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IV. Dissection
3. The indications for stent-graft placement in type B
dissection are limited to persistent or recurrent chest
pain, aortic expansion, dissection progression, and
end-organ malperfusion syndromes.
22.7.9 Long-Term Therapy and Follow-Up
The long-term approach to patients with successful initial treatment of acute aortic dissection begins with the
appreciation of a systemic illness. Systemic hypertension, advanced age, aortic size and the presence of a
patent false lumen are all factors which identify higher
risk, as does the entire spectrum of Marfan's syndrome
[87±89]. All patients merit aggressive medical therapy,
follow-up visits and serial imaging. It has been estimated that nearly a third of patients surviving initial
treatment for acute dissection will experience extension
of dissection, aortic rupture or require surgery for aortic aneurysm formation within 5 years of presentation.
Treatment with effective beta-blockade is the cornerstone of medical therapy. By lowering both blood pressure and dP/dt, beta-blockers have been shown to retard aortic expansion in Marfan's syndrome [90] and
that associated with chronic abdominal aortic aneurysms. Blood pressure should be titrated below 135/80
in usual patients and below 130/80 in those with Marfan's syndrome [83, 90±92].
Serial imaging of the aorta is an essential component
of long-term management (before and after surgery or
stent-graft placement) in Marfan's disease and in all
cases of chronic dissection. The choice of imaging modality is dependent on institutional availability and expertise. Previous recommendations suggest follow-up
imaging at 1, 3, 6, 9, and 12 months following discharge, and annually thereafter [83]; this aggressive
strategy underlines the observation that both hypertension and aortic expansion/dissection are common and
not easily predicted in the first months following hospital discharge. Imaging should not be confined to the region of initial involvement since both dissection and
aneurysm formation may occur anywhere along the entire length of the aorta.
Development of an ascending aortic diameter of 4.5±
5.0 cm is an indication for surgical repair in patients
with Marfan's syndrome. In non-Marfan patients an ascending aortic diameter of 5.5±6 cm warrants repair, as
does distal aortic expansion to 6.0 cm or more in all
types of patients. As with nondissecting aneurysms, the
rate of growth and the size of the aorta are both important factors to consider when it comes to prophylactic
vascular surgery. An ascending aortic aneurysm of
5.0 cm may merit urgent repair in a young patient with
Marfan's syndrome [91]. Conversely, an aneurysm of
5.0 cm for 3 years in an elderly person with well-con-
trolled blood pressure is unlikely to rupture. Patients
who have been treated with surgery and/or endovascular stent-grafting warrant similar follow-up to those
whose initial treatment was limited to medical treatment.
Considering both the aging patient population in
Western societies with prolonged survival despite hypertension and the better diagnostic strategies available
to more patients, the cardiovascular community faces
an increasing incidence of acute and chronic aortic
problems, such as dissection, aneurysm, intramural hematoma, ulcerations and traumatic lesions, that desperately need to be stratified using both early biomarkers
of an inflammatory and dissecting process and functional imaging of the aortic wall. At this pivotal point
in time, an elevated level of awareness in clinical cardiology and the availability of modern imaging technology should trigger interest in diagnosing and treating
the complex of acute aortic syndromes similar to previous efforts in acute coronary syndromes. Cardiologists should improve diagnostic pathways and vascular
staging in acute and chronic aortic diseases, form regional referral networks and allocation systems, and
utilize uniform follow-up programs. Moreover precise
definitions of pathology using clear semantics should
be integrated into prospective registries of aortic diseases by a multidisciplinary team of physicians in an
attempt to validate previous retrospective observations
and to make the best use of evolving diagnostic and endovascular treatment strategies. Finally, cardiologists
are in need of credible prognostic models that can support decisions for individual patient care independent
of investigators, at different times, and in worldwide locations.
Take home message for follow-up
1. Close follow-up by a specialized team includes the
assessment of signs of aortic expansion, aneurysm
formation, signs of leakages at anastomoses/stent
sites, and malperfusion
2. Excellent blood pressure control below 135/80 mmHg
is paramount to prevent complications
3. After hospital discharge, regular outpatient visits
and imaging should be performed at 1, 3, 6, 9, and
12 months and at least yearly thereafter.
