Aortic Dissection

SHORT REVIEW

08.09.2015
• Aortic dissection is defined as separation of the layers
within the aortic wall. Tears in the intimal layer result
in the propagation of dissection (proximally or
distally) secondary to blood entering the intima-media
space.

• An acute aortic dissection (< 2 weeks) is associated

with high morbidity and mortality rates. Mortality is
highest in the first 7 days. Patients with chronic aortic
dissection (>2 weeks) have a better prognosis
• Degeneration of the aortic media, or cystic
medial necrosis, a prerequisite.

• Blood passes into the aortic media through the

tear, separating the intima from the surrounding
media and/or adventitia, and creating a false
lumen.

• Initiating event
-primary rupture of the intima.
-haemorrhage within the media.
 INCIDENCE

• Acute aortic dissection : 2.6 to 3.5 per 100,000

person-years .
• 60- to 80-years
• 70% males
• Women present late (67 versus 60 years)
 RISK FACTORS
• Systemic hypertension
72 % hypertension, 31 % atherosclerosis.

• Less important in young patients

< 40 yr, 34 % hypertension 1% atherosclerosis
• Pre-existing aortic aneurysm – 13%
 Ascending aorta >aortic arch >descending aorta.
 Such a history was more common in patients under age
40 (19 percent).

• Inflammatory diseases that cause vasculitis (giant cell

arteritis, Takayasu arteritis, rheumatoid arthritis,
syphilitic aortitis).
• Disorders of collagen (eg, Marfan syndrome, Ehlers-
Danlos syndrome, annuloaortic ectasia)
 Family history of dissection.
 50 % <40, only 2 percent of older patients.
 Dissection in the third trimester of pregnancy

• Bicuspid aortic valve.

 9 % <40yrs had a bicuspid valve, compared with 1
percent of those over age 40 .
 Always involves the ascending aorta, usually with severe
loss of elastic fibres in the media
• Aortic coarctation.
 Post surgery para coarctation aorta that has intrinsic
medial faults,
 Post BAV,
 Coexisting bicuspid aortic valve.

• Turner syndrome.
 Aortic dissection or rupture, often occurring with
coarctation, is an increasingly recognized cause of
death in women with Turner syndrome.
• Coronary artery bypass graft surgery (CABG).
Ascending aortic dissection is a rare complication of
CABG, perhaps more often, with minimally invasive
off-pump CABG .

• Previous aortic valve replacement. 5 percent

• Cardiac catheterization with or without coronary

intervention - 2percent
• Trauma rarely causes a classic dissection, but can induce
a localized tear in the region of the aortic isthmus .

• More commonly, chest trauma from acute deceleration

(as in a motor vehicle accident) results in aortic rupture
or transection .

• High-intensity weight lifting

• Crack cocaine
 TYPES OF AORTIC DISSECTION
Classification

• The DeBakey and Daily (Stanford) systems

• DeBakey system is based upon the site of origin

 type 1 originating in the ascending aorta and
propagating to at least the aortic arch,
 type 2 originating in and confined to the
ascending aorta, and
 type 3 originating in the descending aorta and
extending distally or proximally.
• The Stanford system is more widely used.

• Type A - The ascending aorta is involved

(DeBakey types I and II)
• Type B - The descending aorta is involved
(DeBakey type III)
Image A represents a Stanford A or a
DeBakey type 1 dissection.

Image B represents a Stanford A or

DeBakey type II dissection.

Image C represents a Stanford type

B or a DeBakey type III dissection.

Image D is classified in a manner

similar to A but contains an
additional entry tear in the
descending thoracic aorta. Note that
a primary arch dissection does not
fit neatly into either classification
• Ascending aortic dissections are almost twice as
common as descending dissections.

• The right lateral wall of the ascending aorta is the

most common site of aortic dissection .

• In patients with an ascending aortic dissection,

aortic arch involvement is seen in up to 30
percent.
• Isolated abdominal aortic dissection is reported
sporadically and can be due to iatrogenic,
spontaneous, or traumatic mechanisms .

• The infrarenal abdominal aorta is more commonly

involved than the suprarenal aorta.
Variants

• Intimal tear without hematoma

• Uncommon variant of aortic dissection characterized by a
stellate or linear intimal tear associated with exposure of
the underlying aortic media or adventitial layers. There is
no progression or separation of the medial layers

• Current imaging techniques may be inadequate

for diagnosing this type of dissection
There are several variations of aortic
dissection. Class I- classic dissection
with separation of intima/media and
dual lumens; there is a flap between
true and false aneurysm and clot in
false lumen;
Class II- intramural hematoma with
separation of intima/media but no
intraluminal tear or flap imaged;
Class III - limited intimal tear without
hematoma and eccentric bulge at tear
site (limited dissection);
Class IV- atherosclerotic ulcer
penetrating to adventitia with
surrounding hematoma that is usually
subadventitial; and
Class V- iatrogenic or traumatic
dissection, as for example due to a
coronary catheter causing dissection.
• Aortic intramural hematoma
 Characterized by blood in the wall of the aorta in the absence of
an intimal tear,
 5 to 13 percent of patients with symptoms consistent with an
aortic dissection .
 The false channel is probably produced by a rupture of the vaso
vasorum into the media of the aortic wall.

