TABLE OF CONTENTS

THORACIC AORTIC DISEASES..................................................................... 1

I. THORACIC AORTIC ANEURYSM ....................................................... 1
A. ANATOMY OF THE AORTA ......................................................... 1
B. DEFINITION .................................................................................. 1
C. CAUSES ....................................................................................... 2
D. NATURAL HISTORY..................................................................... 3
E. CLINICAL MANIFESTATION ........................................................ 3
F. DIAGNOSTIC EVALUATION......................................................... 3
G. TREATMENT ................................................................................ 4
H. PREOPERATIVE ASSESSMENT AND PREPARATION ............... 4
II. AORTIC DISSECTION ......................................................................... 6
A. CLASSIFICATION ......................................................................... 6
B. CLINICAL MANIFESTATION ........................................................ 6
C. DIAGNOSTIC EVALUATION......................................................... 7
D. TREATMENT ................................................................................ 7
III. MARFAN SYNDROME......................................................................... 8
ANEURYSM AND DISSECTION ..................................................................... 8
I. AORTIC ANEURYSM........................................................................... 8
A. CLASSIFICATION ......................................................................... 8
II. ABDOMINAL AORTIC ANEURYSM (AAA)........................................... 9
A. ANATOMY | ............................................................................... 9
B. EPIDEMIOLOGY........................................................................... 9
C. RISK FACTORS............................................................................ 9
D. ETIOLOGY AND PATHOGENESIS ............................................... 9
E. NATURAL HISTORY..................................................................... 9
F. PHYSICAL EXAM ......................................................................... 9
G. CLINICAL MANIFESTATIONS ...................................................... 9
H. DIAGNOSIS ................................................................................ 10
III. RUPTURED ANEURYSM .................................................................. 10
A. DIAGNOSIS OF RUPTURED AAA .............................................. 10
B. SURGICAL MANAGEMENT........................................................ 11
IV. THORACIC AORTIC ANEURYSM (TAA) ........................................... 11
A. CAUSES OF TAA........................................................................ 11
B. DIAGNOSIS OF ASCENDING AORTIC ANEURYSMS ............... 12
C. SURGICAL INTERVENTION....................................................... 12
V. TRANSVERSE ARCH ANEURYSM ................................................... 12
A. INDICATIONS FOR SURGERY .................................................. 12
B. DIAGNOSIS OF DESCENDING AA ............................................ 13
C. SURGICAL MANAGEMENT........................................................ 13 Figure 1. Normal anatomy of thoracoabdominal aorta. Obtained from Schwartz.
D. THORACIC ENDOVASCULAR AORTIC REPAIR (TEVAR) ........ 13
E. THORACIC STENT-GRAFTS ..................................................... 14
VI. ACUTE AORTIC DISSECTION .......................................................... 14
A. TYPE I ........................................................................................ 15
B. MARFAN SYNDROME................................................................ 15
VII. QUESTION AND ANSWER PORTION............................................... 16
REFERENCES.............................................................................................. 16
IV. APPENDIX ......................................................................................... 17
TREATMENT OF THORACIC AORTIC ANEURYSM DEPENDING ON
ETIOLOGY .............................................................................................. 17

MUST KNOW BOOK PREVIOUS TRANS

THORACIC AORTIC DISEASES

I. THORACIC AORTIC ANEURYSM

A. ANATOMY OF THE AORTA

Figure 2. Anatomic location. Obtained from Dr. Purino’s PPT.
● Thoracic aorta is divided into 9 segments:
● From the aortic sinuses of Valsalva → running upwards to the
sinotubular junction → to the mid ascending aorta → to the
proximal aortic arch → mid aortic arch → proximal descending
aorta → mid descending aorta → aortic level of the diaphragm →
abdominal aorta at the celiac axis region
B. DEFINITION
● An aneurysm is a permanent, localized dilatation by at least 50%
increase in diameter compared to a normal segment
→ But according to doc, it is a localized dilatation by more than
50%.
● Can be classified as:
1. TRUE ANEURYSM
A-TG7 | Balilo | Arzadon, Asenci, Austria, Averia, Año Page 1 of 19
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21)
● Consist of all layers of the aorta
● Pulsating |
● Can be fusiform or saccular types |
→ Fusiform aneurysms - more common; symmetrical
dilatations of the aorta; even dilatation of all segments of
the aorta |
→ Saccular aneurysms - localized outpouchings of the aorta;
only one side is dilated |
2. FALSE ANEURYSM (Pseudoaneurysm)
● Only outer layer is aneurysmal/dilated (contained hematoma)
● Pulsating |
● Actually, a contained rupture; with leak that can form a bulge |
● Leaks in the aortic wall contained by the outer layer and/or
periaortic tissue |
● Caused by disruption of aortic wall and lead blood to collect in
pouches of fibrotic tissue |
● As to the shape, it can be either:
→ Fusiform – even dilatation of all segments of the aorta
→ Saccular – only one side is dilated
C. CAUSES
● Normal strength of the aortic wall is because of the medial layer
with interplay of elastin, collagen, smooth muscle cells and
ground substance
● Follow the Laplace Law
→ Tension = pressure x radius
→ As the pressure increases as well as the radius or diameter,
tension within the aneurysm sac increases, thus making it
prone to rupture
→ Rupture risk is directly related to aneurysm size as predicted
by Laplace Law |
■ Considers maximum transverse diameter of the aneurysm
| → Further studies needed to delineate the underlying
● Atherosclerosis is a coexistent factor rather than a direct
cause
GENETIC DISORDERS
● Marfan Syndrome
→ Autosomal dominant |
→ Specific connective tissue defect that leads to aneurysm
formation |
→ Tall stature, high palate, joint hypermobility, eye lens
disorders, mitral valve prolapse, aortic aneurysm
→ This is caused by fragmentation of elastic fibers and cystic
medial degeneration
→ 75-85% have dilatation of the ascending aorta and
annuloaortic ectasia
→ More recent evidence shows that abnormal fibrillin causes
degeneration of the aortic wall matrix by increasing the activity
of transforming growth factor beta (TGF-β) |
→ Aortic complications are the most common cause of death
among patients with Marfan Syndrome |
● Ehlers-Danlos Syndrome
→ Autosomal dominant defect in Type III collagen synthesis
→ Less involvement of thoracic aorta
→ But when they occur, they pose a particularly challenging
surgical problem due to the reduced integrity of the aortic
tissue |
→ Spontaneous arterial rupture, usually involving mesenteric
vessels, is the most common cause of death in these patients
| ● Termed “mycotic aneurysm” |
● Loeys-Dietz syndrome
→ Arterial tortuosity, hypertension, hypertelorism
→ Phenotypically distinct from Marfan syndrome
→ Aneurysmal syndrome with widespread systemic involvement
| → S. aureus, S. epidermidis, Salmonella, Streptococcus
→ Aggressive autosomal dominant condition
→ Triad: Arterial tortuosity and aneurysms, hypertelorism (widely
spaced eyes), and bifid uvula or cleft palate |
Page 2 of 19
→ Increased risk of aortic rupture and dissection
→ Diameter-based thresholds of repair tend to be lower for these
patients than for patients with other heritable disorders |
FAMILIAL AORTIC ANEURYSMS
● At least 20% of the population have a genetic predisposition
● Involved mutations: autosomal dominant with decreased
penetrance and variable expression |
● Involved genes include those related to: TGF-β receptors, TGF-
β ligands, myosin, elastin, elastin microfibril interfacer 1
(EMLIN1), microfibril-associated glycoprotein 2, fibrillin-2, fibulin-
4, lysyl oxidase, α-smooth muscle cell actin |
ANEURYSM-OSTEOARTHRITIS SYNDROME |
● Autosomal dominant; mutations in gene encoding SMAD3
● Characterized by:
→ Aortic and arterial aneurysms, arterial tortuosity, aortic
dissection, mild craniofacial abnormalities, and early-onset
arthritis
CONGENITAL BICUSPID AORTIC VALVE
● Most common congenital malformation of the heart or great
vessels |
● Increased incidence in ascending aortic aneurysm
● Congenital defect involving aortic wall matrix
● Hemodynamic stress because of turbulent flow in the diseased
valve
● Dilatation usually is limited to the ascending aorta and root |
→ Occasionally found in the aortic arch
→ Rarely seen in descending or abdominal aorta
BOVINE AORTIC ARCH |
● Common origin of innominate and left common carotid artery
● Higher prevalence in patients with thoracic aortic disease
● Precursor of aortic aneurysm
mechanism for this association
NONSPECIFIC MEDIAL DEGENERATION |
● Most common cause of thoracic aortic aneurysm |
● Underlying causes remain poorly understood
● Histologic findings of mild medial degeneration:
→ Fragmentation of elastic fibers and loss of smooth muscle cells
- expected in an aging aorta
● In advanced, accelerated form of medial degeneration
→ Progressive weakening of the aortic wall
→ Aneurysm formation
→ Eventual dissection, rupture, or both
AORTIC DISSECTION
● Usually begins as a tear in the inner aortic wall → initiates a
progressive separation of medial layers → creates 2 channels
within the aorta |
● Most common catastrophe involving the aorta |
→ Represents a major distinct cause of thoracic aortic
aneurysms
● Weakens the false lumen caused by the dissection
AORTITIS
● Patients with preexisting degenerative aneurysm can have
infection of that aneurysm
● Cause is unknown
● Ex. Takayasu arteritis, giant cell arteritis, rheumatoid aortitis
INFECTION
● Rare
● Caused by bacteria rather than fungi |
→ Bacterial endocarditis, endothelial trauma, extension from
infected laminar clot
● Often produce saccular aneurysm rather than the fusiform
type |
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PSEUDOANEURYSM → Thoracoabdominal aortic aneurysms can cause duodenal

