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Aortic Dissection
WilliamM.Sherk, MinhajS.Khaja, andDavidM.Williams
Pathophysiology
Aortic dissection is an uncommon but potentially lethal condition. Although aortic pathologies were known to Antyllus
as early as the second century AD, a clearer concept of dissection was not well developed until the nineteenth century
[1]. Over a century passed before Debakey [2] and Wheat [3]
established the rst effective surgical and medical treatments
for aortic dissection. Since that time, diagnostic and treatment modalities have continued to advance, with endovascular procedures including thoracic aortic endograft placement
(TEVAR) and fenestration supplementing or replacing traditional management in select cases.
The “double-barrel” concept described in 1822 by
Shekelton remains relevant to the current understanding of
the pathogenesis and natural history of aortic dissection.
Most commonly, a rupture of the intima and inow of
blood accompany a cleavage plane through the media
forming a new channel called the false lumen. Intimal
tears occur in regions of the aorta subjected to great pulsatility and pressure, in particular, at sites of exure and relative xation (ascending aorta and proximal descending
aorta near the ligamentum arteriosum) [4]. The dissection
ap typically contains the intima and two-thirds of the
media, while the remaining media and adventitia comprise
the thinner false lumen wall. Because of its thinner wall
and decreased elastic recoil, the false lumen expands to a
larger diameter to equilibrate the wall tension. In cases
W. M. Sherk
University of Michigan Health System, Department of Radiology,
Ann Arbor, MI, USA
e-mail: wsherk@med.umich.edu
M. S. Khaja
University of Michigan Hospital and Health Systems, Department
of Radiology, Ann Arbor, MI, USA
e-mail: mkhaja@med.umich.edu; davidwms@med.umich.edu
∙ D. M. Williams (*)
18
where the false lumen pressure exceeds the true lumen
pressure or when true lumen ow is rapid and forceful, the
true lumen may collapse. From the entry tear, the new
intramedial channel (false lumen) can travel proximally or
distally and in certain cases propagate into and obstruct
branch vessels. The Michigan classication [5] illustrates
two mechanisms of branch vessel compromise: static
(xed) obstruction, in which the aortic dissection ap
extends into the branch artery, and dynamic obstruction, in
which the ap prolapses over the ostium of the vessel or
collapses over the true lumen proximal to the branch vessel. Other mechanisms of dissection-related arterial
obstruction include embolic occlusion of true or false
lumen branches and true lumen thrombosis of vessels distal to an obstructing ap or non-reentering false lumen.
The spectrum of acute aortic injury includes two additional entities, intramural hematoma (IMH) and penetrating
atherosclerotic ulcer (PAU), both of which are amenable to
endovascular treatment [6, 7]. IMH is a variant of dissection
in which there is rupture of the vasa vasorum resulting in
hemorrhage in the aortic wall. PAU represents ulceration
through the elastic lamina of the aortic wall with varying
amounts of hematoma within the media.
Contemporary data regarding the epidemiology of aortic
dissection comes from the International Registry of Acute
Aortic Dissection (IRAD), which began in 1996 [8]. The
IRAD data demonstrates multiple risk factors for dissection
(Table 18.1), with hypertension as the most prevalent risk
factor (71% of patients). Men are approximately three times
more frequently affected than women, with an average age
of 63years [8].
Aortic dissections are classied by anatomical location
and temporal relation to the onset of symptoms. The anatomic classication is the primary factor inuencing treatment. Debakey originally proposed nine types of dissection
[1], later rening the classication into three types
(Fig.18.1) [9]:
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_18
209
210
W. M. Sherk et al.
Table 18.1 Risk factors for aortic dissection
Arterial hypertension Connective tissue disorders (Marfan’s and
Smoking Bicuspid aortic valve
Dyslipidemia Coarctation
Trauma Iatrogenic (catheter instrumentation, valvular
Cocaine or
amphetamine use
Fig. 18.1 Classication of aortic dissections by Debakey and Stanford
systems
Ehlers-Danlos syndromes)
or aortic surgery)
Autoimmune disorders (giant cell arteritis,
Takayasu’s arteritis)
• Type I: Dissection involves the ascending and descending
aorta.
• Type II: Dissection involves the ascending aorta only.
• Type III: Dissection involves the descending aorta only,
originating distal to the left subclavian artery.