• Penetrating atherosclerotic ulcer

 complicates an aortic intramural hematoma and can also lead to
aortic dissection or perforation.
 Noninvasive imaging shows an ulcer-like projection into the
hematoma,
 almost always seen with a type B hematoma (31 of 34 cases in
one series)
 CLINICAL MANIFESTATIONS

• Severe, sharp or "tearing" posterior chest or back pain

(distal to the left subclavian) or anterior (in ascending
aortic dissection)

• Radiation

• Associated with syncope, CVA, MI, heart failure or other

clinical symptoms or signs
• Typically abrupt in onset and more often sharp than
tearing

• More common with type A dissections while both

back pain and abdominal pain significantly more
common with type B dissections.
• Painless dissection

 Relatively uncommon, only 6.4 percent

 Older (67 versus 62 years) and more often had a type
A dissection (75 versus 61 percent).
 Diabetes, aortic aneurysm, cardiovascular surgery.
 Syncope, heart failure, or stroke
 In-hospital mortality was significantly higher than for
patients presenting with pain (33 versus 23 percent).
• Syncope
 worse outcomes
 Stanford type A dissection
 cardiac tamponade and stroke

• Hypertension
• Distal (type B) dissection

• Other symptoms - related to impaired blood flow to

an organ or limb induced by the original dissection or
by propagation of the dissection proximally or distally.
• The presence of impaired or absent blood flow to peripheral
vessels is manifest as a pulse deficit, defined as a weak or absent
carotid, brachial, or femoral pulse resulting from the intimal flap
or compression by hematoma.

• Pulse deficit - 19 to 30 percent of patients with an acute type A

dissection compared with 9 to 21 percent with a type B
dissection .

• Higher rate of in-hospital complications and mortality

• Women less likely to have a pulse deficit than men

• Involvement of the ascending aorta

 Acute aortic valve regurgitation, diastolic

decrescendo murmur, hypotension, or heart failure,
in one-half to two-thirds of ascending dissections .

 Acute myocardial ischemia or myocardial infarction

(MI) due to coronary occlusion. The right coronary
artery is most commonly involved

 Cardiac tamponade and sudden death due to rupture

of the aorta into the pericardial space.
• Hemothorax and exsanguination if the dissection extends through
the adventitia, with hemorrhage into the pleural space.

• A considerable variation (>20 mmHg) in systolic blood pressure

between the arms.

• Neurologic deficits, including stroke or decreased consciousness

due to direct extension of the dissection into the carotid arteries or
diminished carotid blood flow.

• Horner syndrome if there is compression of the superior cervical

sympathetic ganglion.

• Vocal cord paralysis and hoarseness due to compression of the left

recurrent laryngeal nerve.
• Elderly > 70 yrs

• Marfan syndrome
• Atherosclerosis, prior aortic aneurysm, iatrogenic
dissection, or intramural hematoma,

• Abrupt onset of pain, any pulse deficit or a

murmur of aortic regurgitation
• Less likely to undergo surgery and had a higher
mortality rate with either surgery or medical
therapy.
• Involvement of the descending aorta — splanchnic
ischemia, renal insufficiency, lower extremity ischemia,
or focal neurologic deficits due to spinal artery
involvement and spinal cord ischemia .

• Chest or back pain – 86 percent

• Abrupt onset of pain – 89 percent
• Migrating pain – 25 percent
• Hypertension – 69 percent
• Hypotension/shock – 3 percent
• Pulse deficit – 21 percent
• Spinal cord ischemia – 3 percent
• Ischemic peripheral neuropathy – 2 percent
• Factors independently associated with in-hospital
mortality include :
 hypotension/shock,
lack of chest pain on presentation,
branch vessel involvement.
• Periaortic hematoma — detected by imaging, may
reflect slow oozing from the damaged acutely
dissecting aorta at or near the site of dissection.
harbinger of impending rupture.

• Higher rates of shock, cardiac tamponade, and

altered consciousness/coma and had a significantly
higher mortality rate
 DIAGNOSIS

• History and physical examination.

• 96 percent -combination of the following three clinical
features :

 Abrupt onset of thoracic or abdominal pain with a sharp,

tearing and/or ripping character
 Mediastinal and/or aortic widening on chest radiograph
 A variation in pulse (absence of a proximal extremity or
carotid pulse) and/or blood pressure (>20 mmHg
difference between the right and left arm)
• Despite the reported utility of this diagnostic
strategy, additional imaging studies are obtained in
almost all patients (98 percent in data from IRAD)
because of the limited sensitivity of the chest
radiograph, especially in type B dissections
• Blood tests — Serum markers are emerging diagnostic
option, particularly screening patients in the setting of chest
pain where the cost of widespread imaging is prohibitive.

• D-dimer — D-dimer is one of the major fibrin degradation

products and is generated from cross-linked fibrin. An
elevated plasma concentration of D-dimer indicates recent
or ongoing intravascular blood coagulation.

• A cut-off of 500 ng/mL has been widely used and levels

below this value are highly predictive for excluding
dissection .
• Other tests —
• The serum lactate dehydrogenase concentration may be
elevated due to hemolysis of blood in the false lumen,
nonspecific finding.

• A rapid 30-minute immunoassay for the serum concentration of

smooth muscle myosin heavy chain has been evaluated in
patients suspected of having an aortic dissection .