● Chronic contained leaks obstruction, or if they erode through bowel wall, GI bleeding |
● Ruptured aneurysm that was contained by surrounding
structures (e.g. adventitia and fatty layer) → Descending thoracic and thoracoabdominal aortic
● Wall develops from organized thrombus and associated fibrosis; aneurysm frequently causes back pain
not formed by intact aortic tissue | → Spinal instability, hemoptysis, airway obstruction,
hematemesis
→ Erosion into the IVC or iliac vein = abdominal bruit, widened
pulse pressure, edema, and heart failure |
● Aortic Valve Regurgitation
→ Causes displacement of the aortic valve commissures, and
aortic root dilatation
● Distal Embolization
→ Descending thoracic and thoracoabdominal aortic aneurysm
are frequently lined with friable atheromatous plaque and
mural thrombus that can embolize and rupture
→ Debris may embolize distally, causing occlusion and
thrombosis of the visceral, renal, or lower extremity branches
|
● Rupture
→ Sudden, severe pain in the
■ Anterior chest (ascending aorta) | ,
■ Upper back or left chest (descending aorta),
■ Left flank (thoracoabdominal aorta)
■ * Can connote a rupture
→ Ascending aortic aneurysm rupture = usually bleed into
Figure 3. Causes of thoracic aortic aneurysm. Obtained from 2020 Trans. | pericardial space → acute cardiac tamponade and death. |
Table 1. Summary table of classifications of Aortic Aneurysm |
Types Location Shape Etiology → Descending aortic aneurysm rupture = into pleural cavity →
True Thoracic Fusiform Degenerative severe hemorrhagic shock and respiratory compromise |
Dissecting Thoracoabdominal Saccular CTD
False Abdominal Congenital F. DIAGNOSTIC EVALUATION
Infectious ● Cross-sectional imaging is needed for definitive diagnosis |
Inflammation ● Plain radiography
Post-dissection → Plain radiography of chest, abdomen, or spine often enough
Post-stenosis to support initial diagnosis of thoracic aortic aneurysm |
Pseudoaneurysm
→ Ascending aortic aneurysm produces a convex shadow to
Miscellaneous
the right of the cardiac silhouette
D. NATURAL HISTORY → Loss of retrosternal space = anterior projection of ascending
● Rate of expansion is about aneurysm |
→ 0.07 cm/yr in ascending aorta, → An aneurysm may be indistinguishable from elongation and
→ 0.19 cm/yr in descending thoracic aorta tortuosity |
● Critical diameter for repair is → Plain CXRs may reveal convexity in the right superior
→ 6.0 cm for ascending aorta, mediastinum, loss of retrosternal space, or widening of
→ 7.0 cm in descending thoracic aorta descending thoracic aortic shadow |
● Certain types have increased risk of rupture → However, most would often appear normal
→ with Marfan Syndrome → Additional studies required to define extent of aortic
→ Saccular type involvement |
● 27% of patients with 5cm ascending aorta during aortic valve
replacement have aortic dissection
E. CLINICAL MANIFESTATION
● Asymptomatic (most common; usually incidental finding) |
● Local compression and erosion
→ Most common symptom of ascending aortic aneurysm =
anterior chest discomfort |
→ Aneurysms of the ascending aorta and transverse aortic
arch can cause symptoms related to compression of SVC, PA,
airway, or sternum |
→ Expansion of the distal aortic arch aneurysm can stretch the
recurrent laryngeal nerve causing vocal cord paralysis and
hoarseness
→ When aneurysm is largest in the aortic hiatus, it may cause
middle back and epigastric pain Figure 4. Chest radiograph showing calcified rim (arrows) in aortic wall of
→ Thoracic and lumbar vertebral body erosion typically causes thoracoabdominal aortic aneurysm; A - AP view, B - Lateral view; arrows point to
the bulging (latent segment of the descending thoracic aorta). Obtained from Dr.
severe, chronic back pain | Purino’s PPT.
→ Descending thoracic aortic aneurysms may cause varying
degrees of airway obstruction, as cough, wheezing, stridor, or ● Ultrasonography
→ Useful in abdominal aorta
pneumonitis. Compression and erosion = hemoptysis |
→ Limited use in thoracic aorta
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21)
● Echocardiography
→ Provides excellent visualization of ascending aorta and aortic
root
→ Both TTE and TEE provide excellent visualization of
ascending aorta and aortic root |
→ TEE: Descending thoracic aorta can be visualized
● Computed Tomography
→ Most common and most useful imaging modality for evaluating
thoracic aortic aneurysms |
→ Determine exact diameter and involved segment, especially in
the presence of laminated clot, and detects aortic calcification
→ Major disadvantage: risk of contrast-induced nephropathy in
patients who are at risk |
■ 1 day after contrast examination - observe renal function
and permit diuresis |
● Magnetic resonance imaging
→ Produces images comparable to CT scan
→ Not suitable for many critically ill patients
● Aortography and Cardiac catheterization
→ Aortography is now replaced by CT scan because it is less
invasive
→ Usefulness is now in the uptrend because of the advent of
endovascular therapy
■ You need aortography to evaluate deployment of your
endovascular grafts or pre-deployment of your
endovascular grafts
→ Cardiac catheterization is still useful for pre-op planning |
■ Risks:
− Limit images to intraluminal diameter
− Can cause thrombus embolization
− 0.6 to 1.2% risk of stroke
− Allergy
− Contrast nephropathy
G. TREATMENT
● Symptomatic patients must be treated as rupture until proven
otherwise |
● If hemodynamically stable and intact aneurysm on CT, admit the
patient for BP control with IV antihypertensives and repair
aneurysm within 12-24 hours |
● If hemodynamically unstable, history of back pain, syncope, and
known unrepaired AAA or with a pulsatile abdominal |
● Determination of the appropriate treatment
→ Management begins with patient education, especially if
asymptomatic
→ Assess pertinent symptoms and signs
→ Assess for presence of genetic defects
→ Become surgical candidates if symptomatic or size reaches its
limit
● Determination of the extent and severity of the disease
→ Serial CT scans are critical when evaluating an aneurysm,
determining treatment, and planning necessary procedures |
→ Staged operative repair in complex aneurysm, rather than
single repair
→ Proximal aneurysm is usually addressed first via sternotomy
approach |
● Indications for operation
→ Elective repair is recommended in either of the following:
■ Ascending aorta >5.5cm
■ Descending aorta >6.5cm
■ Increase in size of >1cm per year (>0.5cm in book) |
→ In patients with heritable disorders such as Marfan and Loeys-
Dietz syndromes, the threshold for operation is based on a
smaller aortic diameter, and in patients with aortic valve
regurgitation|
→ Smaller threshold in patients with genetic defects like Loeys-
Dietz syndrome and in patients with aortic valve regurgitation
→ Presence of symptoms like chest pain also influences decision
to operate
Page 4 of 19
→ Patients who present with symptoms may need urgent
operation. Symptomatic patients are at increased risk of
rupture and warrant expeditious evaluation. The onset of new
pain in patients with known aneurysms is especially
concerning because it may herald significant expansion,
leakage, or impending rupture. Emergent intervention is
reserved for patients who present with aneurysm |
→ Rupture or superimposed acute dissection. |
● Operative Mortality |
→ 4-6%= elective aneurysm repair
→ 19%= urgent aortic repair
→ 50%= repair of ruptured aneurysm
● Open surgical repair |
→ Traditional open operations to repair proximal aortic
aneurysms—which involve the ascending aorta, trans- verse
aortic arch, or both—are performed through a midsternal
incision and require cardiopulmonary bypass.
→ Midline transabdominal incision is the common approach
→ Uses general anesthesia
→ Main advantage: AAA is permanently eliminated because it is
replaced by a prosthetic aortic graft
→ No risk for recurrence and decreased need for long-term
imaging surveillance
→ Other advantages: can properly assess circulation of colon
and allows exploration of other abdominal pathologies
→ Risks: Cardiac complications (most common), ischemic colitis,
renal failure, atheromatous embolization, injury to ureter,
contrast induced nephropathy, or suprarenal aortic clamping
● Endovascular repair |
→ Minimally invasive procedure and shorter hospital stay than
open repair
→ For patients with increased risk for surgery due to age or
comorbidities (severe pulmonary disease and severe
cardiopulmonary dysfunction)
→ Implantation of an aortic stent graft that is fixed proximally and
distally to nonaneurysmal aortoiliac segment
→ Aneurysmal sac is not resected, increase risk for continued
expansion or rupture
→ Uses epidural or regional anesthesia
→ Endoleak can occur - blood flow outside the lumen of the graft
but within the aneurysmal sac |
→ Endovascular repair is accepted especially in descending
thoracic aorta and is the best option in patients who are older
and have significant comorbidities
→ Requirement:
■ Size of proximal and distal neck should be at least 20mm
and appropriate size for adequate sealing, adequate
diameter of access vessels like the femoral or iliac arteries
→ Patients with significant atheroma, and those with connective
tissue disease are best approached via open repair
*Figures for ascending aortic aneurysm of degenerative and genetic
etiologies placed in appendix (Figures 51 & 52)
H. PREOPERATIVE ASSESSMENT AND PREPARATION
● Cardiac evaluation
→ Presence of Coronary Artery Disease and valvular Heart
Disease
→ Coronary Angiography and Cardiac Catheterization
→ Transthoracic echocardiography is a satisfactory noninvasive
method for evaluating both valvular and biventricular function.
|
→ Dipyridamole-thallium myocardial scanning identifies regions
of myocardium that have reversible ischemia, and this test is
more practical than exercise testing in older patients with
concomitant lower-extremity peripheral vascular disease. |
→ Cardiac catheterization and coronary arteriography are
performed in patients who have evidence of coronary disease
|
● Pulmonary Evaluation
→ Pulmonary function screening with ABG and spirometry
→ Good surgical candidates for open surgical repair
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 5 of 19

