Diseases of the

Aorta and
Trauma of the Heart & the Aorta
Nurnajmia Curie Proklamatina
Ruswandiani
Resource Person : dr. Suko Adiarto, PhD, SpJP(K)

DEPARTMENT OF CARDIOLOGY & VASCULAR MEDICINE

FACULTY OF MEDICINE, UNIVERSITAS INDONESIA
November 2015

Outline
Anatomy and Physiology of the Aorta
Aortic Aneurysm
Aortic Dissection
Trauma of the Aorta
Trauma of the Heart

Anatomy and
Physiology
of the Aorta

Anatomy of the Aorta

Anatomically divided into:
Thoracic aorta: ascending, arch, descending
segments
Abdominal aorta: suprarenal, infrarenal segments

Normal aortic diameters usually <40 mm,

taper gradually downstream
Variation influenced by age, gender, body
size, blood pressure
Expansion rate 0.9 mm (men) 0.7 mm
(women) for each decade of life

2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.

2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.

Microscopic Structure of
the Aorta
Aortic wall include three layers:
Tunica intima: lined by endothelial cells, demarcated from media by
internal elastic lamina
Tunica media: concentric layers of elastic fibers alternating with
vascular smooth muscle cells lamellar unit, delineated from
adventitia by external elastic lamina
Tunica adventitia: collagen fibers, fibroblasts, small nerves, blood
vessels

Ascending aorta contains 55-60 elastic lamellae, gradually

decrease to 26 at aortic bifurcation
Oxygen and nutrients supply:
Proximal aortic segments are supplied by vasa vasorum from
adventitia to outer layer of elastic media
Distal segments 29 lamellae are supplied by simple diffusion from
lumen

Physiology of the Aorta

Transmits pulsatile arterial blood pressure
to all points in arterial tree
Function depends on its properties as
elastic conduit role of second pump
through its elasticity (Windkessel function)
Pressure-responsive receptor in ascending
aorta and aortic arch (control of SVR and
HR) increased aortic pressure results in
decreased SVR and HR, vice versa

Pressure-Diameter Curve of
the Aorta
Aortic wall pressure-diameter relationship is nonlinear
Transition from distensible to stiff behavior occurs at
pressure >80 mmHg
Curve become less steep with increasing age (aorta
stiffen, diameter increases), due to:
Increased collagen-to-elastin ratio (decreased elastin,
increased collagen)
Changes in wall (progressive disordered medial elastic
fibers and lamellae displaying thinning and fragmentation)
Increased wall thickness (collagen and other ECM
macromolecules deposition and elastic fibers calcification)
Arteriosclerotic changes (wall stiffening)

Evaluation of the Aorta

Can normally be palpated in
midabdominal region, depending on body
habitus may be detected by deep
palpation adjacent to spine
Plain radiography is insensitive in
evaluating thoracic and abdominal aorta
More diagnostic detail can be obtained
with ultrasound (including
echocardiography), CT, MRI, aortography

Aortic Aneurysms

Overview of Aortic Aneurysms

Pathologic aortic segment dilation that tend to expand and
rupture
Increased diameter 50% than expected for same aortic
segment in unaffected individuals of same age and sex
Described in terms of:
Size (cross-sectional diameter on imaging)
Morphology
Fusiform symmetric, entire circumference
Saccular localized, only a portion of wall circumference, appear as focal
outpouching)
Pseudoaneurysm bleeding through wall, results in contained periaortic
hematoma in continuity with lumen (trauma or contained rupture of
aneurysm, dissection, penetrating ulcer)

Location (thoracic, abdominal)

Cause (degenerative, genetic disorder, etc)

http://www.uchospitals.edu/onlinelibrary/

Abdominal Aortic
Aneurysms

Overview of AAA
Increased abdominal aorta
diameter >3 cm
Most common form of
aortic aneurysm
Occurs in 3-9% men >50
years old
80% infrarenal, 10%
pararenal/visceral, some
extend to thoracoabdominal segment

Risk factors:

Men (5x)
Older age (>60 years old)
Cigarette smoking (5x)
Emphysema
Hypertension
Hyperlipidemia
Family history (20%)