• Sensitivity and specificity of this assay in the first 3 hours are

similar and possibly superior to those of TTE, conventional CT,
and aortography, but were lower than those of TEE, helical CT, or
MRI.

• Utility needs further evaluation.

• Electrocardiogram

 ECG normal in 30 percent,

 Nonspecific ST and T wave changes in 45 percent
(commonly, LVH and strain associated with hypertension),
 Ischemic changes in 15 percent,
 Acute MI in 5 percent .
 Involvement of a coronary artery in an aortic dissection
may not manifest changes in the electrocardiogram
• Imaging

• Imaging studies to establish the diagnosis of aortic

dissection are not performed until the patient is stabilized
medically

Initial study :
 CT in 61 percent,
 TEE in 33 percent,
 Aortography in only 4 percent, and
 MRI in only 2 percent .
• Important to rapidly identify acute dissections involving
the ascending aorta.

• Transthoracic echocardiography may be useful to

identify proximal ascending aortic dissections,
particularly with regard to coexistent aortic
valve disruption/regurgitation and hemopericardium

• Not sufficient to delineate the extent of the dissection, or

any associated bleeding or complications of dissection.
• Imaging studies can identify the presence of aortic
dissection and the following associated features :

 Involvement of the ascending aorta

 The extent of dissection and the sites of entry and reentry
 Thrombus in the false lumen
 Branch vessel or coronary artery involvement
 Aortic valve regurgitation
 Pericardial effusion
• Chest radiograph

• Conventional chest radiographs may show widening of the

aorta with aortic dissections .
• Mediastinal widening : 63 % with type A dissections, 11%
normal
• Pleural effusion was found in 19 %

• Other findings
 widening of the aortic contour,
 displaced calcification,
 aortic kinking, and
 opacification of the aorticopulmonary window
Aortography

 Site of dissection
 Relationship between dissection and major branches
 Communication site between the true and false lumen
 Coronary angiography and evaluation for AR
 Generally been replaced by non invasive testing
 Sensitivity of 88 % and a specificity of 94 %
 Positive and negative predictive values were 96 and 84 %
• False negative Aortography

 Simultaneous opacification of the true and false lumen ,

intimal flap between them is not visible,
 thrombosis of the false lumen results in lack of
opacification with contrast, or
 intramural hematoma with non communicating dissection
CT scan

• After injection of intravenous iodinated contrast, two

distinct lumens with a visible intimal flap are identified
• Ready availability ,identification of intraluminal
thrombus and pericardial effusion.

Disadvantages of standard CT
 Intimal flap is seen in less than 75 percent of cases and
that the site of entry is rarely identified .
 Potentially nephrotoxic iodinated contrast is required,
 No capability to assess for AR
 The accuracy substantially improved with spiral (helical) CT
and perhaps with multidetector (multislice)
 CT (Spiral CT may be more accurate than MRI or TEE in the
detection of aortic arch vessel involvement .
 Potential limitation is a spiral CT artifact that can simulate
an aortic dissection flap in patients if performed without
ECG gating
Patient with an
ascending type
A aortic
dissection
showing the
intimal flap.
Patient with a
type A aortic
dissection
involving the
ascending and
descending
aorta
• MRI

• Less commonly used , MRI is a highly accurate non invasive

technique for evaluating the thoracic aorta in patients with
suspected dissection.

• The presence of a double lumen with a visible intimal flap

is the diagnostic criterion for aortic dissection .

• Additional suggestive findings include widening of the

aorta with a thickened wall and thrombosis of the false
lumen.
• Sensitivity and specificity of MRI were both 98%,
85 % sensitivity for identification of the site of entry

• MRI is safe in adequately monitored patients

• MR contrast agents have a more favorable safety

profile than iodinated contrast agents.

• Ability to assess branch vessels, AR

• TTE
• Limited utility for evaluation of the thoracic aorta for
dissection

• Inability to adequately visualize the distal ascending,

transverse, and descending aorta .

• Undulating intimal flap may be seen in the proximal aorta in

some patients, the sensitivity and specificity of TTE are inferior
to those with CT, MRI, and TEE .

• TTE is most useful for the assessment of cardiac complications

of dissection, including AR, PE/tamponade, and regional LVEF.
• TEE

 Close proximity of the esophagus to the thoracic aorta and

the absence of an intervening lung or chest wall.

 Easily performed in the emergency department and yields

diagnosis within minutes from the start of the procedure.

 Useful in patients too unstable or inappropriate (eg,

pacemaker or other contraindication) for MRI .

 Procedural sedation, experienced operators

• TEE in patients with aortic dissection
 Intimal dissection flaps can be identified with high spatial resolution.

 M-mode echocardiography demonstrates lack of relation between

movement of the intimal flap and the aortic wall .

 True and false lumens can be identified.

 Color Doppler permits clear identification of flow within and between the
true and false lumens .

 The presence of flow does not absolutely distinguish the true lumen from
the false lumen.

 The true lumen has an endothelial lining and is contiguous with the aortic
valve.
 Thrombosis in the false lumen, pericardial effusion, concomitant
AR, and proximal coronary arteries can be readily visualized.

 The 135º long axis view from TEE can define the severity and
mechanism of aortic regurgitation that complicates acute type A
dissections .