■ FEV1 > 1.0 L

■ PaCO < 45 mmHg
2

→ Poor pulmonary risk; smoking cessation, weight loss, change

operative approach
→ Preserve the recurrent laryngeal nerve, phrenic nerve and
diaphragmatic function
● Renal Evaluation
→ Measure serum electrolytes, blood urea nitrogen and
creatinine
→ Evaluate kidney from CT Aortogram
→ Patients with severe renal impairment have higher mortality
and often need dialysis after surgery
→ Patients with renal artery stenosis can undergo
endarterectomy, stenting or bypass during aneurysm repair Figure 7. Extensive Thoracoabdominal aneurysm featuring a 2-stage approach.
Obtained from Dr. Purino’s PPT.

Figure 5. Crawford Classification. Repair is according to classification. Obtained

from Dr. Purino’s PPT.
● Indications for repair
→ Rupture
→ Acute dissection resulting in malperfusion or other life altering
complications
Figure 8. First stage. The elephant trunk approach with a concomitant island
→ Symptomatic states brachiocephalic artery reattachment. Contemporary Y-graft arch repairs include.
→ Pain consistent with rupture and unexplained by other causes Repair ascending aorta then leave a limb of the graft inside the descending
→ Compression of adjacent organs thoracic aneurysm. Obtained from Schwartz.
→ Documented enlargement more than or equal to 1cm/year, or
substantial growth approaching absolute size criteria
→ Absolute size >6.5cm or >6cm in patients with connective
tissue disorders

Figure 9. Second stage. The distal repair uses the floating “trunk”/limb for the
proximal anastomosis. Obtained from Schwartz.

