished flow to the abdomen and legs
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The interventional management of Stanford type B
(De Bakey type III) dissection and the use of stentgrafts evolved to avoid of the risk of paraplegia from
spinal artery occlusion as seen in up to 18% of patients
after open surgery. In the near future combined surgical
and interventional procedures even for proximal dissection are likely to evolve [77, 78].
22.7.4 Indications for Stent-Graft Placement
There appears to be a role for interventional concepts
in the treatment of static or dynamic obstruction of
aortic branch arteries; static obstruction of a branch
can be overcome by placing endovascular stents in the
ostium of the compromised side branch, and dynamic
obstruction may benefit from stents in the aortic true
lumen. In classic aortic dissection, successful fenestration leaves false lumen pressure unchanged. Sometimes
bare stents deployed from the true lumen into side
branches are useful to buttress the flap in a stable position [79]. Conversely, fenestration may increase the
long-term risk of aortic rupture because a large reentry
tear promotes flow in the false lumen and provides the
basis for aneurysmal expansion of the false lumen;
moreover, there is risk of peripheral embolism from a
perfused, but partially thrombosed false lumen.
The most effective method to exclude an enlarging
and aneurysmal dilated false lumen is the sealing of
proximal entry tears with a customized stent-graft; the
absence of a distal reentry tear is desirable for optimal
results but is not a prerequisite. Adjunctive treatment
by fenestration and/or ostial bare stents may help establish flow to compromised aortic branches. Compression
of the true aortic lumen cranial to the main abdominal
branches with distal malperfusion (so called pseudocoarctation) may also be corrected by stent-grafts that
enlarge the compressed true lumen and improve distal
aortic blood flow [71±73, 76]. Depressurization and
Table 22.5. Interventional therapy in aortic dissection
Recommendation
Stenting of obstructed branch origin for
static obstruction of branch artery
Balloon fenestration of dissecting membrane
plus stenting of aortic true lumen for dynamic
obstruction
Stenting to keep fenestration open II a
Fenestration to provide reentry tear for
dead-end false lumen
Stenting of true lumen
+ to seal entry (covered stent) II b
+ enlarge compressed true lumen IIa
a
All recommendations are level of evidence C
a
Class I, II a,
II b, III
IIa
IIa
IIa
shrinking of the false lumen is the most beneficial result to be gained, ideally followed by complete thrombosis of the false lumen and remodeling of the entire
dissected aorta, and in rare occasions even in retrograde type A dissection. Similar to previously accepted
indications for surgical intervention in type B dissection, scenarios such as intractable pain with descending
dissection, rapidly expanding false lumen diameter and
extraaortic blood collection as a sign of imminent rupture or distal malperfusion syndrome are accepted indications for emergent stent-graft placement [73, 79±81].
Moreover, late onset of complications such as malperfusion of vital aortic side branches may justify endovascular stent-grafting as a first option (Table 22.5).
22.7.5 Interventional Therapy in an Elective Setting
With both bare stents in side branches and sometimes
fenestrating maneuvers compromised flow can be restored in more than 90% (range, 92±100%) of vessels
obstructed from aortic dissection. The average 30-day
mortality rate is 10% (range, 0±25%) and additional
surgical revascularization is rarely needed. Most patients remain asymptomatic over a mean follow-up time
of about 1 year. Fatalities related to the interventional
procedure may occur as a result of irreversible ischemic
complications, progression of the dissection or complications of additional reconstructive surgical procedures
on the thoracic aorta. Potential problems may arise
from unpredictable hemodynamic alterations in the true
and the false lumen after fenestration and side branch
stenting. These alterations can result in loss of previously well-perfused arteries or initially salvaged side
branches.
Recent reports suggest that percutaneous stent-graft
placement in the dissected aorta is safer and produces
better results than surgery for type B dissection [72,
73]. Paraplegia may occur after use of multiple stentgrafts but still appears to be a rare phenomenon, especially with a stented segment of less than 16 cm. The results of short-term follow-up are an excellent 1-year
survival rate of more than 90%; tears can be readapted
and aortic diameters generally decrease with complete
thrombosis of the false lumen. This suggests that stent
placement may facilitate healing of the dissection,
sometimes of the entire aorta, including abdominal segments (Fig. 22.7). However, late reperfusion of the false
lumen has been observed occasionally, underlining the
need for stringent follow-up imaging.
232
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IV. Dissection
Fig. 22.7. Acute type B aortic dissection in a
44-year-old man; note the communications
between the true and the false lumen at the
thoracic and abdominal level. After stentgraft placement across the proximal thoracic entry, the entire aorta including the abdominal segment is reconstructed with
time, with complete ªhealingº of the dissected aortic wall and closure of distal
communication
22.7.6 Interventional Stent-Graft Therapy
as an Emergency
The concept of emergent stent-graft placement for urgent endovascular aortic repair of dissection is attractive, and a growing number of acute type B aortic dissections are subjected to endovascular repair with little
evidence of periprocedural morbidity with the result of
aborted malperfusion or sealed leakage, and eventually
reconstruction of the dissected aorta; stent-graft placement in complicated distal aortic dissection is an
emerging concept not associated with excessive peripheral or neurological complications in experienced hands
[80±82] and yields better short-term and midterm outcome than surgical or medical treatment in high risk
groups of type B dissection.