Molecular genetics:
Up to 20% of infrarenal AAA
have family history of AAAs,
suggest inherited component
Sequence variant on
chromosome 9p21 is associated
with 31% increased risk for AAA

Pathogenesis of AAA
Chronic aortic wall inflammation, increased
local expression of proteinases, degradation of
structural connective tissue proteins
Response to foreign antigens and microbial
infection, autoimmune response postulated in
AAA development
Aneurysmal dilation and rupture result from
mechanical failure of medial elastin and
adventitial collagen
Natural history of AAAs balance between
degradative and reparative processes

Inflammat Elastin
ory Cells

Collag
en

MMP

Vascular SMC

Infiltrate
aortic wall

Medial
elastin
destruction
and
marked
decrease in
elastin
concentrati
on

Increas
ed
collage
n
content
(wall
tensile
strengt
h)

Most prominent
elastin- & collagendegrading enzymes
in AAA degrade
broad range of
matrix proteins

Normally produce
elastin and collagen
during aortic
development

Damage to
lamellae
Proinflamma by
-tory
elastolytic
cytokines:
proteinase
TNF-, IL-1
s leads to
, IL-6, IF-
aneurysma
l dilation

Enzyme
s
initiatin
g
interstit
ial
collage
n
cleavag
e
rapid
aneurys
m
expansi
on and
rupture

Release
matrixdegrading
enzymes
lead to
medial
degeneratio
n

MMP-2, 7, 9, 12
exhibit activity
against elastin
MMP-1, 8, 13
initiate intact
fibrillar collagen
degradation

Predominate within
elastic media
mediate repair of
connective tissue
within AAAs

Depletion of medial
SMCs due to
apoptosis initiated
by medial ischemia,
signaling molecules,
MMP-9 expression is or cellular immune
markedly elevated
responses
in aneurysm tissue
potential use of
Vasa vasorum
doxycycline and
absence supply to
other MMP
media depends on
inhibitors to
diffusion from lumen
suppress
may be
progression
jeopardized by
intimal thickening
and atherosclerotic

Clinical Features
Insidious over years, rarely symptomatic in
absence of distal thromboembolism, rapid
expansion, rupture
Mostly small, large ones have high risk of
rupture
Mostly detected by screening/incidental finding
Physical examination is insensitive, abdominal
palpation may reveal pulsatile
epigastric/periumbilical mass
AAA present in up to 85% femoral artery
aneurysm, 60% popliteal artery aneurysm

Screening
Aneurysm screening &
repair above given size
threshold 50% reduction
in rupture and death
Ultrasound
High accuracy detection,
sensitivity- specificity
almost 100%, inexpensive,
noninvasive, avoid radiation
and contrast agent, serial
measurement
Less accurate diameter
than CT (not recommended
for larger AAA >4.5 cm)
2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.

Other Diagnostic Imaging

CT
Extremely accurate for detection and diameter measurement, esp.
with contrast enhancement, thin slice techniques, 3D reconstruction
Extent of disease, AAA relationship to renal/visceral/iliac arteries,
mural thrombus patterns, calcification, coexist occlusive
atherosclerosis, which might influence repair

MRI
High accuracy in detecting and measuring diameter, avoids radiation
exposure and iodine-based contrast

Aortography
Initial step in EVAR, also used in subsequent interventions following
AAA stent-graft repair, such as embolization of lumbar or iliac artery
branches
Enlarged abdominal aortic segment marked by calcification, lumen
may or may not appear enlarged because of mural thrombus
presence

Natural History
Gradual expansion over years
and eventual rupture
Average expansion rate of 35.5 cm ranges 0.2-0.3 cm/year
Aneurysm size, wall thickness,
intraluminal thrombus
thickness, and peak wall
stress contribute to rupture
1-year risk for rupture:
6.0-7.0 cm: 10-20%; 7.0-8.0 cm:
2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.
20-40%; >8.0 cm: 30-50%

5-year risk for rupture:

3.0-4.0 cm: 5%, 4.0-5.5 cm: 1020%, 5.5-6.0 cm: 30-40%, >7.0
cm : >80%

Ruptured AAA
Symptomatic AAA related to
overt rupture or rapid expansion
and impending rupture
Rupture into peritoneal cavity
acute hemorrhage, severe
abdominal pain, hypotension