Figure 10. Illustration of a “Zone 0” hybrid approach—which combines open and

endovascular techniques—for repair of an extensive aortic aneurysm.
Debranching the arch and thoracoabdominal segments allows the use of a series
Figure 6. Treatment of Aortic Aneurysm. Ascending aorta replaced by graft.
of endovascular stent grafts (more proximal) to exclude the entire aneurysm.
Obtained from Schwartz.
Note that the arterial inflow for the debranched visceral arteries comes from the
left common iliac artery. Obtained from Schwartz.
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 6 of 19

Table 3. DeBakey Classification of Aortic Dissection

Type I Type II Type III
Entry tear Proximal to the left Proximal Beyond the left
subclavian artery to the left subclavian artery
subclavian
artery
Aorta Ascending and Ascending Descending
involved descending aorta aorta aorta
(entire aorta)
Type IIIa
Involves only the
Figure 11. Thoracic Endovascular Aortic repair (TEVAR). Access vessel thoracic aorta
(Femoral Artery) is canulated. Guide wire is used to measure the size and sight
where to deploy the graft. On the third picture, stent graph is excluding the
aneurysm. You must have a good sealing proximally and distally so there would Type IIIb
be no flow to aneurysmal sac otherwise there could be embolus leading to the Both thoracic
aneurysmal sac being pressurized and ultimately ruptured. Obtained from Dr. and abdominal
Purino’s PPT. aorta
II. AORTIC DISSECTION
● The most common catastrophic event involving the aorta.
● A progressive separation of the aortic wall layers that usually
occurs after a tear forms in the intima and inner media. |
● Is an event of sudden onset in which blood leaves the normal
aortic channel through a usually discrete point of exit (intimal
tear) and rapidly dissects the inner from the outer layer of the
media to produce a false channel. |
● Results in creation of true and false lumen
● Complications: rupture, malperfusion, pain, ischemia, stroke
● Can happen anytime and in high frequency
● Acute: diagnosis is made within 2 weeks after onset of
Figure 13. DeBakey Classification of Aortic Dissection. Obtained from 2022 trans.
symptoms. |
● Dissection: development of a hematoma within the middle to ● The Stanford type A corresponds to DeBakey types I & II while
outer third of the aortic media. | Stanford type B corresponds to DeBakey type III.

A. CLASSIFICATION B. CLINICAL MANIFESTATION

● Basis: entry tear |
● Two classifications used:
→ Stanford Classification
→ DeBakey Classification
Figure 12. Illustration of the classification of aortic dissection based on which
portions of the aorta are involved. Ascending aorta (left), descending aorta
(middle) or entire aorta (right). Obtained from Schwartz.
Table 2. Stanford Classification of Aortic Dissection
Type A
~60%
Entry tear Proximal to the left
subclavian artery
Management Surgery
Complications - Coronary artery
occlusion
-Aortic incompetence/
regurgitation
- Rupture into the
pericardial sac →
cardiac tamponade
● Associated with severe “tearing” chest pain that migrates distally
as the dissection progresses along the length of the aorta
● Location of the pain reflects what segments of the aorta are
involved. (Anterior chest – ascending aorta; back and abdomen
– descending thoracoabdominal aorta)
● Dynamic Malperfusion |
→ The artery is perfused by the true lumen, which is compressed
by the false lumen
● Malperfusion syndrome |
→ Malperfusion of the arteries and organs of the lower abdomen
(those supplied by the abdominal aorta)
Table 4. Anatomic manifestations of aortic dissection and their associated signs
and symptoms.
Anatomic Manifestation Signs & Symptoms
Aortic valve insufficiency Dyspnea
Murmur
Pulmonary rales
Shock
Coronary malperfusion Chest pain with characteristic of
angina
Nausea, vomiting
Type B Shock
~40% Ischemic changes on ECG
Beyond the left Elevated cardiac enzymes
subclavian artery Pericardial tamponade Dyspnea
Medical Jugular vein distention
(w/ BP control) Pulsus paradoxus
Muffled cardiac tones
Shock
Low-voltage ECG
Subclavian or iliofemoral Cold, painful extremity
artery malperfusion Extremity motor and sensory
deficit
Peripheral pulse deficit
Carotid artery malperfusion Syncope
Focal neurologic deficit
(transient or persistent)
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 7 of 19

Carotid pulse deficit → Delayed treatment maybe done in stable and closely
Coma monitored patients to make the aortic tissues less friable
Spinal malperfusion Paraplegia ● Chronic Ascending Aortic Dissections
Incontinence → Treated as same as the Acute Dissection
Mesenteric malperfusion Nausea, vomiting ■ Difference: the septum between the true and false lumen is
Abdominal pain not remodeled but rather fenestrated to supply both lumen
Renal malperfusion Oliguria or anuria ● Chronic Dissection
Hematuria → False lumen is not obliterated
■ The septum must be fenestrated/cut to have blood flow
C. DIAGNOSTIC EVALUATION from the prosthetic graft to the true and false lumen
● Needs high index of suspicion especially in younger patients − Because in chronic dissection, some of the arteries
● Clinical signs and symptoms | would be supplied by the false lumen and some by the
● Most would experience pain in the chest, back or abdomen true lumen
characterized as sudden, sharp or tearing, severe pain as − You can’t occlude the false lumen because some
dissection migrates distally. | arteries may also be occluded which may cause
● There would be discrepancy in the blood pressures in the symptoms
extremities ● Descending Thoracic Aortic Dissection
● CT aortogram has a sensitivity of 98% and specificity of 87% → Usually managed medically except in presence of
● MRA is 98% sensitive and specific and is now considered the complications like rupture, malperfusion, intractable pain,
gold standard | ischemic symptoms
→ Not readily available in other institutions OPEN REPAIR FOR ACUTE ASCENDING AORTIC DISSECTION
→ Of limited use in critically-ill patients ● False lumen is obliterated and sandwiched between two
● For unstable patient TEE is 98% sensitive and 95% specific for prosthetic graft
ascending aortic dissection ● The ascending aorta is replaced by a polyester (Dacron) graft
● Coronary angiography should be done prior to repair → Flow of blood will now be from the dacron graft to the true
● Especially in patients at risk of or with existing coronary artery lumen
disease
D. TREATMENT

Figure 15. Proximal aortic repair for acute ascending aortic dissection. Obtained
from Schwartz.
*You may want to check p.883 of Schwartz for the step-by-step procedure
OPEN REPAIR FFOR DESCENDING AORTIC DISSECTION
● Patient is put in a decubitus position
● Done with a cardiopulmonary bypass machine
→ Left heart bypass

Figure 14. Algorithm for acute aortic dissection. Obtained from Schwartz.
● The same for all types and focuses on initial medical therapy
● Aim: is to lower cardiac contractility and blood pressure |
● Medications used:
→ Beta adrenergic blockers
→ Vasodilators
→ CCBs
→ ACEIs
● Ascending Aortic Dissections
→ Treated as an emergency because of high rate of complication
and mortality if delayed
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 8 of 19

