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Acute aortic syndrome: Imaging & endovascular
treatmentVesna Đurović Sarajlic
Clinic of Radiology
University Clinical Center Sarajevo
BCR 2017, Budapest , Hungary
The term “AAS” was first introduced into the literature in
1998 to describe a variety of acute aortic pathologies:
• Aortic dissection (AD)
• Intramural hematoma (IMH)
• Penetrating ulcer (PAU)
• Clinically usually indistinguishable
• They are interrelated, and one condition may evolve into
another, or coexists with another
IMH � AD
PAU � AD
The common denominator of AAS is disruption of the media layer of the aorta
Clinical signs and symptoms
• Sudden onset of tearing and ripping chest, neck or back pain
• Pulse differences
• Acute congestive heart failure
• Neurological deficit
• Abdominal pain
• Shock
• Multi - detector CTA is the modality of choice in AAS
Sensitivity up to 100%, specificity of 98 – 99%
I. Non CE phase
II. CE arterial phase (with ECG gating)
III. CE delayed phase
• TTE & TEE in unstable patients (aortic valve insufficiency,
pericardial effusion..)
• Magnetic resonance and catheter angiography are seldom
used in acute conditions
Aortic dissection
• Represents the majority of the AAS
• Prevalence 10 – 30/million/ year, twice that of AAA rupture
• Male predominance, but in women has a higher mortality rate
• Ascending aorta app. 60%, descending aorta app. 40%
• > 40 y, hypertension
Risk factors
• Congenital & hereditary
Bicuspid aortic valve, coarctation, Connective tissue disorders
Marfan syndrom, Ehl. Danlos , policystic kidney disease
• Acquired
hypertension
aneurysms, atherosclerosis
• Iatrogenic
cardiac surgery, wires and catheter caused
• Other conditions
smoking, dyslipidemia, cocain and amphetamine abuse
Classification systems for AD
• Stanford classification (extension of dissection):
Stanford type A – Affects Ascending Aorta
Stanford type B – Distal to the left subclavian artery
• DeBakey classification (location of the entry tear):
DeBakey type I – ascending & descending aorta
DeBakey type II – ascending aorta
DeBakey type III – descending aorta
Stanford A Stanford B
• There is no consensus about
the classification of arch AD
without involvement of the
ascending aorta
ESVS Guidelines Descending Thoracic
Aorta
Diagnostic features of AD:
Intimomedial flap and double lumen
True lumen
• Smaller
• Brighter in the arterial phase
• Outer wall calcification
False lumen
• Larger (as more pressurized)
• Wrapping at the level of the
aortic arch
• Thrombosis
Intimomedial flap Double lumen
Coronal plane VR reconstruction
What do we report in AD?
• Primary entry tear
• Re - entry tear
• Complications:
- malperfusion of the aortic branches
- pericardial effusion & tamponade
- rupture
Stanford A Stanford B
63-year old female, hypertension, chest pain, weaknes in the left hand, confusion
Brain malperfusion – bad prognostic factor
68 year-old male, chest pain, left arm and left leg pulse deficite
Right kidny and left leg malperfusion
53 year female, hypertensive crisis, sudden onset of back pain
Intramural hematoma IMH
A hematoma within the aortic wall
• without intimomedial flap
• no visible intimal tear
• no flow in hematoma
- The classical theory of
pathogenesis of IMH is that of
“rupture of the vasa vasorum”
• Incidence – app. 12% of all suspected AAD cases are IMH
(IRAD)
• A significant number of IMH will progress to plain dissection
• Up to 10% of IMH will resolve spontaneously
• The higher incidence in Asians than in Europeans and
Americans
Diagnostic feature and classification
• > 0.5mm crescentic or
circular thickening of the
media, hyperdense on the
non CE scans
• Stanford classification to
IMH type A and type B
IMH vs. AD
• Descending aorta
• Older patients
• Rupture is more frequent
• No compression of the
lumen
• No involvement of the
branch arteries
• Ascending aorta
• Patients with Marfan Sy.