Rupture into retroperitoneum

temporarily contained periaortic
hematoma, severe abdominal or
back pain radiate to flank or groin,
tender pulsatile abdominal or flank
mass, hypotension, syncope

30-50% die before

hospitalization, 30-40% die at
hospital before treatment, OSR
mortality rate 40-50%, may be
2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.
lower
with EVAR

Surveillance/Medical
Therapy
Small AAAs can be observed
safely with imaging
surveillance and little risk for
rupture
Society of Vascular Surgery
guidelines:

2.6 -2.9 cm, imaging/5 years

3.0-3.4 cm, imaging/3 years
3.5-4.4 cm, imaging/12 months
4.5-5.4 cm, imaging/6 months

Uncertainty for 4.5-5.4 cm,

recommendations must be
individualized:
Young, healthy, esp. women with
5-5.4 cm may benefit from early
repair

Medical therapy objectives:

prevent CV events
limit AAA growth
prepare patient optimally to
reduce perioperative risk
once intervention is indicated

Risk factor management:

smoking cessation
(mandatory)
diet & exercise (reasonable)

Medical therapy:

reduce wall shear stress or

inflammation statin, ACE-I

Experimental therapy:

BB, doxycycline, ARB, aspirin

Surgical Therapy
Elective repair of
asymptomatic patient (at least
5.0-5.5 cm) depends on life
expectancy, risk for rupture,
risk associated with repair
Symptomatic aneurysms and
rapid growth (>1 cm/year)
require surgical consultation
Morbidity and mortality
influenced by CAD, CKD,
COPD, DM
Selection of OSR or EVAR
depends on individual
anatomy, age, risk associated
with anesthesia and surgery
Braverman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Techniques and
Outcomes of OSR
Infrarenal
transperitoneal/left
retroperitoneal approach
Prosthetic graft is sutured
to proximal aorta
sutured to distal aorta
(tube graft)/common iliac
arteries (bifurcation graft)
after lower extremity
flow restoration,
aneurysm sac is sewn
together to prevent graft
and GI tract contact

Mortality rate 4-8%,

complication rates 10-30%
cardiac, pulmonary, renal
complications and colonic
ischemia
Late complications 15-30%
related to incision, paraanastomotic aneurysm, graft
infection, graft-enteric
erosions/fistula, graft limb
occlusions with lower
extremity ischemia
Follow-up with 5-year
intervals CT after OSR

EVAR
Fluoroscopically guided
endograft insertion
through femoral arteries
to re-line aorta
Less invasive, requires
adequate nonaneurysmal
proximal and distal
attachment sites
Early lower mortality and
complication rate (>5
years similar to surgical
repair, esp. age >70
years), higher number of
repeated interventions

Complications: endoleaks, endotension,

endograft migration, limb thrombosis,
implant-related complications, graft infection

Contrast-Enhanced CTA at 1 month/6

month/annually after device implantation

Color duplex ultrasonography to detect

endoleaks and AAA enlargement for those
with stable imaging findings

Braverman AC. Diseases of the aorta. In:

Braunwalds Heart Disease. 10th Edition. 2015.
2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.

Braverman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.

Thoracic Aortic
Aneurysms

Overview of TAA
Incidence 5-10 per 100,000 person-years
Cause, natural history, treatment vary
depending on TAA location
Aortic root/ascending aorta 60%,
descending aorta 35%, aortic arch <10%
Thoracoabdominal descending
thoracic extend distally to involve
abdominal aorta

Cause and Pathogenesis

Genetically triggered, degenerative or
atherosclerotic, mechanical, inflammatory, and
infectious diseases
Genetic disorder tend to involve root& ascending
aorta
Risk factor: smoking, HT, age, COPD, CAD, fam
history
CMD (MFS, other genetically triggered TAA, aging,
HT): elastic fibers degeneration & fragmentation, loss
of SMCs, increase collagen deposition, replacement
with interstitial cysts of mucoid-appearing
basophilic-staining ECM progressive weakening of
aortic wall, result in dilation and aneurysm