A. CLASSIFICATION
● I (Type)
→ True
→ Dissecting
→ False
● II (Location)
→ Thoracic
→ Thoracoabdominal
→ Abdominal
● III (Shape)
→ Fusiform
→ Saccular
● IV (Etiology)
→ Degenerative
→ CTD
→ Congenital
→ Infectious
→ Inflammation
→ Post-dissection
→ Post-stenosis
→ Pseudoaneurysm
→ Miscellaneous
ACCORDING TO TYPE
● True Aneurysm
→ dilatation involving all layers of the aortic wall
→ Pulsating
→ Two forms: saccular and fusiform |
● False Aneurysm/Pseudoaneurysm
→ a break in the wall producing a contained hematoma sac
→ May enlarge overtime and rupture
→ Pulsating |
→ Actually, a contained rupture |
→ With leak that can form a bulge |
Q ● Dissecting Aneurysm
Figure 16. Distal aortic repair of a chronic aortic dissection. Obtained from → progressive separation of the aortic intima from the rest of the
Schwartz.
*You may want to check p.886 of Schwartz for the step-by-step procedure
media
ENDOVASCULAR REPAIR
● Same principle as for aneurysm but the goal is to cover the entry
tear and remodel the distal aorta
● Needs spinal cord protection because of the coverage of spinal
arteries
● Limited by the presence of visceral and renal vessels
III. MARFAN SYNDROME
● An autosomal dominant genetic disorder characterized by a
specific connective tissue defect that leads to aneurysm
formation |
● Mutation in fibrillin gene on the long arm of chromosome 15 | Figure 17. Types of Aneurysm. Obtained from 2022 transcript.
● Phenotype:
→ Arm span is longer than height ACCORDING TO SHAPE
→ Tall stature, high palate, joint hypermobility, eye lens ● Fusiform
disorders, mitral valve prolapse, and aortic aneurysms → an exert circumferential dilatation of the aortic wall
● Signs: → An even dilatation of all segments of the aorta
→ Thumb sign → More common |
→ Wrist sign → Symmetrical dilatation |
● Saccular
ANEURYSM AND DISSECTION → Only one side is dilated
→ eccentric dilatation
I. AORTIC ANEURYSM
→ More prone to rupture; must be treated aggressively
● The most dreaded form of aortic pathology → Localized outpouchings of the aorta |
● Weakness in the aortic wall due to plaque deposition in the intima
leads to dilatation of the aorta |
● ANEURYSM
→ Greek “ANEURYSMA”- a widening
→ A permanent localized dilatation of an artery having at least
50% increase in diameter compared with the expected normal
diameter (Rutherford 2005).
→ >½ of normal diameter
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 9 of 19

● Excessive activity of proteolytic enzymes leads to deterioration

of elastin and collagen in the aortic media
● Aneurysm size
→ Single most important predictor of aneurysm rupture |

Figure 18. Types of Aneurysm according to shape. Obtained from 2022

transcript.

II. ABDOMINAL AORTIC ANEURYSM (AAA)

● Incidence is increasing due to improvements in diagnostic
imaging and growing elderly population
● Inflammatory AAA Figure 19. Pathogenesis of Aneurysm. Obtained from 2022 transcript.
→ presence of aneurysmal wall thickening, adjacent peritoneum
fibrosis, and rigid adherence of adjacent structures to anterior ACC/AHA Atherosclerotic Risk Factors Recommendations
aneurysmal wall Class I
● Infectious or mycotic AAA ● In patients with AAAs, BP and fasting serum lipid values should
→ associated with high mortality be monitored and controlled as recommended for patients with
atherosclerotic disease (LOE:C)
A. ANATOMY | ● Patients with aneurysms or a family history of aneurysms
● Defined as a pathologic focal dilation of the aorta greater than should be advised to stop smoking and be offered smoking
30mm or diameter is 1.5 times more than the adjacent normal cessation interventions, including behavior modification, nicotine
aorta replacement, or bupropion (LOE: B)
● Males tend to have larger aortas *LOE = Level of Evidence
● 90% are infrarenal and have a fusiform morphology
E. NATURAL HISTORY
● Women have higher chance for juxtarenal and suprarenal AAA
● Exhibits a “staccato” pattern of growth, alternating between
B. EPIDEMIOLOGY quiescence and expansion
● There is an “age-related” increase in abdominal aortic diameter ● Natural history is to expand and rupture
● Prevalence of aneurysm (aortic diameter of ≥3 cm) in men ● Average aggregate growth is 3-4mm/year
increases 6% per decade ● Rupture risk is directed related to aneurysm size as predicted by
● Clinically significant aneurysms (≥4 cm) occur in 1% of men 55- Laplace’s Law.
64 years → Considers the maximum transverse diameter of the aneurysm
→ Prevalence increases 2-4% per decade thereafter ● Below 5.5cm, elective repair is recommended provided that the
→ Warrants regular follow-up due to increased rate of rupture surgical mortality is below 5%
● Women are at higher risk for rupture, therefore elective repair is
C. RISK FACTORS recommended until 4.5-5cm
● Advancing age ● Expansion below this can be monitored by UTZ or CT scan every
● Male gender (M:F 2-6:1) (strong risk for inflammatory AAA) 6 months
● Family history ● Unless symptomatic or ruptured, AAA repair is a prophylactic
● Tobacco use repair
→ Strongest independent risk factor |
→ 90% of cases have smoked F. PHYSICAL EXAM
→ Smoking for >40 years has 6-fold increased risk ● Pulsatile mass (+/- tenderness)
→ Cessation of smoking reduces risk to 1/30 ● No risk is known to be associated with palpation of abdominal
→ Strong risk factor for inflammatory AAA | aorta
● Atherosclerotic Diseases | → Palpation is the best guide in 75% of AAA
→ Careful palpation of a pulsatile abdominal mass is a
● Hypertension- faster rate of enlargement |
confirmatory finding for diagnosis of AAA |
● Coronary Artery Disease |
→ Small size has lesser chance to be detected |
● COPD | → Sensitivity of abdominal palpation = more sensitive as the
● Incidence rises rapidly after aneurysm enlarges |
→ 50 years of age in Men → Palpate lower extremity artery pulses
→ 60 years of age in Women (protected by menstruation) |
Table 5. Sensitivity of abdominal palpation
● Maximum prevalence:
→ 5.9% in males 80-85 y/o AAA Dimension Sensitivity
→ 4.5% in females >90 y/o 3.0-3.9 cm 29%
4.0-4.9 cm 50%
D. ETIOLOGY AND PATHOGENESIS ≥5.0 cm 76%
● Pathogenesis is complex and multifactorial
● Most common cause of AAA development - aortic wall ● Bruits arising from associated narrowed arteries
degeneration due to atherosclerosis; MMP and proteolytic ● “To and fro” murmur - may suggest an aorto-caval fistula
enzymes are abundant in AAA walls → Fistula = blood from aorta to IVC
Infrarenal Abdominal Aorta G. CLINICAL MANIFESTATIONS
● Above and below the umbilical area ● Asymptomatic
● Most affected by atherosclerosis ● Pain - if present, surgery becomes more urgent |
● Most common site of abdominal aneurysm formation → Most frequent complaint |
→ Bifurcation of the aorta to R & L iliac in the umbilical area → Hypogastric or lower back
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 10 of 19

→ Hip claudication ● Difficult to establish in the field but it is possible to recognize

→ Steady, lasting for hours to days, gnawing certain salient features
→ Pressure on adjacent structures ● Imaging techniques: expedient CT Scan, and timely surgical
→ Leakage of blood intro retroperitoneum repair will save patients from sure mortality
● Once rupture has taken place, mortality, despite surgery, might
be as high as 50-60%
→ Hypotension, syncope, cold clammy perspiration
→ Retroperitoneum
■ Hypotension, pulsatile abdominal mass
→ GIT
■ Hematemesis, melena
→ Vena cava
Figure 20. Patient with a relaxed abdomen after anesthesia. Aneurysm becomes
■ Continuous bruit, prominent veins, cardiac failure, wide
more prominent. Obtained from 2022 transcript. pulse pressure

Figure 21. Left-sided retroperitoneal pulsatile mass is typical on exploration.