The Stanford system [10] simplies aortic dissection into
two types (see Fig.18.1):
Table 18.2 Exam ndings in aortic dissection
Cardiovascular Differential blood pressure between
extremities [13]
Changing pulse exam over time
New aortic regurgitation murmur
(18–50% in proximal dissection [4])
Hypertension or hypotension
Neurologic Stroke, focal neurologic decits (5–10%)
Altered mental status
Syncope
Spinal cord ischemia, paraplegia
Ischemic peripheral neuropathy
Gastrointestinal Acute abdomen if mesenteric ischemia
Clinical Indication
The classic presentation of aortic dissection is abrupt,
catastrophic, tearing pain in the chest, back (often intrascapular region), or abdomen [4] (Table18.2). The location of the
pain often reects the location of the dissection. The pain can
be migratory as the dissection progresses but does not typically radiate like in acute coronary syndrome [4].
Patient presenting symptoms can signal involvement of
secondary organ systems or compression of structures by the
expanding dissection or leaking blood. Malperfusion to the
extremities, brain, spinal cord, and bowel can cause associated acute signs and symptoms. The enlarging dissected aorta
may also compress adjacent structures. In the mediastinum,
compression of structures such as the superior vena cava,
superior cervical ganglia, bronchi, or esophagus can result in
SVC syndrome, Horner’s syndrome, airway compromise,
and dysphagia, respectively [4].
Key Point
Differential blood pressure between extremities is the
most specic sign of aortic dissection, but is only seen
in 38% of cases.
• Type A: Dissection involves the ascending aorta (61% of
cases).
• Type B: Dissection is limited to the descending aorta.
Dissections are additionally classied by acuity [11]:
• Hyperacute, <24h
• Acute, 2–7days
• Subacute, 8–30days
• Chronic, >30days
Both ECG and chest radiography, commonly performed
for the emergency room patient with chest pain, are unreliable
to detect or exclude aortic dissection (Fig.18.2). The presence or absence of ischemic ndings on ECG does not predict aortic dissection. Chest radiography may occasionally
show widening of the mediastinum. The conrmation of aortic dissection relies on either transesophageal echocardiogram (TEE) or CT or MR angiography. TEE can be performed
on unstable patients at bedside with accurate results but cannot
18 Aortic Dissection
211
Fig. 18.2 Imaging ndings of dissection on chest radiograph (a), CTA
(b), MRA (c), and intravascular ultrasound (IVUS) (d). Note the nondescript appearance of the chest radiograph, which is unreliable for the
detection of dissection. The dissection plane and extent of involvement
determine the distal extent of involvement. CT angiography
with ECG gating is valuable for treatment planning.
Once triaged, a patient with aortic dissection follows a
complex treatment algorithm based primarily on the anatomic classication of the dissection and the presence or
absence of complications. All require aggressive medical
management, including anti-impulse therapy with
β-blockers. Patients with type A (Stanford classication)
aortic dissection (TAAD) complicated by rupture, acute aortic insufciency, or involvement of the coronary arteries
undergo emergent open repair. In those patients with TAAD
with prolonged malperfusion of the gut or lower extremity,
restoration of the blood ow to the compromised branch
arteries by endovascular interventions may be considered
[14–16], followed by repair of the ascending aorta when feasible. Uncomplicated type B aortic dissection (TBAD) is
treated medically, while TBAD complicated by false lumen
rupture, malperfusion due to branch artery obstruction, continuing pain and hypertension despite full medical therapy,
or early false lumen expansion is treated by endovascular
techniques [17].
Conventional Therapy
Wheat and colleagues rst advocated medical therapy for
aortic dissection in 1965 [3]. The idea of antihypertensive
treatment of dissection stems back to the poultry industry,
where spontaneous dissections aficted turkeys before the
introduction of reserpine [1]. β-Blockers (e.g., esmolol) and
aggressive blood pressure control are initiated emergently in
all patients with acute dissection. The exception is patients
with profound hypotension. The overarching goal is to
diminish the shear stress on the aorta by reducing the force of
left ventricular contraction, pulsatility of the aortic ow, and
systemic arterial pressure [4]. These factors in turn hinder
are delineated on the CT and MR. On IVUS, the dissection ap is
shown as a hyperechoic band (arrowheads). The true (T) and false (F)
lumens can be distinguished. The IVUS device has a characteristic circular, hyperechoic appearance (arrow)
Key Point
Medical management with aggressive blood pressure
control is the standard of care for uncomplicated type
B aortic dissection.
further propagation, diminish dynamic obstruction, and
possibly reduce the risk of rupture.