Braverman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

*Abnormalities in aortic media, vascular SMCs, or contractile proteins, overactivation of signaling

pathways and downstream mediators
Braverman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Clinical Manifestations
Most are asymptomatic, discovered incidentally on imaging study
Symptoms usually related to :
Local mass effect, progressive AR, HF from root dilation, systemic
embolization from mural thrombus or atheroembolism
SVC/innominate vein obstruction, trachea/bronchus/esophagus
compression
Direct mass effect with compression of intrathoracic structures/erosion into
adjacent bones may cause persistent chest/back pain

Most serious complications rupture and dissection

Rupture sudden severe chest/back pain
Rupture into:
Pleural cavity (usually left) or mediastinum is associated with hypotension
Esophagus leads to hematemesis from aortoesophageal fistula (common in infected
TAA)
Bronchus or trachea results in hemoptysis

Acute aortic expansion, contained rupture, and pseudoaneurysm can cause

severe chest or back pain

Chest X Ray
Widened mediastinum,
prominent aortic knob,
displaced trachea
Smaller aneurysms, esp.
saccular, may not be visible
Aneurysms of sinuses of
Valsalva and aortic root often
hidden behind sternum,
mediastinal structures, and
vertebrae
Aortic tortuosity and unfolding
in older adults may mimic or
mask TAAs
CXR cannot exclude
Braverman AC. Diseases
of the aorta. In: Braunwalds Heart Disease. 10
diagnosis
of TAA

th

Edition. 2015.

Trans Thoracic
Echocardiography

Excellent for imaging

aortic root, can be
used to visualize TAAs
involving sinuses of
Valsalva, proximal
ascending aorta,
aortic arch, proximal
descending aorta
Aortic root size is
dependent on age,
height or body
surface area, gender
Braverman AC. Diseases of the aorta. In:
Braunwalds Heart Disease. 10th Edition. 2015.

Other Modalities
Contrast-enhanced CT
and MRA are preferred
over aortogrpahy to
define both aortic and
branch vessel
anatomy
CT and MRI measure
external diameter of
aorta, 0.2 -0.4 cm
larger than internal
diameter in
echocardiography

verman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Natural History
Relatively indolent, growth rate 0.1-0.2 cm/ year and marked
individual variability
Other risk factors for increased growth and rupture: older age,
female, BSA, COPD, hypertension, cigarette smoking, rapid
aneurysm growth, pain, aortic dissection, positive family history
Factors Influencing
Natural History

Description

Cause

MFS: rapid growth rate (0.5 1 mm/year), RR for aneurysm

dissection/rupture 3.7, female 2.9
FTAAs: growth rate up to 2.1 mm/year (combined ascending
and descending)
LDS: growth rate up to >10 mm/year, death at mean age of
26 years
BAV: BAV ascending aortic aneurysms have higher growth
rate (0.19 cm/year) than tricuspid AV (0.13 cm/ year)

Location

Descending aorta have greater growth rate (3 mm/year) than

ascending aorta (1 mm/year)

Diameter Size

Most important risk factor for aneurysm rupture, dissection,

and death
Larger aneurysm grow faster
Mean rupture or dissection rate 2% per year for aneurysms
<5 cm, 3% per year 5.0-5.9 cm, 7% per year >6.0 cm

Coexisting condition

Dissected TAAs grow more rapidly (0.14 cm/year) than

without dissection (0.09 cm/year)

Aortic Size Index

ASI <2.75 cm/m2 complication rate 4%, ASI 2.75-4.25 cm/m 2

event rate 8%, ASI >4.25 cm/m2 event rate 20-25%

Surveillance/Medical
Therapy
Medical treatment:
Hypertension treatment
(ARB/ACE-I)
Cholesterol lowering
(atherosclerotic TAA statin)
Beta blockers (MFS)
MMP inhibitor (doxycycline)

Lifestyle modification:
Awareness of condition and
risk for dissection and rupture
Smoking cessation
Avoidance of strenuous
physical activity (isometric
exercise)

Braverman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

2014 ESC Guidelines on the diagnosis and treatment of aortic diseases.

Surgical Treatment (1)