Obtained from 2022 transcript.
Figure 22. Plain x-ray of abdomen may show calcification pattern along
H. DIAGNOSIS aneurysm wall. Obtained from 2022 transcript.
● Preoperative evaluation should include: history and PE, Symptomatic Aortic Aneurysm Recommendations
particularly to symptoms referable to aneurysm, history of pelvic ● CLASS I
surgery or radiation, claudication, lower extremity bypass or other → In patients with the clinical triad of:
femoral reconstructive procedures, chronic renal insufficiency, ■ Abdominal and/or low back pain
and contrast allergy ■ Pulsatile abdominal mass
● Cross-sectional imaging is needed for definitive diagnosis ■ Hypotension
● CT scans remain the gold standard for determination of → Immediate surgical evaluation is indicated. (LOE: B)
anatomic eligibility for endovascular repair ● In patients with symptomatic aortic aneurysms, repair is indicated
III. RUPTURED ANEURYSM regardless of diameter. (LOE: C) |
● Heralded by new or worsening pain that is constant, severe Abdominal Ultrasound
located in the lower back ● Most practical screening method |
● Triad: (sure signs of impending rupture) → Least expensive, non-invasive
→ Abdominal and/or low back pain → Can be performed at bedside
→ Pulsatile abdominal mass → Detects peritoneal blood
→ Hypotension ● Accurately defines size within +/- 0.3 cm
Table 6. Annualized risk of rupture of aortic aneurysm based on size. ● Limitations:
ANNUALIZED RISK OF RUPTURE OF AAA BASED ON SIZE → Cannot detect - suprarenal involvement and pelvic extent
Description Diameter of Estimated Estimated 5- → Limited by bowel gas and obesity
Aorta Annual Risk of year Risk of ● Ideal screening test |
Rupture (%) Rupture (%)
Normal Aorta 2-3cm 0 0 (unless AAA CT Scan
develops) ● Gold standard in determining eligibility for endovascular repair |
Small 4-5cm 1 5-10
Moderate 5-6cm 2-5 30-40 ● Better defines shape, extent, and local anatomical relationships
Large 6-7cm 3-10 >50 ● Accurate method for diagnosing and sizing to within +/- 0.2 cm
Very Large >7cm >10 Approaching ● Higher cost
100 ● Use of contrast material
● <5.5 cm = elective repair is recommended, provided that surgical ● Provides detailed image of aneurysm, especially if surgery is
mortality is <5% contemplated |
● Women are at a higher risk for rupture, therefore elective repair ● If the patient is hypotensive, don’t do CT anymore. Proceed to
is recommended until 4.5-5 cm surgery! |
● Expansion below this can be monitored by UTZ or CT scan every Aortography
6 months ● Gold standard imaging modality for pre-operative definition of
● Unless symptomatic or ruptured, abdominal aortic aneurysm AAA anatomy |
repair is prophylactic repair ● Excellent for defining adjacent arterial involvement
A. DIAGNOSIS OF RUPTURED AAA → Renal artery anatomy
● 65% of patients with ruptured AAA die from sudden CV collapse → Mesenteric arterial anatomy
before reaching the hospital → Iliofemoral artery
→ Requires a high index of suspicion ● Evaluation prior to endovascular procedure
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 11 of 19

● Because of CT Scan and MRI, aortograms are not performed as

frequently |
● Indications for angiography: |
→ Isolated concomitant iliac occlusive disease (in <10% of AAA
patients)
→ Unusual renovascular anatomy

Figure 27. Endovascular Aortic Repair (EVAR) as alternative to Open Repair,

especially in high-risk patients. Obtained from 2022 transcript.

B. SURGICAL MANAGEMENT
● Elective aneurysmectomy doubles life-span of the patient
● Operative mortality
→ 4-6% = elective aneurysm repair
→ 19% = urgent aortic repair
→ 50% = repair of ruptured aneurysm
● Symptomatic patients must be treated as rupture, until proven
otherwise |
● If hemodynamically stable and intact aneurysm on CT, admit the
patient for BP control with IV antihypertensives, and repair
Figure 23. Illustrations of some of the important steps in open repair of an aneurysm within 12-24 hours |
abdominal aortic aneurysm, such as isolation, proximal and distal control, ● If hemodynamically unstable, history of back pain, syncope, and
resection and graft interposition. Obtained from 2022 transcript. known unrepaired AAA or with pulsatile abdominal mass - bring
to OR immediately! |
| KEY POINTS
● Surgical repair provides best outcome due to its durability, and less
incidence of reintervention
● Abdominal aortic aneurysms should be repaired when the risk of
rupture (mainly by size), exceeds the risk of death due to
perioperative complications or concurrent illness
● Endovascular repair is associated with less perioperative morbidity
and mortality compared to open reconstruction, and is preferred for
high-risk patients who meet specific anatomic criteria
Figure 24. Actual case of AAA as seen intraoperatively after isolation. Obtained
from 2022 transcript. IV. THORACIC AORTIC ANEURYSM (TAA)
● Approach is different from AAA
A. CAUSES OF TAA
● Non-specific medial degeneration
● Aortic dissection
● Atherosclerosis is commonly cited as a cause of thoracic aortic
aneurysms |
● Genetic disorders
→ Marfan syndrome, Ehlers-Danlos syndrome, Familial aortic
aneurysm
● Post-stenotic dilatation
● Infection
Figure 25. Proximal anastomosis of the graft. Obtained from 2022 transcript. ● Aortitis
→ Takayasu arteritis, Rheumatoid aortitis
● Trauma
● Diagnostic Evaluation:
→ Needs high index of suspicion especially in younger
population.
→ Most would experience pain in chest, back/ abdomen
characterized as sudden, sharp or tearing, severe pain which
migrates distally.
→ There would be discrepancy in the blood pressures in the
extremities.
Figure 26. After-graft interposition. Obtained from 2022 transcript. → CT aortogram has a sensitivity of 98% and specificity of 87%
→ MRA is 98% sensitive and specific and is now considered as
the gold standard. However, this is not readily available to
some institutions and is limited use in critically ill patients.
→ For unstable patients, TEE is 98% sensitive and 95% specific
for ascending aortic dissection.
→ Coronary angiogram should be done prior to repair especially
in patients who are at risk of coronary artery disease.
● Treatment:
→ The same for all types and focuses on medical therapy.
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 12 of 19