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C. A. Nienaber Chapter 22 Medical Treatment or Endovascular Stent-Graft Treatment for Acute Aortic Syndrome
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Physiopathology
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of Ischemic Complications
of Aortic Dissections
David M. Williams, Bora Peynircioglu
Chapter
23
Contents
23.1 Introduction .......................
23.2 Identification of the True and False Lumens ..... 239
23.3 Importance of Abdominal Aortic Dissection .....240
23.4 Classification of Branch Artery Obstruction .....241
23.5 Diagnosis of Branch Artery Obstruction ....... 242
23.6 Setting Priorities and Avoiding Pitfalls ........243
23.7 Conclusion ......................... 243
239
23.1 Introduction
Acute aortic dissection typically kills by tamponade or
exsanguination owing to false-lumen rupture or by organ ischemia owing to the malperfusion syndromes [4,
8, 9, 12, 13]. Until recently, the purview of angiography
was treating the malperfusion syndromes, with the goal
of restoring flow to obstructed arteries and treating
medically the ensuing reperfusion injury as best we
could. This treatment consisted of fenestration and deployment of uncovered stents on the basis of complete
evaluation of the aorta and critical branch arteries, as
directed by the clinical examination of the patient, intravascular ultrasound survey of the aorta, and branch
arteriography and manometry. The availability of endografts initiated the opportunity of treating the malperfusion syndromes more expeditiously and, in addition,
preventing rupture by inducing thrombosis of the false
lumen [3, 5, 10, 11]. As in any medical endeavor, errors
in diagnosis lead to errors in treatment. The goals of
this chapter are to survey the mechanisms by which
aortic dissection leads to organ or limb malperfusion
and to consider a few of the pitfalls in establishing the
diagnosis. In particular, the discussion of malperfusion
in the setting of aortic dissection will be divided into
these topics:
l Identification of the true and false lumens
l Importance of abdominal aortic dissection
l Classification of branch artery obstruction
l Clinical diagnosis of malperfusion
l Setting priorities and avoiding pitfalls.
23.2 Identification of the True
and False Lumens
Identification of the true and false lumens is crucial in
the endovascular treatment of aortic dissection. The
true and false lumens behave differently. In most acute
aortic dissection, the false lumen is prone to ectasia
and is at risk of rupture, and the true lumen is prone
to collapse and is at risk of compromise of its branch
arteries. Numerous steps in the endovascular treatment
of dissection require real-time knowledge of which lumen the guidewire, the diagnostic catheter, and treatment devices lie within. These steps include:
l Deploying an endograft across the entry tear within
the true lumen
l Stenting a branch artery to the aortic true lumen
l Stenting the aortic true lumen after fenestration, to
reduce a prolapsing flap
l Aligning both iliac arteries with the aortic true lu-
men during aortoiliac stenting
l Avoiding complicating future transfemoral catheter
procedures, retrograde aortic perfusion, or endograft
treatment because of injudicious placement of aortic
or branch artery stents.
In chronic dissections, the distinction between the true
and false lumens is usually straightforward. For most of
these patients, the interventionalist will have the benefit
of a chest, abdomen, and pelvis computed tomography
(CT) scan. In acute dissections, a complete CT examination may not be available. Features identifying the
false lumen include aortic cobwebs and the ªbeakº sign
[6, 7, 14]. Aortic cobwebs are remnants of media
stretching (like cobwebs) between the dissection flap
and the outer wall of the false lumen (Fig. 23.1). The
beak sign is the acute angle by which the dissection
flap meets the outer wall of the aorta (Fig. 23.1). As
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IV. Dissection
a
b
Fig. 23.1. Cordlike remnants of media, ªaortic cobwebs,º are a reliable marker
of the false lumen (a, arrows). Characteristically, they stretch from the dissection flap covering the true lumen (a, arrowheads) to the outer wall of the
false lumen). On the computed tomography examination of this patient, a
cobweb is visible in the distal thoracic aorta (
ªbeakº (b, arrowhead) marks the junction of the dissection flap with the
aortic wall and lies within the false lumen
b, arrow). The acute angle or
abc
Fig. 23.2. Two distinct lumens are present in the thoracic aorta
(a) and in the common iliac arteries (b). In the intervening abdominal aorta, the second lumen has nearly disappeared (c).