Ascending TAA:
resection and grafting of
ascending aorta
concomitant AVR

Aortic Arch:
proximal hemiarch resection
arch vessels left intact, with
descending aorta as roof, and
remaining arch is replaced

extended arch resection

remove entire arch tissue and
use branched grafts to replace
arch and great vessels
reimplant island of arch tissue
including great vessel origins

averman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Surgical Treatment
(2)
Descending TAA:
resection and grafting of
aneurysmal segment with a
polyester graft

Thoracoabdominal
aneurysm:
depends on Crawford
classification

http://clinicalgate.com/vascular-surgery/

TEVAR:
less invasive
aortic anatomy must have
adequate proximal & distal
landing zones of at least 20-25
mm in length and diameters
that accommodate endograft
and adequate vascular access
Braverman AC. Diseases of the aorta. In: Braunwalds Heart Disease. 10 th Edition.
2015.

Acute Aortic
Syndrome (AAS)
Classic Aortic
Dissection
Aortic Intramural
Hematoma
(IMH)
Penetrating
Atherosclerotic
Ulcer
( PAU)

Aortic Dissection

Epidemiology
US 2-3.5 cases per 100.000 person-years
Incidence is higher in men than n women and
increases with age
The prognosis is poorer in women, as a result
of atypical presentation and delayed
diagnosis.
The most common risk factor associated with
AD is hypertension (6575%), mostly poorly
controlled.
IRAD registry, the mean age was 63 years;
65% were men

Pathophysiology

 The pressure of the pulsatile blood within the aortic wall

after dissection leads to extension of the dissection.
Usually propagate in an antegrade direction because of
the pressure wave from the aortic blood, but
occasionally extend in a retrograde direction.
The dissection flap may be localized or mayspiral the
entire length of the aorta
Arterial pressure and shear forces further tears in the
intimal flap produce exit sites or additional entry
sites for flow of blood into the false lumen
Distention of the false lumen with blood the intimal
flap to compress the true lumen and narrow its caliber
malperfusion syndromes.

Classification
De Bakey
I : Originates in the ascending aorta and
extends at least to the aortic arch and
often to the descending aorta ( and
beyond)
II : Originates in the ascending aorta and
confined to this segment
III : Originates in the descending aorta,
usually just distal to the left subclavian
artery and extends distally
a : stops above the diaphragm
b : extends below the diaphragm

Stanford

A : Dissections involving the ascending

aota ( with or without extension into the
descendig aprta)
B : Dissections not involving the
ascending aorta

Classification
Duration

Acute : < 2 weeks

Chronic : > 2 weeks

Subacute : 2- 6 weeks

Chronic : > 6 weeks

Predilection

65% ascending aorta

30% descending aorta

< 10% aortic arch

1% abdominal aorta

Clinical
Manifestations

Pain
Pain may be sharp, ripping, tearing, knife-like
Typically different from other causes of chst pain
Onset : abrutness
Site : chest (80%)-> anterior ( Type A) , back (40%),
abdominal (25%) Type B
May radiate from the chest to the back or vice versa
Pain in the neck, throat, jaw or head predicts
involvement of the ascending aorta ( and often the
great vessels)
Pain in the back, abdomen, or lower extremities
descending aorta

Aortic Regurgitation
41-70 % Type A
Incomplete coaptation of the aortic leaflets
because of concurent dilation of the aortic root
and anuulus or because of acute aortic dilatation
from an expanding false lumen leading to central
aortic regurgitation
Aortic leaflet prolapse caused by the dissection
flap propagating into the aortic leadlets or
commissures or by distortion of prope leaflet
alignment by an asymmetric dissection flap
leading to eccentric aortic regurgitation

FIGURE 57-14 Aortic regurgitation complicating acute type A aortic

dissection.
The dissection flap distorts the normal aortic leaflet alignment,
thereby leading to
malcoaptation of the aortic valve and subsequent aortic
regurgitation. In this
example the dissection flap extends into the ostium of the right
coronary artery
(arrow).

Diagnostic Test

Electrocardiogram

Biomarkers

D- dimer

D dimer > 1600 mg/ dl within the first 6 hours after

initial evaluation

Sensitivity 94%, specifity 40-100%.