 Patients with an intrinsically normal valve who have aortic

regurgitation due to a correctable aortic lesion (incomplete
leaflet closure, leaflet prolapse, or dissection flap prolapse) can
undergo aortic valve repair .

 In contrast, unrepairable abnormalities (eg, Marfan syndrome,

bicuspid valve, aortitis) require valve replacement.
• Aortic intramural hematoma on TEE - Regional thickening of the aortic
wall of more than 7 mm in a crescentic (primarily if nontraumatic) or
circular shape (primarily if traumatic) and/or evidence of intramural
accumulation of blood

• The sensitivity 95 % , specificity 90- 100%

• Monoplane TEE - Inability to visualize the upper portion of the ascending

aorta due to the interposed trachea (between the aorta and esophagus).

• Biplane and multiplane TEE circumvent this deficiency by permitting the

observation of the ascending aorta in multiple imaging planes

• Large series data on real-time three-dimensional (3D) TEE are lacking.

• Choice of imaging study

• Information required and access to and experience with the

imaging modality

• Thoracic MRI, thoracic CT, and multiplane TEE are the preferred
methods, if available.

• Most centres generally perform multiplane TEE at the bedside or

in the Emergency Department for patients who present with acute
chest pain and/or are clinically unstable .

• Hemodynamically unstable patients with a very strong suspicion of

dissection can be emergently brought to the operating room and
undergo TEE after induction of anesthesia.
• Thoracic MRI is preferred in patients with chronic chest pain
and in those who are hemodynamically stable, or are seen for
follow-up of a chronic dissection .

• CT chest with contrast often indicated as an initial screening

study in patients with suspected aortic dissection, especially in
the emergency department setting where TEE is less available,
and especially after hours.

• If CT is equivocal, or further delineation of the dissection is

needed, TEE or MRI is indicated.
• Digital subtraction aortography is used when ascending aortic
dissection is strongly suspected, but noninvasive tests are
unavailable or inconclusive.

• Coronary angiography is safe in stable patients, but delay to

surgical invention should be minimized.
• Retrospective data suggest no in-hospital benefit to coronary
angiography .

Coronary angiography is generally attempted in all patients with

a prior history or angina or MI, patients older than 60 years of
age, and patients with multiple risk factors for coronary disease.
Management of aortic dissection

• GENERAL PRINCIPLES

• Acute dissections involving the ascending aorta are considered surgical

emergencies.

• Reasons for medical therapy includes advanced age, comorbidity, patient

refusal, intramural hematoma, or death prior to planned surgery.

• Confined to the descending aorta are treated medically unless the patient
demonstrates progressive dissection with end-organ ischemia or
continued hemorrhage into the pleural or retroperitoneal space.

• Only 20 percent of those with a type B dissection undergo surgery.

Surgical therapy involves:
• Excision of the intimal tear
• Obliteration of entry into the false lumen proximally
• Reconstitution of the aorta with interposition of a synthetic
vascular graft
• Restoration of aortic valve competence : resuspension of the native
aortic valve or by aortic valve replacement

Medical therapy of involves :

• Lowering the blood pressure and
• Decreasing the velocity of left ventricular contraction, both of
which will decrease aortic shear stress and minimize the tendency
for the dissection to propagate.
ACUTE MANAGEMENT

 Admit to ICU, pain relief with morphine , blood pressure control

 Intubation : Hemodynamically unstable / airway compromise

 Blood pressure control, IV beta blocker to reduce the heart rate

and aortic shear stress.

 Propranolol (1 to 10 mg load, followed by 3 mg/h) / labetalol

(20 mg initially, followed by 20 to 80 mg every 10 minutes to a
total dose of 300 mg) or as an infusion (0.5 to 2mg/min).
 Esmolol has advantages in the acute setting, short half-life
and ability to titrate to effect, patients who might be
intolerant of beta blockers due, to asthma, or heart failure

 Verapamil or diltiazem are alternatives in patients who

cannot tolerate beta blockers
 Switched to oral beta blocker therapy
 Target BP 100-120, lowest possible in range
 Systolic blood pressure remains elevated , use
nitroprusside
 The initial dose of nitroprusside is 0.25 to 0.5 mcg/kg per
minute.
 Do not use without initial beta blockade
 Continuous monitoring
• Hypotensive patients should be evaluated to determine if the cause is
blood loss, hemopericardium with tamponade, valvular dysfunction, or left
ventricular systolic dysfunction before volume is administered.

• Inotropic agents should be avoided since they will increase aortic wall
shear stress and worsen the dissection.

• In patients with cardiac tamponade, percutaneous pericardiocentesis can

accelerate bleeding and shock.

• Diagnostic evaluation, bedside TEE is the procedure of choice . In more

stable patients chest computed tomography (CT) or thoracic magnetic
resonance imaging (MRI)
• DEFINITIVE THERAPY
• Descending (type B) aortic dissection

• Medical therapy — Uncomplicated aortic dissections confined to the

descending thoracic aorta (Stanford type B or DeBakey type III)

• In a series of 384 patients with type B dissections from the IRAD, 73 percent
were managed medically. In-hospital mortality for these patients was 10
percent .

• The reported long-term survival rate with medical therapy is approximately

60 to 80 percent at four to five years and approximately 40 to 45 percent at
10 years .

• Survival is best in patients with non-communicating and retrograde

dissections
• With medical therapy disappearance of false lumen is
uncommon.