Here, the true lumen has collapsed completely and is visible as
such, this angle (or beak) is the imaging correlate of
the cleaving wedge of hematoma which splits the medial layers to form the false lumen. These signs are highly
reliable identifiers of the false lumen. Generally reliable
characteristics of the true lumen are continuity with the
aortic root, which remains the source of the majority of
a curvilinear filling defect along the anterior margin on the
aorta (c, arrow), where it lies across the origin of the superior
mesenteric artery (asterisk)
then two are present in the abdomen, although one of
them may be difficult to identify (Fig. 23.2). Sources of
branch artery perfusion are identified as exclusively
true lumen, exclusively false lumen, or shared true and
false lumens. Branches with shared perfusion are
further characterized as with or without reentry tears.
the large-diameter aortic branches, and continuity with
the femoral arteries.
Once the lumens have been identified, they should
be traced from root to groin. A reliable anatomical rule
to use while drawing a mental path within the aorta
23.3 Importance
of Abdominal Aortic Dissection
from slice to slice on a CT examination is that every
time the path crosses the flap it changes the lumen. A
second reliable anatomical rule is that, in acute dissections, the lumens are continuous. If two lumens are observed in the chest and two are observed in the pelvis,
Renal, mesenteric, or spinal cord malperfusion approximately doubles the mortality of patients with acute aortic
dissection [2]. Most of these malperfusion syndromes
arise as complications of the dissection path through
D.M. Williams, B. Peynircioglu Chapter 23 Physiopathology of Ischemic Complications of Aortic Dissections
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Fig. 23.3. A single lumen is prominent at the level of the aortic
crura near the diaphragm in the same patient as in Fig. 23.2.
Careful tracing of this lumen back to the heart shows that it is
the false lumen, and that the true lumen is completely collapsed and nearly invisible. Until proven otherwise, the bowel
must be considered at risk. The true lumen has collapsed
against the anterior wall of the aorta, scalloping the anterior
margin of the false lumen
Fig. 23.4. Anatomical drawing, static vs dynamic obstruction.
Reprinted with permission [19]
In static obstruction, the dissection flap intersects the
origin of a branch and potentially encroaches on the lumen. If the dissection enters the vessel origin but does
not reenter, the true lumen of the vessel is narrowed,
the abdominal aorta, the source of the critical branch arteries. Because of its crucial prognostic role, separate discussion of the abdominal aorta is worthwhile. The false
lumen which tapers and disappears at the diaphragm
may be of little consequence; however, the true lumen
which tapers and disappears at this location represents
a lethal, if not mortal, injury (Fig. 23.3), because every
true lumen branch distal to the disappearing flap is at
risk of obstruction and end-organ infarction. In some
cases, the true lumen is so completely collapsed that it
is visible only as a scalloping of the anterior aortic lumen
(Fig. 23.3). If a lumen ªendsº at the diaphragm, make sure
it is the false lumen, not the true lumen.
and a pressure gradient may be measured across the
stenosis between the aorta and the arterial trunk. If the
false lumen reenters through a large enough tear, it can
completely compensate for a narrowed true lumen, and
no pressure gradient may be present. Treatment is
aimed at relieving the branch artery stenosis.
In dynamic obstruction, the dissection flap spares the
vessel origin, but prolapses across it like a curtain. This
obstruction is dynamic in two senses. It is observed only
during cross-sectional imaging with the aorta pressurized and conducting flow; it disappears when the aorta
is observed at aortotomy or at necropsy (Fig. 23.5).
Furthermore, it may disappear during medical treatment
with antihypertensives and beta-blockers, and recur
when medications are discontinued (Fig. 23.6). Treatment
must be directed at the dissection flap in the aorta.
23.4 Classification
of Branch Artery Obstruction
Static and dynamic obstruction can simultaneously
contribute to branch artery obstruction. In addition,
complete occlusion of a vessel by either mechanism can
The Michigan classification of branch artery obstruction [15] is based on the anatomical relationship of the
dissection flap to the branch artery in question
(Fig. 23.4). It is an intuitively appealing classification
because this anatomic distinction forms the basis of
distinct treatment strategies. The causes of obstruction
may be distinguished as follows:
l Static obstruction
l Dynamic obstruction
l Mixed static and dynamic obstruction
l Miscellaneous
± Related to dissection: thrombosis, embolism
± Unrelated to dissection: atherosclerosis, fibromus-
cular dysplasia.
lead to thrombosis of the true lumen distally. In the
kidney, which has no effective collateral supply, this can
lead to diffuse renal branch artery thrombosis, an unsalvageable condition. In the pelvis, iliac artery thrombosis is often arrested at the iliac bifurcation, where
collateral supply from lumbar arteries or the contralateral internal iliac artery reconstitutes the obstructed internal and external iliac arteries.