Medical management with aggressive blood pressure
control is the standard of care for uncomplicated TBAD. As
early as the 1970s, patients with TBAD treated medically
were shown to have similar in-hospital mortality rates to
those treated surgically [10]. Unlike surgery or thoracic
endovascular aortic repair (TEVAR), however, medical
therapy does not directly affect aortic remodeling. Patients
treated with medical management alone carry a high risk
of future aneurysm formation [18, 19]. Chronic, continued perfusion of the false lumen in medically treated
patients represents an added risk factor for future rupture and
survival [20].
The rst effective surgical management of aortic dissection
by Gurlin, Bulmer, and Derby in 1935 [21] was performed
on a patient with a pulseless lower extremity. During the procedure, the right external iliac artery was exposed and found
to have “inltration of dark blood in its lateral third, extending as far as could be seen in both directions” [21]. A longitudinal incision was made on the unaffected side of the
artery, revealing the narrowed true lumen. The intima and
media opposite the false lumen were incised from within the
vessel. Through the new opening, bright red arterial blood
spurted after release of the proximal clamp. The technique
restored ow to the lower extremity, but the patient died
6days later of renal failure.
Michael Debakey, a pioneer in the surgical treatment of
aortic dissection, recognized the importance of establishing
212
W. M. Sherk et al.
an articial “reentry” from the false lumen into the true lumen
of the aorta to reduce false lumen pressure and prevent distal
dissection and the invariably lethal rupture [2]. His work with
surgical fenestration as well as aortorrhaphy (aortic excision
and homograft placement) established a clear benet of surgical intervention over the natural course of dissection [9].
Further advances in surgical and anesthetic technique, including upgraded prosthetic graft materials, improved management of the aortic root and valve, and intraoperative cardiac
and cerebral protection, have reduced morbidity and mortality since Debakey’s early work [22].
Open surgical repair remains the standard treatment for
TAAD. In IRAD, the in-hospital mortality rate for patients
with TAAD receiving surgery was 26.6% versus 55.9% for
those treated with medical therapy alone. Of patients who
survived to hospital discharge and had documented follow up, 96.1% and 90.5% of those treated surgically for TAAD
versus 88.6% and 68.7% treated medically were alive at 1 and
3years after discharge [8]. In contrast, endovascular procedures have gradually replaced open surgery for the treatment
of complicated TBAD. The results of surgery in this setting
have been variable, with reported mortality rates up to
25–50% and substantial risk of spinal cord ischemia [11, 12].
Interventional Therapy
Background andIndications
Endovascular procedures treat two of the most lethal complications of acute aortic dissection, false lumen rupture and malperfusion syndrome [14, 15, 23, 24]. Thoracic endovascular
aortic repair (TEVAR), fenestration with or without stenting, or
a combination is employed in these patients. The guiding principle of endovascular treatment is to dene the anatomy of the
dissection, the location of the entry tear with respect to nearby
critical vessels, and the mechanism (static or dynamic) of arterial obstruction: these factors determine treatment. Endograft
placement over the entry tear of a dissection can be a single-step
treatment in the relief of many (especially dynamic) arterial
obstructions; stent placement within the true lumen encourages thrombosis of the false lumen and deters aneurysm formation [25]. When the arterial anatomy prohibits deployment
of a stent graft, or when malperfusion persists despite coverage of the entry tear, fenestration or stenting (or both) can
treat the recalcitrant branch vessel obstruction in a targeted,
piecemeal fashion. The goal of the fenestration is to create a
large, controlled tear in the dissection ap separating the true
and false lumens, allowing blood ow and pressure equilibration across the ap to reperfuse branches of the true lumen that
have been excluded by the dissection [26].