• Compression of the true
lumen
• Proximal and distal
malperfusion sindromes
• Longer lesions
Predictors of the adverse IMH outcome
• Age of the patient > 68y
• Location of the IMH –IMH type A
• Coexistance of PAU
• Hematoma thickness
> 10 mm
• Aortic diameter
> 50 mm
Penetrating atherosclerotic ulcer (PAU)
• Progressive erosion of an
atheromatous plaque that
penetrates the elastic lamina
into the aortic media
• It counts for 2- 7% of all
AAS
• Usually asymptomatic
• PAUs are closely associated with
atherosclerosis of the aorta
(hypertension, hyperlipidemia,
AAA)
• 85% -90% are located in the
descending aorta
• PAUs in the ascending aorta and the
arch are more prone to rupture
PAU type A PAU type B
Complications of PAU
PAU > 20 mm x 10 mm
increases the risk of :
• Hematoma formation
• Pseudoaneurysm
• Rupture
Treatment concepts in the ASCENDING thoracic aorta
• Surgical repair - AAS
involving ascending aorta
• Endovascularrepair - in the
early phase of application
Treatment concepts in the DESCENDING thoracic aorta
• Level A evidence does not exist in the management of DTA
• “Management of Descending Thoracic Aorta Diseases”
(Clinical Practice Guidelines of the ESVS 2017)
- offer the best medical evidence available and the best
consensus amongst key experts in the field
Uncomplicatedacute type B dissection
• Acute dissection- within the first 14 days after the onset of
symptoms
• Medical therapy with antihypertensive drugs is widely
accepted to be the first line treatment ( SBP 100-120; HR <60
beats/min)
• Adequate clinical and imaging surveillance (MR or CTA 3m,
6m, yearly)
TEVAR in Uncomplicatedacute type B AD “To treat or not to treat”
Pros
• To prevent late dilatation and
rupture of the aorta
• IRAD reported reduced mortality
in patients treated with TEVAR
(Fattori R at al, 2013)
• ADSORB study – increased false
lumen thrombosis and remodeling
of the aorta after TEVAR
(Brunkwall J at al, 2014)
Cons
• Complications of the
endovascular procedure
• Retrograde dissection of the aorta
• Stroke
• Spinal cord ischemia
• Paraplegia/ paraparesis
• Migration of the stent-graft
Selection of the patients
Radiologic pred. of growth
• One entry tear (ET) , the size
>10mm
• Entry tear at the concavity
• False lumen > 22 mm
• Eliptic true lumen and round false
lumen
• Early thoracic endografting may be considered selectively to
prevent aortic complications in uncomplicated acute type B
dissection, (recommendation 18, ESVS’ CPG)
• To facilitate the patient selection process, important clinical
and anatomical features were summarized in a new
categorization scheme DISSECT (M.Dake at al, 2013)
Complicated acute type B dissection
• Endovascular repair with thoracic endografting should be the first
line therapy (recommendation 16, ESVS CPG)
• Endovascular repair is associated with lower peri-operative
morbidity and mortality rate than OR (2,5 9,8% : 25-50% mortality rate)
• Technical success of TEVAR ranges from 95 to 99%, hospital
mortality from 2,6 to 9,8%, neurological complications from 0,6
to 3,1 % (6,96,97)
The goals of TEVAR are:
- Coverage of the primary
entry tear
- Decreased pressure in the
false lumen/ repressurisation
of the true lumen
- Reperfusion of branch
vessels
- Thrombosis of the false
lumen
• In complicated type B AD,
patients presenting with
malperfusion, experience the
poorest outcome
• Endovascular fenestrationshould
be considered in these patients to
treat malperfusion
(recommendation 17, ESVS CPG)
Acute type B IMH and PAU
• Uncomplicatedtype B IMH
and PAU should be treated
medically, followed by
serial imaging surveillance
(recommendation 20, ESVS CPG)
• Complicated type B IMH
and PAU should be treated
by endovascular approach –
TEVAR
(recommendation 21&22, ESVS CPG)
Future prospectives
• To assess the management controversies of uncomplicated acute
type B dissections, larger randomized controlled trias should be
conducted
• The timing of the procedure is of special interest in
uncomplicated type B aortic dissections
• Definition of early unfavourable clinical and imaging signs to
select the patients who would benefit the most from an early
TEVAR procedure