→ Aim is to lower cardiac contractility and blood pressure. Segmental Graft Replacement (Graft Interposition)
→ Medications used: beta adrenergic blockers, vasodilators, ● Done under cardiopulmonary bypass; or
calcium channel blockers and angiotensin converting enzyme
inhibitors.
B. DIAGNOSIS OF ASCENDING AORTIC ANEURYSMS
● Usually asymptomatic
→ Diagnosis is likely to be delayed
● Incidental chest x-ray finding
● May present with CHF secondary to AR
● PPE: Aortic insufficiency (e.g. diastolic murmur, widened pulse Figure 29. Segmental Graft Replacement. Obtained from 2022 transcript.
pressure)
● Diagnostics: CT Scan, Aortography Classic Bentall Procedure
● Treatment: (Ascending Aortic Dissection) ● May entail an additional coronary artery bypass graft
→ Treated as an emergency because of high rate of complication
and mortality if delayed.
→ Delayed treatment maybe done in stable and closely
monitored patients to make aortic tissues less friable.
● Treatment: (Chronic Ascending Aortic Dissection)
→ Treatment as the same as the acute dissection with one
difference, the septum between true and false lumen is not
remodeled but rather fenestrated to supply both lumen.
Figure 30. Classic Bentall Procedure. Obtained from 2022 transcript.
C. SURGICAL INTERVENTION
● Decision to intervene surgically is based on clinical judgment Bentall-Button Modification
specific to:
→ Size of aneurysm
→ Associated co-morbid conditions
→ Patient’s life expectancy
→ Risk of surgery

● Indications:
→ Diameter of ascending segment: ≥5.5 cm
→ 5.0 cm (Marfan Syndrome) Figure 31. Bentall-Button Modification. Obtained from 2022 transcript.
→ Symptomatic: pain, compression, AR
→ Documented enlargement: >1 cm growth/year Aortic Valve Repair/Replacement
● May be done: ● If aortic root has been involved
→ Under cardiopulmonary bypass; or
→ May entail an additional coronary artery bypass graft; or
→ Bentall repair; or
→ Aortic valve repair
Open Repair
● To repair ascending aortic dissection.
Figure 32. Aortic Valve Repair/Replacement. Obtained from 2022 transcript.

V. TRANSVERSE ARCH ANEURYSM

● Almost always due to atherosclerosis
● Patients >60 years of age with associated coronary and cerebral
diseases
● Less urgent, but repair requires antegrade cerebral perfusion
A. INDICATIONS FOR SURGERY
● Size: 6-8 cm in diameter
● Compression of trachea and bronchi
● Pain
● Major surgical concern: preservation of brain viability

Figure 28. Open Repair. Obtained from Dr. Purino’s PPT. In this illustration, the
ascending aorta is being repaired. The technique here is that the false lumen
is obliterated and sandwiched between the prosthetic graft. Then, the
ascending aorta is replaced by the Dacron graft. The blood flow now will be
from the Dacron graft to the true lumen.
Note: For the chronic dissection, the false lumen is not obliterated but it will
still persist. To have a flow to the false lumen, fenestrate/ cut the septum so
that the blood from the prosthetic graft will flow to the false and true lumen
because in chronic dissection some of the arteries are supplied by the false
lumen and some will be supplied by the true lumen. If the false lumen will be
occluded, some of the arteries will be occluded as well leading to symptoms.
Unlike in acute, you can still remodel/ obliterate the false lumen so that all Figure 33. Arch vessels are reimplanted as a group, but may require pre-formed
arteries will have one, the true lumen. graft prior to surgery Obtained from 2022 transcript.
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 13 of 19

Figure 34. When arch vessels are already involved, requiring individual
reconstruction. In this picture, left carotid artery is being anastomosed to the
middle branch of the graft. Obtained from 2022 transcript.

Figure 35. Arch aneurysm after interposition and reconstruction of head vessels.
Obtained from 2022 transcript.
Figure 37. Open Repair. Obtained from Dr. Purino’s PPT. This is a completed
repair with the whole of the ascending and abdominal aorta replaced by Dacron
graft/ prosthetic graft.
Endovascular Repair
● Same principle as for the aneurysm but the goal is to cover the
entry tear and remodel the distal aorta.
● Needs spinal cord protection because of the coverage of the
spinal arteries.
● Limited by the presence of visceral and renal vessels.

B. DIAGNOSIS OF DESCENDING AA Recommendations for Surgery

● PE: essentially normal ● Diameter
● CXR: accidental finding of asymptomatic mass → ≥6.5 cm
● Compression symptoms → 6.0 cm (Marfan Syndrome)
→ Bronchus - cough and dyspnea ● Aortic rupture
→ Erosion – hemoptysis ● Symptomatic
→ Recurrent laryngeal nerve - hoarseness → Pain, compression syndromes, AR
● Diagnostics: CT Scan and Aortography ● Documented enlargement
● Treatment: ● >1 cm growth/year
→ Usually managed medically except the presence of ● Requires “complication-specific” approach
complications like rupture, malperfusion, intractable pain, Complications of Resection
ischemic symptoms. ● Paraplegia
C. SURGICAL MANAGEMENT → Compromise of spinal arteries at level of T10-T12 (artery of
● Timing of surgery: used to be once diagnosed Adamkiewiez)
● Exceptions: small aneurysms with associated significant → Paraplegia rates
coronary and carotid disease ■ 15-20% = 605 pts, Crawford, 1982
● May observe: with frequent CT Scan ■ 6.5% = 360 pts, Cooley, 1985
● Operative risk for elective surgery: <5% ■ 4% = 230 pts, Coady, 1997
→ Avoided by spinal fluid monitoring, and drainage to prevent
Open Repair cord ischemia
● To repair descending thoracic aortic dissection. D. THORACIC ENDOVASCULAR AORTIC REPAIR (TEVAR)
● Alternative treatment for high risk patients
● Offers minimally invasive option, but requires expertise and
costly devices done under angiographic guidance
● Usually done in hybrid cardiovascular OR with angiography and
c-arm as required setup
1. Delivery system insertion

Figure 36. Open Repair. Obtained from Dr. Purino’s PPT. Place the patient in
decubitus position. Then, with the help of the cardiopulmonary bypass machine
usually to the left heart bypass so protect the brain, kidney and implant spinal Figure 38. Delivery System Insertion. Obtained from 2022 transcript.
artery, clamp the involved segment and replace with Dacron graft/ prosthetic
graft.
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21)
2. Stent-Graft positioning
Figure 39. Stent-Graft Positioning. Obtained from 2022 transcript.
3. (L) TEVAR after deployment of proximal end; (R) deploy
remaining stent-graft
Figure 40. (L) TEVAR after deployment of proximal end; (R) deploy remaining
stent-graft. Obtained from 2022 transcript.
4. Remove delivery system - after complete deployment of TEVAR
Figure 41. Removal of Delivery System. Obtained from 2022 transcript.
5. Ballooning to optimize sealing - ends are distended with a
pressure balloon to effect sealing
Figure 42. Ballooning. Obtained from 2022 transcript.
E. THORACIC STENT-GRAFTS
● However, problematic endoleaks may cause progression of the
aneurysm
● If uncorrected, may require re-intervention or open repair in the
future
Page 14 of 19
Figure 43. Types of Endoleak in thoracic stent-grafts Obtained from 2022
transcript.
● Types:
→ Type I: end of graft
→ Type II: aortic branches
→ Type III: graft overlap
→ Type IV: graft fabric leak
→ Type V: sac expansion without cause
Classification of Common Treatment Strategies for Endoleak
● Type I - incomplete seal between stent-graft and aorta
→ Treatment: early intervention to improve seal or conversion to
open surgery
● Type II - retrograde perfusion of sac from excluded collateral
arteries
→ Treatment: surveillance; as-needed occlusion percutaneous
● Type III - incomplete seal between overlapping stent-grafts or
fabric
→ Treatment: early intervention to cover gap or conversion to
open surgery
● Type IV - perfusion of sac due to porosity of material
→ Treatment: surveillance; as-needed reintervention to reline
stent-graft
● Type V - expansion of sac with no identifiable source
→ Treatment: surveillance; as-needed reintervention to reline
stent graft
● Close follow-up is mandatory
| KEY POINTS
● Assessing urgency of repair is essential to develop the
appropriate management plan
→ Careful planning and close monitoring are key strategies for
successful management
● Emergent repair carries a greater risk, but delay of repair risk
death
● Clinical progression leads to expansion and eventual rupture, thus
regular non-invasive imaging is recommended
● Ascending aortic aneurysms that are symptomatic or >5.5 cm
should be repaired, but may be earlier for those with connective
tissue disorders
● Optimize patient’s health status before surgical intervention
● Antegrade cerebral perfusion and CSF drainage have
significantly reduced the morbidity rates associated with complex
aortic repair (in TAA)
● Endovascular repair devices are approved for the treatment of
descending thoracic aortic aneurysms, and some of the newer
devices are also approved for the treatment of aortic trauma and
penetrating aortic ulcer
VI. ACUTE AORTIC DISSECTION
● Often misdiagnosed condition that is life-threatening and difficult
to manage
● An event of sudden onset in which blood leaves the normal aortic
channel through a usually discrete point of exit (intimal tear) and
rapidly dissects the inner from the outer layer of the media to
produce a false channel
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 15 of 19