A false lumen which thromboses without a reentry
tear can completely fill an artery (or even the aorta), effectively obliterating the true lumen. Furthermore, retrograde thrombosis beginning distally in the vessel can
proceed to complete occlusion of that vessel. We have
observed this in the iliac, renal, and superior mesenter-
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IV. Dissection
abc
Fig. 23.5. a Computed tomography shows collapse of the true
lumen against the anterior wall of the abdominal aorta, occluding the superior mesenteric artery (SMA). Small rulers were
inserted medially into the false lumen on the autopsy specimen
Fig. 23.6. A patient with acute type B dissection was being eval-
uated for renal artery involvement. Intravascular ultrasound
when the patient was at her well-treated normotensive state (
of 90/50 showed a capacious true lumen with unimpeded SMA
perfusion. During treatment for impending sedation-induced
ic arteries. When it occurs in the aorta, the patient may
present with symptoms of spinal cord ischemia. A true
lumen may thrombose distal to a dissection flap which
covers yet does not enter the vessel origin. This occurs
most often in the common iliac artery, when the dissection spares one common iliac origin but enters the
other. Complete stasis is present on the nondissected
side, and thrombosis ensues. Cross-pelvic collaterals
from the contralateral dissected side generally arrest
this thrombosis at the iliac artery bifurcation. When the
iliac artery is completely thrombosed, it may be difficult to tell whether the thrombosis is within the true or
the false lumen, but the distinction is crucial. When
thrombosis is present in the false lumen, the obstruction may be treated by means of a stent in the true lumen. When the thrombosis is in the true lumen, the
thrombosis must be cleared by mechanical or other
thrombolysis before flow in the true lumen is restored
by endograft or fenestration.
Embolic occlusion of false and true lumen branches
is unusual. Embolism to false lumen branches usually
originates from thrombus poorly adhering to the dissection flap. Embolism to true lumen branches usually
originates from thrombus forming in regions of stasis,
as outlined in the previous paragraph. Other sources include thrombus on the true lumen side of the dissection
flap forming at sites of spontaneous reentry tears, or
(b) up to the anterior margins of the dissection. These confirm
that the dissection flap spared the SMA origin, despite diffuse
bowel infarction (
respiratory arrest, her pressure was driven up to 159/83, resulting in collapse of the true lumen and obstruction of the SMA
a)
(b). When her pressure returned to the baseline, the true lumen also returned to its baseline state, reopening the SMA (c).
The dissection flap is marked by arrowheads
c)
from thrombus within a false lumen extruded into the
true lumen through an iatrogenic reentry tear during
an angioplasty or stent delivery.
Special situations are beyond the scope of this chapter. These include presentation of dissection and malperfusion in patients with a prior aortic endograft or
interposition graft, causes of malperfusion in patients
with aortic dissection unrelated to the dissection flap,
and causes of malperfusion in patients with previous
negative angiographic workup.
23.5 Diagnosis
of Branch Artery Obstruction
Cross-sectional imaging is useful to ruling out ªischemic anatomy.º If the true lumen is of reasonable caliber from entry tear to termination, and if the dissection
flap spares every major branch artery, branch artery
obstruction is unlikely. However, if the flap crosses a
vessel origin, or the true lumen is collapsed, malperfusion may be present, and should be evaluated by angiography. Evaluation begins with inspection of the flap
in relation to branch artery origins. This can be done
most expeditiously using intravascular ultrasound. Pressure measurements are made simultaneously in the aor-
D.M. Williams, B. Peynircioglu Chapter 23 Physiopathology of Ischemic Complications of Aortic Dissections
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ab
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Fig. 23.7. Pressure tracings at the level of the SMA from the pa-
tient in Fig. 23.3. True and false lumen pressures are nearly
a), despite nearly total collapse of the true lumen. In
equal (
a
contrast, a profound pressure deficit is present in the SMA,
which arises exclusively from the true lumen (b). TL true lumen, FL false lumen
b
c d
Fig. 23.8. Pressures. No aortorenal gradient is present in the
proximal renal artery (a). However, the renal artery injection
shows that the dissection flap (arrow) extends to the renal hilum (b), and so the proximal renal artery pressure may not re-
tic root and abdominal aortic true and false lumens. If
these are equal, subsequent pressure measurements can
be made using the abdominal aortic pressure as a surrogate for root pressure. If they are unequal, then a
search for a pressure drop across a coarctation-like obstruction within the aorta should be made.