• Continued flow through the false lumen (patent false

lumen), which occurs with either partial thrombosis or
no significant thrombosis, is postulated to prevent
healing.

• The mean three-year mortality rate is significantly

worse in patients with partial thrombosis compared
with those with complete patency (32 versus 14
percent)
• Intervention — (surgical or endovascular) for descending aortic
dissection is reserved for complicated course.

• Indications for intervention

 occlusion of a major aortic branch leading to end-organ
ischemia,
 persistent severe hypertension or pain,
 propagation of the dissection (as may be manifested by
persistent or recurrent pain),
 aneurysmal expansion, and rupture .
 Acute distal dissections in patients with Marfan syndrome may
also be best treated surgically
• In-hospital mortality for surgical patients was 32
percent compared with 10 percent for those
treated medically

• There were two independent predictors of surgical

mortality: age ≥70 years and hypotension or shock
on admission .

• Endovascular stent-grafting has been employed as

a less invasive alternative to surgery, particularly in
stable patients with type B dissections
• Ascending (type A) aortic dissection

• Acute ascending aortic dissections (Stanford type A)

should be treated as a surgical emergency as patients are
high risk for a life-threatening complication such as aortic
regurgitation, tamponade, and myocardial infarction.

• Mortality rate as high as 1 to 2 percent per hour early after

symptom onset .

• The in-hospital mortality was 27 and 56 percent for

surgical and medical therapy,
• Not myocardial infarction but hemorrhagic stroke
is a relative contraindication to urgent surgical
intervention.

• Women and elderly – less likely to be treated

surgically.
Poor prognostic factors include

●Age over 70 years

●Abrupt onset of chest pain
●Hypotension, shock, or tamponade at presentation
●Renal failure at presentation and before surgery
●Pulse deficit
●Abnormal ECG, particularly ST segment elevation
●Prior myocardial infarction
●Previous aortic valve replacement
●Renal and/ or visceral ischemia
●Underlying pulmonary disease
●Preoperative neurologic impairment
●Perioperative bleeding and massive blood transfusion
●Prolonged clamping time

The first six factors were the most important predictors of in-hospital
mortality in the IRAD review
• Survival after repair

• Long-term survival after surgical repair of type A

dissections is relatively good.
• Survival at one and three years 96 and 91 percent,
respectively.
• Patient survival at 5 and 10 years 68 and 52 percent,
respectively
• The overall risk of reoperation was 16 percent at 10 years.
• Endovascular stent-grafts

• Endovascular stent-grafting has been employed as a

less invasive alternative to surgery, primarily in
patients with complicated type B dissections .

• The stent graft is positioned to cover the intimal flap

and seal the entry site of the dissection, resulting in
thrombosis of the false lumen.
• Type B dissections

• In the IRAD series of 384 type B dissections, 46 (12

percent) were managed with endovascular stent
grafting . This technique was reserved for patients
who had undergone at least eight weeks of medical
management. Only three (6.5 percent) died during
the initial hospitalization.
• Outcome of stent grafting compared with surgery in a non
randomized evaluation of 24 consecutive patients with a
subacute or chronic thoracic type B dissection who had at
least one indication for surgery .

• There was no morbidity (paraplegia, stroke, embolization,

side-branch occlusion or infection) or mortality with stent
grafting, while surgery was associated with a 33 percent
mortality and a 42 percent incidence of adverse events
within 12 months.

• At three months, thrombosis of the false lumen had

occurred in all patients undergoing stent grafting.
• Stent grafting has also been evaluated for acute and, in some cases, life-
threatening dissections, but the outcomes are not as good .

• One report evaluated 19 patients with an acute dissection (four type A)

and an indication for surgery . This included involvement of aortic
branches in 14, which led to symptomatic compromise of multiple branch
vessels in 7.

• Complete thrombosis was achieved in 79 percent, and revascularization

of ischemic branch vessels with relief of symptoms occurred in 76
percent of obstructed branches.

• However, the morbidity rate was 21 percent (small bowel and renal
infarction and lower extremity gangrene) and 30-day mortality was 16
percent.

• Among patients who survived this period, there were no deaths or

instances of aneurysm or aortic rupture during the subsequent 13-month
follow-up period.
Meta-analysis of 39 studies involving a total of 609 patients
who underwent stent-graft placement for a type B dissection .

 Procedure success 98 %
 Major complications 11.1 %
 Neurologic complications, the most serious, in 2.9 percent,
mostly peri-procedural stroke and paraplegia (1.9 and 0.8
percent, respectively)
 The major complication rate higher with acute compared
with chronic dissections (21.7 versus 9.1 percent)
 Minor complications - 2.5 percent.
 The rate of complications compared favourably with
previously reported surgical series.
• Type A dissections
• Possible alternative to surgery in patients with
type A dissections with ischemic complications.
• Limited experience .In one series, the false lumen
was completely obliterated in 14 of 15 patients
within three months .
• Further study is required to determine the role for
this approach in such patients.
• A hybrid approach to the repair of type A aortic dissection,
sometimes referred to as the “frozen elephant trunk
repair,” uses an open approach to surgically repair the
ascending aorta while using a stent-graft to manage the
descending aorta.
• Fenestration and other stents

• In life-threatening ischemia of distal organs, mortality can

exceed 60 percent.
• Surgical repair of the dissection often results in resolution of
peripheral ischemia,
• Stenting and/or balloon fenestration of the dissecting
membrane may be non invasive alternatives for patients with
- type A dissection in whom mesenteric, renal, or
peripheral ischemia persists after surgical repair, or
- type B dissection treated medically in whom mesenteric,
renal, or peripheral ischemic complications arise
• PROGNOSIS

• The 10-year actuarial survival rate of patients with an aortic

dissection who leave the hospital has ranges from 30 to 88 %

• Survival appears similar for both type A and type B dissections .