Multiple consensus statements support the use of endovascular interventions for treatment of complicated TBAD
[27–29] despite the lack of robust, randomized data comparing
Table 18.3 From the IRAD data: in-hospital management and outcomes
of all patients with type B aortic dissection
Denitive management Overall Survived Died
Surgery 56 (15%) 38 (67.9%) 18 (32.1%)
Medical treatment 282 (73%) 255 (90.4%) 27 (9.6%)
Percutaneous intervention
(fenestration, stent)
a
Adapted from [24]
Table 18.4 Comparison of pooled mortality and complication rates
between medical therapy, open surgery, and TEVAR for acute type B
dissections
Early mortality rate, % 6.4 17.5 10.2
Stroke and spinal cord ischemia, % 4.2, 5.3 5.9, 3.3 4.9, 4.2
Long-term survival rate, % 70.2–89 44–64.8 56.3–87
Aortic adverse event freedom at
5years (including aortic death,
rupture, new dissection, enlargement,
reintervention), %
a
Adapted from [29]
a
46 (12%) 43 (93.5%) 3 (6.5%)
Medical Surgery TEVAR
75–88.5 58.7–68 45–77
endovascular therapies to open surgery or to medical management. Pooled data from IRAD suggests a lower early
mortality with endovascular treatments relative to open
surgery [24, 29] (Tables 18.3 and 18.4). In patients with malperfusion and TBAD, isolated medical therapy represents an
independent mortality risk factor [23].
Malperfusion also aficts patients with TAAD in 16–33%
of cases, and ongoing research indicates improved outcomes
when endovascular therapy precedes traditional open repair
[14, 15]. Compared to a historical cohort of patients with malperfusion, patients who underwent medical stabilization, percutaneous intervention, and delayed operative repair for type
A dissection with malperfusion had signicantly lower mortality (89% versus 25%, including 15% mortality from rupture) [24]. Patients who followed this algorithm of delayed
operative repair after reperfusion by IR had similar mortality
as the uncomplicated type A dissection group [15].
For uncomplicated TBAD, the ADSORB trial demonstrated
favorable long-term aortic remodeling for patients treated with
TEVAR and medical therapy versus medical therapy alone
[30]. For patients with chronic, uncomplicated type B dissections, the INSTEAD-XL trial showed better aorta-specic mortality at 5years for TEVAR versus medical therapy alone [31].
Key Point
CTA evaluation checklist:
• Evidence of false lumen leak or rupture
• Signs of possible organ malperfusion
• Identication of lumen supplying each critical artery
• Presence of thrombosis in false lumen of aorta or
branch arteries
• Localization of entry and reentry sites
18 Aortic Dissection
213
Preprocedure Work-Up
CT angiography is commonly performed in cases of suspected
aortic dissection and provides vital information for intervention planning, including location of aortic rupture, presence
and mechanism of branch artery obstruction, and spatial relationships of the true and false lumen. Markers of end-organ
ischemia, such as elevated creatinine, lactate, or liver enzymes,
The How To: TEVAR (Fig. 18.3)
During endovascular treatment, absolute certainty of
guide-wire location and identification of true and
false lumens are essential. Pre-operative cross-sectional
imaging is critical to define the orientation of the
lumens, location of intimal tears, and proximity of tears
to critical vessels such as left common carotid, left
subclavian, and celiac arteries.
1. For percutaneous access, the common femoral
graft device (22–24 Fr access). Alternative access
methods must be pursued if this is not the case (e.g.,
cutdown arteriotomy, pre-rupture with placement of
endograft conduit, or Dacron graft conduit to the
iliac artery via open incision).
2. The endograft delivery catheter is closely inspected
and prepared, taking care to remove any air bubbles.
3. Over a stiff (e.g., Lunderquist) guidewire, the stent
graft is positioned across the entry tear.
4. Thoracic aortography is performed, with careful
attention to left common carotic and subclavian
origins and the entry tear.
5. The endograft delivery catheter position is adjusted
according to angiographic landmarks, and the
endograft is deployed.
6. An angiogram is repeated. Fenestration or branch
artery stenting may be required if there is persistent
branch artery malperfusion despite coverage of the
entry tear or there is unsuitable anatomy for endograft placement. The following steps describe the
fenestration procedure.
The How To: Fenestration (Figs. 18.4, 18.5, and 18.6)
1. In general, percutaneous access is obtained in
the bilateral common femoral arteries via the
Seldinger technique (refer to Chap. 8 for more
information).
2. Intravascular ultrasound (IVUS) is used to demon-
3. Digital subtraction angiography is used to identify
the extent of dissection within branch arteries, distal
emboli, and incidental arteriopathy. Aortography is
rarely needed.