● Its sudden onset and rapid progression prevent early

management and requires aggressive approach to surgical
management
A. TYPE I

Figure 47. Aortic wall of patient with Marfan Syndrome Obtained from 2022
transcript.

Figure 44. Acute aortic dissection Type I Obtained from 2022 transcript.
● Type I can dissect retrogradely, and produce cardiac tamponade
and cardiac arrest

Figure 48. Bentall’s repair of ascending aorta with aortic valve replacement.
Obtained from 2022 transcript.

Figure 45. Type I AAD extending to infrarenal aorta. Obtained from 2022
transcript.

B. MARFAN SYNDROME

Figure 49. Coronary artery reimplantation. Obtained from 2022 transcript.

Figure 53. Patient with Marfan Syndrome Obtained from 2022 transcript.
● Arm span is longer than height
● Increased elasticity in Marfan Syndrome makes them prone to Figure 50. CT aortogram Obtained from 2022 transcript.
aortic aneurysm and dissection
Table 7. Anatomic complications of aortic dissection and associated signs and
→ Weakness in the aortic wall makes them prone to aneurysmal symptoms.
dilatation and dissection ANATOMIC MANIFESTATION SIGNS AND SYMPTOMS
● Repair is difficult due to weakened aortic wall Aortic valve insufficiency Dyspnea, murmur, rales, shock
● Diagnosis: CT aortogram can delineate aortic dissection without
Coronary malperfusion Angina, nausea/vomiting, shock,
being invasive ischemic pattern on ECG,
elevated cardiac enzymes
Pericardial tamponade Dyspnea, jugular vein distention,
pulsus paradoxus, muffled heart
sounds, shock
Subclavian or iliofemoral artery Cold, painful extremities with
malperfusion sensory/motor deficits,
diminished pulses
Carotid artery malperfusion Syncope, FNDs, decreased
carotid pulse, coma
Figure 46. Tests for hyper-elasticity: (L) Thumb sign (R) Wrist sign in Marfan | KEY POINT
Syndrome. Obtained from 2022 transcript. ● Proximal aortic dissection is a life-threatening condition, and
immediate operative repair is generally indicated, although
definitive aortic repair may be delayed until after severe
malperfusion has been treated
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 16 of 19

VII. QUESTION AND ANSWER PORTION

1. Indications for Carotid Intervention
a. Symptomatic patients with ≥50% ICA stenosis
b. Asymptomatic patients ≥80% ICS stenosis
c. Patients with TIA or ulcerated plaque
d. AOTA
2. True of peripheral arterial diseases
a. Most with intermittent claudication will require surgical
intervention
b. Few patients respond to pharmacotherapy and risk factor
modification
c. Rest pain or tissue necrosis will require urgent
revascularization
d. AOTA
3. Indications for AAA repair
a. Size >5 cm
b. 4 cm AAA with low back pain
c. 2 cm saccular aortic aneurysm
d. AOTA
4. The following have reduced morbidity associated with TAA
repair
a. Early surgery
b. CSF drainage with pressure monitoring
c. Antegrade cerebral perfusion
d. AOTA

5. Some anatomic complications of aortic dissection include the

following, EXCEPT:
a. Pericardial tamponade
b. Carotid artery malperfusion
c. Pulmonary hemorrhage
d. Coronary malperfusion
END OF TRANSCRIPT
REFERENCES
Purino, P.V. Jr., (2020), Thoracic Aortic Diseases, Aneurysm, and Dissection
[PowerPoint Presentation]. Manila, Philippines: Faculty of Medicine
and Surgery, University of Santo Tomas, TCVS
Brunicardi F.C, Andersen D.K., Billiar, T.R., Dunn, D.L., Hunter, J.G., Kao, L.S.,
Matthews, J.B., & Pollock, R.E. (2019). Schwartz’s Principle of Surgery
[11th Ed.]. USA: McGraw-Hill Education. (Chapter 22 & 23, pp. 853-
896, 907-927, 950-968)
2022 Transcript: BAUTISTA, A., BELZA, DE CHAVEZ, DE GUZMAN | DAVID, M.,
DAVID, R., DE CASTRO
 [TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 17 of 19

IV. APPENDIX

TREATMENT OF THORACIC AORTIC ANEURYSM DEPENDING ON ETIOLOGY

V.
VI.
VII.
VIII.
IX.
X.
XI.
XII.
XIII.
XIV.
XV.
XVI.
XVII.
XVIII.
XIX.
XX.
XXI.
XXII.
XXIII.
XXIV.
XXV.
XXVI.
XXVII.
XXVIII.
XXIX.
XXX.
XXXI.
XXXII.
XXXIII.
XXXIV.
XXXV.
XXXVI.
XXXVII.
XXXVIII.
XXXIX.
XL.
XLI.
XLII.
XLIII.
XLIV.
XLV.
XLVI.
XLVII.
XLVIII.
XLIX.
L.
LI.
LII.
LIII.
LIV.
LV.
LVI.
LVII.
LVIII.
LIX.
LX.
LXI.

Figure 51. Ascending aortic aneurysm of degenerative etiology. Critical size is 5.5cm. Obtained from Dr. Purino’s PPT.
LXII.
LXIII.
[TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 18 of 19

LXIV.
LXV. Figure 52. Ascending aortic aneurysm associated with genetic disorder. Critical size is >5.5 cm. Obtained from Dr. Purino’s PPT.
LXVI.
[TCVS] 2.01 – Thoracic Aortic Diseases, Aneurysm and Dissection (21 OCTOBER 21) Page 19 of 19

Figure 53. Management of Descending Thoracic Aorta. Obtained from Dr. Purino’s PPT.