• Adverse events, such as recurrent dissection or complications of

aneurysm formation in the descending aorta, occur in both type
A and type B dissection.

• Late aneurysm formation and adverse outcomes, including

death, related to the initial diameter of the false lumen in the
upper thoracic aorta.
• Initial false lumen diameter of ≥22 mm at the upper thoracic
aorta, significantly more likely to develop late aneurysm
formation (42 versus 5 percent) or death.

• The causes of death were illustrated in a report of 380 survivors

of an initial type A dissection in which there were 31 late deaths

• The causes were stroke (12 patients), aortic reoperation for

redissection or progressive dilatation of the false lumen (seven
patients), malignancy (five patients), myocardial infarction (four
patients), and heart failure (three patients).
• LONG-TERM MANAGEMENT

• Medical therapy
• Life-long therapy with an oral beta blocker to reduce
systemic blood pressure and the rate of rise in systolic
pressure, both of which will minimize aortic wall stress
• Target blood pressure of less than 120/80 mmHg .
• Avoidance of strenuous physical activity is also
recommended as another method to minimize aortic
shear stress.
• Serial imaging — Baseline thoracic MRI or chest CT scan
prior to discharge with follow-up examinations at 3, 6, and
12 months, even if the patient remains asymptomatic .
Subsequent screening studies are then performed every one
to two years if there is no evidence of progression.

• Abnormalities on serial imaging:

• Extension or recurrence of the dissection
• Aneurysm formation
• Leakage at anastomoses or stent sites
• MRI is as accurate as TEE and, because it is non invasive, is
more acceptable for serial studies.
• MRI does not expose patients to iodinated contrast and
ionizing radiation, which are important factors for younger
patients.
• CT scanning is an alternative, but exposes the patient to
considerable ionizing radiation and requires iodinated
contrast, which may cause nephrotoxicity.

• Alternating chest CT and thoracic MRI is a reasonable

option for patients with good renal function.
• Non-contrast MRI can be used for patients with impaired
renal function to avoid the risk of nephrogenic systemic
fibrosis.
• Reoperation
• Repeat surgery is required in 12 to 30 percent of
patients,

• extension or recurrence of dissection at the previous

site of intervention,
• localized aneurysm formation remote from the site
of repair,
• graft dehiscence or infection, or aortic regurgitation.

• The reoperation rate is higher in patients with

Marfan syndrome
• Planning of TEVAR—type B TAD

• Planning of TEVAR includes clinical examination, laboratory

tests and imaging to classify the type of dissection (classical
dissection, intramural haematoma (IMH), penetrating
atherosclerotic ulcer, traumatic dissection), its duration and
potential complications.

• Localization of all tears, with emphasis on identifying the

primary entry tear, is important.

• The next step is to define the extension of dissection and

possible static, dynamic or complex involvement of
supraaortic, visceral and pelvic vessels resulting in
malperfusion .
• Perfusion of side branch vessels through the false
lumen does not automatically exclude patients from
TEVAR, as a distal communication is often present
or the visceral vessel may receive a contribution
from both lumina.
• TEVAR for type B aortic dissection
• Complicated acute type B aortic dissections .
• Further subgroups benefiting from immediate
TEVAR are being defined.
• In an uncomplicated type B dissection.
• Definition of endoleak after TEVAR for TAD
• The only important types of endoleaks in TAD
are type IA (antegrade perfusion of the false
lumen) and type II (perfusion of the false
lumen via the over stented left subclavian
artery). Retrograde flow from distal entry
tears must not be considered as endoleaks.
• Procedural ‘technical’ success is defined as closure of the
primary entry tear (i.e. absence of type Ia endoleak) and
induction of false lumen thrombosis.

• The aim of endovascular treatment is to overcome or resolve

complications of aortic dissection including malperfusion,
imminent rupture and bleeding.

• Does not imply complete immediate thrombosis of the false

lumen, as further thrombosis and remodelling processes are a
matter of time.
• Specifics of TEVAR for TAD
• The focus is the occlusion of the primary entry tear.

• The size of the selected stent graft should be based on

the diameter of the aorta proximal to the dissected
segment, applying almost no oversizing.

• The technical challenge, especially in complicated type

B dissections, may be to cannulate the narrowed,
sometimes collapsed true lumen.

• To assure access to the true lumen, TEE may often be

necessary .
• Procedure-related difficulties may be overcome by an antegrade
approach via the brachial artery with the guidewire being
snared in the aorta.

• After deployment, ballooning is not recommended, even if the

stent graft is not fully expanded, because of the self-expanding
nature of the stent and the time required for the remodelling
process of the aorta.