4. Pressure measurements are recorded between the
aortic root and branch arteries, taking care to ensure
that the pressure recorded in the branch vessel is
distal to reentry tear or thrombosed false lumen and
cially in the SMA, branch artery IVUS is necessary. The branch vessels are inspected by order of
importance, with gut perfusion (SMA) given the
5. The level of fenestration is selected close to the
arteries that are being salvaged. A steerable needle
(such as a Rosch-Uchida needle) is advanced to
the desired level and oriented perpendicular to the
is acquired from the pre-intervention CT or MR
angiogram and intraprocedural IVUS.
6.
to perform the puncture from the smaller, usually true, lumen into the larger, usually false,
lumen, as the smaller lumen stabilizes the needle and minimizes the risk of extraluminal passage [29].
7. Passage into the false lumen during the transseptal
puncture is almost always confirmed with IVUS,
either by visualization of the needle, catheter, or
wire; or by saline injection through the catheter.
Seldom is contrast injection needed or used.
8.
eter is used to expand the hole to create the fenestration. A waist may not be seen in the balloon
9. If true lumen collapse persists despite fenestration, large-diameter self-expanding stents are
used to buttress the true lumen. These are placed
alongside the fenestration tear entirely within
the true lumen.
10. Additional steps including branch vessel stenting
may be indicated based on the intraoperative
dynamic imaging. Static obstruction of branch
vessels may persist after initial interventions,
requiring stent deployment within the true lumen
of the affected branch.
-
-
respect to branch artery origins, size and orientation of the true lumen, and location of entry and
reentry tears, both at baseline and in response to
interventions.
214
W. M. Sherk et al.
Fig. 18.3 A 59-year-old woman with intractable chest pain after med-
ical management of TBAD. The partially thrombosed false lumen was
identied on both preoperative CTA and intraprocedural IVUS (star in
a and b, respectively). The dissection ap extended from the origin of
the left subclavian artery to the left external iliac artery. TEVAR was
can be signs of ongoing malperfusion syndrome and should
be correlated with CT demonstration of threatened vessels
and closely followed. Peripheral pulses and compartments
should be closely monitored for signs of lower extremity vessel occlusion and subsequent compartment syndrome following revascularization. In all cases of aortic dissection, the
interventionalist should be in close communication with cardiothoracic surgery, anesthesia, and critical care colleagues to
implement and maintain appropriate care in these profoundly
ill patients. Invasive hemodynamic monitoring is required.
Post-procedural Management
The patient will continue to require aggressive medical management after endovascular treatment. Restoration of blood
ow to previously compromised branch arteries can result in
reperfusion injury, where reintroduction of oxygen in previously ischemic tissues can cause the dissemination of
inammatory cytokines and reactive oxygen species. In the
gut, reperfusion injury can cause increased intestinal permeability to bacteria and subsequent translocation into the
performed, and overlapping endografts (arrows in c) were deployed
from just beyond the left common carotid artery origin to just above
the celiac artery. Preoperatively, subclavian artery transposition was
performed; the patent transposed vessel can be seen on the aortogram
(arrowheads in d)
bloodstream, resulting in sepsis. After correction of prolonged leg or gut arterial obstruction, it is useful to request
clinical consultations from vascular or general surgery, in
case lower extremity fasciotomy or exploratory laparotomy
is needed soon after the angiographic procedure. Repeat
endovascular procedures to treat malperfusion are occasionally required. Malperfusion may also appear in a postoperative setting, hours or days after repair of the ascending
aorta. Principles of treatment are the same. Periodic followup imaging surveillance is recommended to evaluate for
endograft complications and evolving changes in the true
and false lumens (Table18.5). Typically, this is performed at
1, 3, and 6months and annually thereafter.