Aortic pressures should be compared with arterial
trunk pressures in the organ of clinical concern as well
flect renal perfusion pressure. A catheter in the true lumen distal to the dissection (c) documents a small aortorenal pressure
gradient (d). Other renal branches may be subject to different
deficits in perfusion pressure
as in those branches suspected of being compromised
on the basis of imaging. Equal pressures in a false lumen and a collapsed true lumen do not mean that the
branch artery pressures are also equal (Fig. 23.7). Pressure measurements should be made within the branch
artery of interest. Furthermore, branch artery manometry should be followed by selective arteriography, to
make sure that measurements are representative of per-
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IV. Dissection
fusion pressure at the organ level. This precaution is
necessary in instances of static obstruction, wherein the
reentry tear may be several centimeters deep in the
trunk; unless the measurement is distal to the reentry
tear, it may underestimate the branch artery deficit in
perfusion pressure (Fig. 23.8).
As already noted, dynamic obstruction may be demonstrably pressure-dependent (Fig. 23.6). An occasional
scenario is the patient who arrives in the emergency department with tearing chest pain, loss of leg pulses, and
refractory hypertension, is aggressively treated with antihypertensives and beta-blockers, and finally arrives,
chatty and serene, in the angiography suite to rule out
malperfusion. In cases such as this, especially when the
clinical history suggests the patient is noncompliant with
medications or clinical follow-up, a negative workup for
malperfusion is followed by reassessment after tapering
down the dose of the beta-blocker. For this reason, we request patients with subacute dissection and a history suggesting sporadic episodes of malperfusion be converted
to short-acting beta-blockers, antihypertensives, and sedation. Patients with acute dissection are, ordinarily, already being treated with short-acting drugs.
23.6 Setting Priorities and Avoiding Pitfalls
whom aortic root reconstruction may be delayed. For
example, deploying a Wallstent through a fenestration
tear, from the false lumen above to the true lumen below, may effectively treat the malperfusion. However, by
compressing the true lumen adjacent to the false lumen
component of the Wallstent, this procedure greatly complicates future transfemoral access to the brachiocephalic vessels and may preclude future cardiac bypass using
retrograde transfemoral perfusion. Instead, the stent
should be deployed entirely within the aortic true lumen. A similar consideration in patients with acute
type A dissection complicated by malperfusion is pertinent to creation of the circumferential tear in the flap
during the so-called scissor technique [1].
23.7 Conclusion
The malperfusion syndromes greatly increase the mortality of acute aortic dissection. Endovascular techniques, if timely and if carried out with clear and complete understanding of the vascular pathoanatomy of
the individual patients, are highly successful in correcting malperfusion.
The leaking false lumen (which heralds impending rupture or tamponade) and florid aortic insufficiency take
precedence over malperfusion, and are indications for
immediate open repair in patients with reasonable operative risk. The De Bakey and Stanford classifications
provide straightforward anatomical criteria for stratifying patients into immediate surgical or medical management. Patients with prolonged malperfusion of gut
or lower extremity may be unsuitable for immediate repair even with type A dissection, and in such cases immediate therapy is directed at restoring flow to critical
vessels. The mechanism of arterial obstruction determines the appropriate treatment in a given case, and so
the first principle of treatment is to define arterial anatomy and assess visceral perfusion. In particular, assuring the integrity of the superior mesenteric artery, or
restoring perfusion to the compromised superior mesenteric artery, has the highest priority of any endovascular goal in this group of patients. Even when resection of dead bowel is necessary, preoperative endovascular restoration of superior mesenteric artery perfusion will give the general surgeon reliable margins between uncompromised and unsalvageable bowel.
While correcting life-threatening malperfusion is the
goal of these procedures, nevertheless the endovascular
physician should bear in mind that additional endovascular procedures may be necessary in the future. This
is especially important when treating patients with
type A dissections complicated by malperfusion, in
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