• Retrograde dissection and rupture of the dissection membrane

has been reported due to ballooning.
 INTRAPROCEDURAL MONITORING AND BLOOD
PRESSURE CONTROL

• Invasive blood pressure monitoring

• Pharmacological lowering of blood pressure <80 mmHg systolic

during stent-graft deployment may be sufficient in many cases
to avoid displacement of the device.

• If further blood pressure lowering is required in proximal aortic

procedures, then rapid pacing is the method of choice
• VASCULAR ACCESS

• Surgical cut-down is traditionally regarded as the safest way

to fully control access vessels.

• Percutaneous approaches are increasingly used with a wide

variety of techniques.

• At present, the diameter and calcification of the vessel

represent major limitations of these devices .

• Further reduction in the profile of stent-graft delivery device

will expand the indication for percutaneous approaches.
 TECHNIQUES FOR NON-SURGICAL SIDE BRANCH
ACCESS

• Aortic pathologies involving major side branches are a

complex challenge for endovascular repair.
• Implantation of a stent-graft may result in critical ischaemia
and organ dysfunction.

• Approaches include:
• (1) development of dedicated stent-graft prostheses with
fenestrations or branches for direct side branch access, and
• (2) modification of readily available interventional techniques
to establish extra-anatomic side branch perfusion (e.g.
‘Chimney’, ‘Sandwich’ technique etc.).
 Outcome parameters
• The closure rate of the primary entry tear and
thrombosis of the false lumen of the stented
segment of the thoracic aorta is high in most series,
but needs to be reported in the long term .

• Reasonable to accept continued perfusion of the

false lumen in the abdomen distal from the stent-
graft site as long as aortic dilatation does not occur
• Follow-up after TEVAR

• Lifelong clinical and morphological surveillance is

mandatory after TEVAR as late treatment failure may
develop even years after the initial treatment .

• Currently CTA is recommended prior to discharge.

Further follow-ups at 6 and 12 months is based on
CTA, thereafter MRI/CTA in addition to annual clinical
follow-up should be implemented.
 PENDING QUESTIONS
Malperfusion
• The value of extending the stented aortic segment into the
abdominal aorta for persisting malperfusion after TEVAR by
implantation of additional uncovered stents distally (PETTICOAT
concept) requires further data collection and evaluation .

Endoleaks
• The majority of endoleaks can be avoided by careful selection
particularly with regard to important morphological details such
as the length of the landing zone, use of multiple stents, length of
overlapping segments as well as severe angulation and massive
aortic calcification (porcelain aorta)
 PENDING QUESTIONS

• TEVAR induced neurologic injury: brain

• Brain injury after TEVAR is a major complication and most often
associated with the underlying pathology, excessive device
manipulation within the arch or intended or inadvertent
overstenting of one or more of the great vessels.

• Aggressively maintaining antegrade cerebral perfusion through

prior vascular transposition .
• Overstenting of the left subclavian artery is permissible in the
emergency setting (e.g. traumatic aortic injury), but is
inadvisable in elective cases due to a heightened risk of stroke
and spinal cord injury. Therefore, detailed information on
cerebral blood supply is required in elective situations
 PENDING QUESTIONS
• TEVAR induced neurologic injury: spinal cord

• Spinal cord injury can occur immediately after TEVAR or be delayed

• The risk may be increased with extended lengths of the covered
thoracic aortic segments .
• Recent reports underline the importance of maintaining collateral
blood supply via the left subclavian artery, lumbar arteries as well
as hypogastric arteries.
• Special attention has to be paid to patients with previous treatment
of AAA and intended coverage of subclavian artery by TEVAR. In
such cases pre-deployment subclavian transposition would appear
mandatory.
• In high-risk patients, preventive cerebrospinal fluid (CSF)
drainage, which has proven efficacy in spinal cord protection
during open thoraco-abdominal aneurysm surgery, is strongly
recommended .

• Reversal of paraplegia can be achieved by the immediate

initiation of CSF drainage and pharmacological elevation of blood
pressure (>90 mmHg mean arterial pressure).

• Hypotensive episodes during the procedure should be avoided.

Neurological outcomes seem to be better with delayed
occurrence of paraplegia than with immediate paraplegia after
TEVAR
• CONCLUSIONS

• The early results of TEVAR for non-acute Stanford type B

aortic dissection are favourable.

• However, for cases with patent false lumens, complete

obliteration of the false lumen of the entire aorta was
difficult to achieve.

• Absence of the primary entry at the outer curvature of the

distal aortic arch, younger age, small aortic diameter and
absence of the abdominal aortic branches arising from the
false lumen were the key success factors.
THANK YOU
Endovascular Versus Medical Therapy for Uncomplicated Type B Aortic Dissection
A Qualitative Review
1Division of Vascular and Endovascular Surgery, New York University School of