Table 18.5 Complications after endovascular treatment of aortic
dissection
E conversion of TBAD to TAAD
E Endograft endoleak
E stroke, spinal cord ischemia (paraplegia, paraparesis)
B reperfusion injury
B peripheral vascular injury due to large sheaths
(E, endograft; B, both fenestration and endograft)
Left carotid
Celiac
A
a
BCD
18 Aortic Dissection
215
FT
F
T
F
F
F
T
T
Left subclavian
Thrombus
Left renal
Left common iliacRight common iliac
Left external iliacRight external iliac
Innominate
True
False
Celiac
SMA
Celiac
SMA
Left
renal
F
Left
renal
Inguinal ligament
Right femoral
b
SMA
Fig. 18.4 (a) In this drawing, the primary entry tear is situated in the
proximal descending thoracic aorta. The dissection ap distal to this
shows evidence of collapse of the true lumen with dynamic obstruction
of the celiac and superior mesenteric arteries. In these vessels, the dissection does not extend into them but rather occludes them by intermittent obstruction of the ap during the cardiac cycle. In contrast, the left
renal artery shows evidence of dissection without reentry in the course
of the branch vessel. In this branch, there is formation of thrombus in
the left renal artery false lumen, which in turn causes a static obstruction and renal malperfusion. F=false lumen; SMA=superior mesenteric artery; T=true lumen. (b) The true lumen is cannulated, and a
Rosch-Uchida needle (Cook, Bloomington, IN) is then placed from
the true into the false lumen in a perpendicular manner with IVUS
Left
renal
Left femoral
Fenestration
tear
monitoring (A). The site of fenestration is at the branch vessels that are
intended for therapy. A wire and subsequently a 5 Fr catheter are then
placed into the false lumen (B). IVUS or small-dose contrast delivery
can conrm the false lumen location of the catheter. A 14-mm balloon
is then placed at the puncture hole in the ap (C) and then inated often
without seeing a “waist” to create a fenestration (D). RU= RoschUchida needle; SMA=superior mesenteric artery. (c) Although fenestration can equalize pressures across the dissection ap, self-expanding
16- to 22-mm- diameter Wallstents (Boston Scientic, Natick, MA) are
usually placed to buttress open the aortic true lumen and are typically
placed near the compromised branch vessel (A). These are usually
inserted via the already obtained percutaneous access sheaths and
deployed by IVUS guidance. Care is taken to withdraw the guidewire
Stent
A
c
Thrombus
Fenestration
tear
Celiac
False
Celiac
SMA
True
Left
renal
Stent
False
lumen
To left
kidney
SMA
Left
renal
Fig. 18.4 (continued) from across the fenestration tear and readvance
it within the aortic true lumen, so as to deploy the stents exclusively
within the aortic true lumen, rather than straddle the tear from true to
false lumen. Neglecting this critical step adds greatly to the complexity
of the procedure. Fenestration and stenting of the aortic true lumen
treats the dynamic obstruction of the depicted mesenteric vessels, but
not the static obstruction seen in the depicted left renal artery. In this
B
branch, pressure measurements conrm a signicant (≥20 mm Hg)
systolic gradient requiring additional treatment (B). SMA =superior
mesenteric artery (Figures adapted from Operative Techniques in
Thoracic and Cardiovascular Surgery, 14(1), Patel HJ, Williams DM,
Endovascular Therapy for Malperfusion in Acute Type B Aortic
Dissection, 10, Copyright 2009, with permission from Elsevier)
Fig. 18.5 A 49-year-old man with TAAD with diminished pulses and
pain in right leg. CTA (a) demonstrated the dissection ap (black
arrowheads) extending into abdominal aorta. During intraprocedural
IVUS (B), a similar appearance of the dissection ap (white arrowheads) was seen at the level of the SMA (S) (b). Manometry via a catheter positioned in the SMA (c) conrmed a signicant pressure gradient
relative to the aortic root due to dynamic obstruction, requiring
fenestration. After fenestration and stent placement in the supramesenteric aortic true lumen (d), the pressure gradient improved. Repeat
IVUS demonstrated persistent collapse of the true lumen near the aortic
bifurcation, necessitating additional fenestration 2cm below the renal
artery origins and aortoiliac true lumen stenting (e). A nal uoroscopic image demonstrated the supramesenteric and aortoiliac stents
(arrows)
18 Aortic Dissection
217
Fig. 18.6 A 29-year-old man with TAAD complicated by visceral and
lower extremity malperfusion. CT angiography through the thoracic
aorta (a) demonstrated a narrow true lumen and perfused false lumen
(F) within the ascending and descending thoracic aorta. In the abdominal aorta, the true lumen was nearly completely decompressed, with
minimal contrast opacication of the SMA (b, arrow). Manometry conrmed a 35 mmHg pressure gradient across the SMA (mean arterial
pressure of 67 mmHg in aortic root versus 32 mmHg in proximal SMA)
due to dynamic obstruction. IVUS before (c) and after (d) fenestration
and true lumen stent placement above the SMA demonstrated improved
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