In conclusion, current advances with stent-graft thoracic intervention must be viewed as exciting new developments that offer hope to many patients with type B
dissection. Technical strategies and devices continue to
evolve and it is likely that these techniques will soon
become first-line therapy for most patients presenting
with anatomically suitable thoracic and thoraco-abdominal aortic lesions.
22.7.7 Role of Endovascular Therapy
The exact role of percutaneous fenestration and stent
placement in aortic dissection is still evolving. Patients
with acute aortic dissection may have life-threatening
complications manifested by end-organ ischemia. The
mortality rate of patients with renal ischemia is 50±70%
and as high as 87% in patients with mesenteric ischemia. Although the surgical success rate at reversing peripheral pulse deficits is high, the surgical in-hospital
mortality rates in the setting of end-organ ischemia re-
main as high as 89%. As such, percutaneous management of this complication has emerged as a viable therapy before or after definitive surgical management if
needed.
In 384 patients with acute type B aortic dissections
in the IRAD registry, 46 (12%) were managed with endovascular stent-grafting, which was similar to the
number of patients treated with surgery (56, 15%) [11].
Only three (6.5%) died during the initial hospitalization. Nienaber et al. [72] compared the outcome of
stent-grafting with surgery in a nonrandomized evaluation of 24 patients with chronic type B aortic dissection
with at least one indication for surgery. Stent-graft
placement resulted in no morbidity or mortality,
whereas surgery for type B dissection was associated
with four deaths (33%) and five serious adverse events
within 12 months. Dake et al. [73] studied the placement of endovascular stent-grafts across the primary
entry tear in 19 patients with acute aortic dissection
(four patients with type A and 15 with type B). Dissections involved aortic branches in 14 of the 19 patients
(74%) and symptomatic compromise of multiple branch
vessels was observed in seven patients (37%). Placement
of a stent-graft across the primary tear was technically
successful in all 19 patients. Complete thrombosis of
the false lumen was achieved in 15 patients (79%). Revascularization of ischemic branch vessel was successful
in 76% of the obstructed branches. Three of 19 (16%)
patients died at 30 days without further death during
the subsequent average follow-up of 13 months.
The European Society of Cardiology Task Force on
acute aortic dissection released its recommendations for
the indications for stent-graft placement and/or fenestration [83]. Additionally, in high-risk patients not suitable for surgery because of age, comorbid conditions or
personal preference, endovascular repair offers palliative
treatment to those who otherwise would have been left
to follow the natural course of the disease.
Take home message for endovascular therapy
C. A. Nienaber Chapter 22 Medical Treatment or Endovascular Stent-Graft Treatment for Acute Aortic Syndrome
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1. Endovascular stent grafts have been successfully utilized as a less invasive procedure for patients with
surgical indications for chronic type B aortic dissections
2. Endovascular therapies continue to evolve in the
treatment of malperfusion syndromes in type A and
type B aortic dissections and serve to complement
or sometimes replace the need for open surgical procedures.
22.7.8 Descending (Type B) Aortic Dissection
233
In the current era, endovascular stent-graft intervention
for acute descending (type B) aortic dissection is reserved for complications of the disease because surgical
repair has no proven superiority over medical or interventional treatment in stable patients. Patients with uncomplicated aortic dissections confined to the descending thoracic aorta (Stanford type B or De Bakey type III) are best treated with medical therapy. Medical treatment consists of invasive hemodynamic monitoring,
beta-blockade and arterial vasodilators if needed to
keep systolic blood pressure less than 120 mmHg. Pain
control with morphine sulfate is also important to attenuate the sympathetic release of catecholamines to
pain with resultant tachycardia and hypertension. Once
the patient is stable, oral beta-blockers and other antihypertensive medications if necessary are substituted
and the patient is discharged with very close follow-up.
In a series of 384 patients with type B dissections
from the IRAD registry, 73% were managed medically.
In-hospital mortality for these patients was 10% [11].
The reported long-term survival rate with medical therapy is approximately 60±80% at 4±5 years and approximately 40±45% at 10 years [84±86]. Survival is best in
patients with noncommunicating and retrograde dissections.
Indications for endovascular operation in patients
with acute type B aortic dissections are generally lim-
Fig. 22.9. Survival curves due to acute type B aortic dissection
for all patients and by management group based on KaplanMeier analysis of 40-day mortality. P. I. percutaneous intervention. (Taken from Ref. [11])
ited to prevention or relief of life-threatening complications. These complications include aortic rupture, ischemia of limbs and organ systems, renal hypertension,
persistent or recurrent intractable pain, progression of
dissection and aneurysm expansion, all more likely with
a patent false lumen and enlarging aortic diameter
(Fig. 22.8), and uncontrolled hypertension. In most series, classic open operations for acute type B aortic dissections carry a higher mortality that historically
ranges between 35 and 75%. Furthermore, patients with
a complicated course may preferentially undergo endovascular procedures rather than surgery, which may
lower the short-term mortality for such patients
(Fig. 22.9) [11].
Take home message for therapy: type B aortic dis-
section
1. Patients with uncomplicated aortic dissections confined to the descending aorta are best treated with
medical therapy
2. Medical therapy includes beta-blockers, other antihypertensives and adequate analgesia to keeps systolic
blood pressure below 120 mmHg
Fig. 22.8 Actuarial survival curves for patients clas-
sified by thrombosis of the false lumen and total
aortic diameter. (Taken from Ref. [93])
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