Medicine, New York, NY, USA

• Abstract
• Background: Uncomplicated type B dissections have been traditionally managed
with antihypertensive therapy. In the endovascular era, this dictum has been
revisited. This review pooled the available studies to compare the outcomes of
best medical therapy (BMT) to thoracic endovascular aortic repair (TEVAR) for
uncomplicated type B dissections.
• Methods: A literature search was performed to identify studies on uncomplicated
type B dissections managed with BMT with and without TEVAR. The primary
outcome measures were mortality rates at 30 days and at 2 years following
intervention.
• Results: A total of 6 studies included 123 patients who underwent TEVAR/BMT,
and 566 patients who had BMT alone. The mortality rates at 30 days (6.5%
TEVAR/BMT vs 4.8% BMT, P = .21) and at 2 years (9.7% vs 11.9%, P = .32) were
similar. Renal failure was greater in TEVAR/BMT (15.4% vs 2.1%, P < .01). Rates of
surgical reintervention/intervention were similar (17.6% vs 20.1%, P = .31).
• Conclusion: The TEVAR with BMT does not provide survival benefit compared to
BMT alone, 2 years following uncomplicated type B aortic dissection.
 Anatomy

• The aorta is composed of the intima, media, and adventitia. The intima,
the innermost layer, is thin, delicate, lined by endothelium, and easily
traumatized.
• The media is responsible for imparting strength to the aorta and consists
of laminated but intertwining sheets of elastic tissue. The arrangement of
these sheets in a spiral provides the aorta with its maximum allowable
tensile strength. The aortic media contains very little smooth muscle and
collagen between the elastic layers and thus has increased distensibility,
elasticity, and tensile strength. This contrasts with peripheral arteries,
which, in comparison, have more smooth muscle and collagen between
the elastic layers.
• The outermost layer of the aorta is adventitia. This largely consists of
collagen. The vasa vasorum, which supplies blood to the outer half of the
aortic wall, lies within the adventitia. The nervi vascularis, bundles of
nerve fibers found in the aortic adventitia, are involved in the production
of pain, which occurs with acute stretching of the aortic wall from a
dissection.[11] .The aorta does not have a serosal layer.
• The aorta plays an integral role in the forward circulation of
the blood in diastole. During left ventricular contraction,
the aorta is distended by blood flowing from the left
ventricle, and kinetic energy from the ventricle is
transformed into potential energy stored in the aortic wall.
During recoil of the aortic wall, this potential energy is
converted to kinetic energy, propelling the blood within the
aorta to the peripheral vasculature.
• The volume of blood ejected into the aorta, the compliance
of the aorta, and resistance to blood flow are responsible
for the systolic pressures within the aorta. Resistance is
mainly due to the tone of the peripheral vessels, although
the inertia exerted by the column of blood during
ventricular systole also plays a small part.
• The aorta has thoracic and abdominal regions. The thoracic aorta is
divided into the ascending, arch, and descending segments; the
abdominal aorta is divided into suprarenal and infrarenal segments.
The ascending aorta is the anterior tubular portion of the thoracic
aorta from the aortic root proximally to the innominate artery
distally. The ascending aorta is 5 cm long and is made up of the
aortic root and an upper tubular segment.
• The aortic root consists of the aortic valve, sinuses of Valsalva, and
left and right coronary arteries. It extends from the aortic valve to
the sinotubular junction and supports the base of the aortic
leaflets. The aortic root allows the 3 sinuses of Valsalva to bulge
outward, facilitating the full excursion of the leaflets in systole. The
left and right coronary arteries arise from these sinuses.
• The upper tubular segment of the ascending aorta starts at
the sinotubular junction and ends at the beginning of the
aortic arch. The ascending aorta lies slightly to the right of
the midline, with its proximal portion in the pericardial
cavity. Structures around the aorta include the pulmonary
artery anteriorly; the left atrium, right pulmonary artery,
and right mainstem bronchus posteriorly; and the right
atrium and superior vena cava to the right.
• The arch of the aorta curves upward between the
ascending aorta and descending aorta. The brachiocephalic
arteries originate from the aortic arch. Arteries that arise
from the aortic arch carry blood to the brain via the left
common carotid, innominate, and left subclavian arteries.
• The initial part of the aortic arch lies slightly left and in front of the
trachea; the arch ends posteriorly to the left of the trachea and
esophagus. Inferior to the arch is the pulmonary artery bifurcation,
the right pulmonary artery, and the left lung. The recurrent
laryngeal nerve passes beneath the distal arch, and the phrenic and
vagus nerves lie to the left. The junction between the aortic arch
and the descending aorta is called the aortic isthmus. The isthmus is
a common site for coarctations and trauma.
• The descending aorta extends from the area distal to the left
subclavian artery to the 12th intercostal space. Initially, the
descending aorta lies in the posterior mediastinum to the left of the
course of the vertebral column. It passes in front of the vertebral
column in its descent and ends behind the esophagus before
passing through the diaphragm at the level of the 12th thoracic
vertebra.
• The abdominal aorta extends from the descending aorta at the level
of the 12th thoracic vertebra to the level of bifurcation at the fourth
lumbar vertebra. The splanchnic arteries branch from the
abdominal aorta. The thoracoabdominal aorta is the combination of
the descending thoracic and abdominal aorta.
• With increasing age, the elasticity and distensibility of the aorta
decline, thus inducing the increase in pulse pressure observed in
elderly individuals. The progression of this process is exacerbated
by hypertension, coronary artery disease, or hypercholesterolemia.
• Histologically, the loss of distensibility is marked by fragmentation
of elastin and the resultant increase in collagen and, thus, a higher
collagen-to-elastin ratio. This, along with impairment in flow in the
vasa vasorum, may be responsible for the age-related changes.
These factors cumulatively lead to increased left ventricular systolic
pressure and wall tension with associated increases in end-diastolic
pressure and volume.