Braverman. Braunwald Heart Disease 10th ed. Elsevier:

2015

Chest Radiograph

Non Spesific
In many cases, completely normal
80- 90 % Abnormal aortic contour or widening of the aortic
silhouette
20% pleural effusions

Calcification of the aortic knob occur detect

separation of the intimal calcification from the
outer aortic soft tissue border by more than 0.5
to 1.0 cmthe calcium sign

Echocardiography
Detect intimal flaps in
the aorta
The tear is defined as
disruption of flap
continuity with fluttering
of the ruptured intimal
borders
Complete obstruction of
an FL, sepatation of
intimal layes from the
thrombus.
Sensitivity 77-80%,
specifity 93-96%

Contrast CT
Most common used for ecaluate Aortic Dissection and best perfomred
with electrocardiographically gated, multidetector scanner, which may
eliminate aortic pulsation motion artifacts.
Presence of two distinct lumina with a visible intimal flap
Detection of two lumina by their diggering rates of opaficitaion with
contrast material.
False lumen completety thrombosed low attenuation
Sensitivity and spesicifity 98-100%
Spiral (helical) contrast enhanced CT allows 3D reconstrutcion
evaluation dissection & branch vessel endovascular repair
IV contrast
Idenntifity the presence of thrombus ( partial or complete in the false
lumen and detect hemopericardium, periaortic hematoma, aortic rupture,
and branch involvement and blood supply from the true and false lumina.
Limitations : motion artifact ( cardiac movement), contrast agent
( nephropathy)

FIGURE 57-10 Contrast-enhanced CT scan of an

aortic dissection demonstrating a fenestration in the
intimal flap (arrow) with contrast material flowing from
the small, densely opacified true lumen into the less
opacified and larger false lumen of the aorta.

FIGURE 57-12 Contrast-enhanced CT scan

demonstrating acute type A aortic dissection with
enlargement of the ascending aorta and intimal
flaps (arrows) in the ascending and descending
aorta. Both the true lumen (TL) and the false lumen
are opacified with contrast material in this
example.

Magnetic Resonance
Imaging
Accuracy similar to or
higher than CT
Does not require IV
contract or radiation
CI : patients with certain
implantable devices
( pacemaker, defibrilator)
and other metallic
implants.
More time needed than CT
For long term follow up of
aortic dissection

Aortagraphy
direct angiographic
visualization of the intimal flap (a negative,
frequently mobile, linear image) or the
recognition of two separate lumens;
indirect signs including aortic lumen contour
irregularities, rigidity or compression, branch
vessel abnormalities, thickening of the aortic
walls, and aortic regurgitation
no longer used for the diagnosis of AD,
except during coronary angiography or
endovascular intervention

MANAGEMENT

Risk Assesment
High-risk condition
MFS or related connective tissue disease, family history of aortic
disease, known aortic valve disease [such as BAV], recent aortic
manipulation, or known TAA)

High-risk pain features,

chest, back, or abdominal pain described as abrupt in onset,

severe in intensity, and of ripping/tearing/sharp or stabbing
quality;

High-risk examination features

perfusion deficit (pulse deficit, blood pressure differential, focal

neurologic deficit), murmur of aortic regurgitation, or hypotension.
Braverman. Braunwald Heart Disease 10th ed. Elsevier:
2015

Braverman. Braunwald Heart Disease 10th ed. Els

Braverman. Braunwald Heart Disease 10th ed. Elsev

BP Reduction

BP approximately 100-120 mmHg or to the

lowest level appropriate for adequate
perfusion

Beta blockers goal HR <= 60x/ min

Short acting B blocker esmolol initial bolus

500 m/kg and continous infusion 50-200
mikro/kg/min
If contraindicated CCB Non DHP verapamil
or diltiem.

Management
Cardiac Tamponade

Indications for Surgical, Endovascular,

and Medical Therapy for Acute Aortic
Dissection

Surgical
Therapy

8-31% in type A AD

Have hypotension, syncope, or altered

mental status

Pericardiocentesis for acute

hemopericardium recurrent bleeding &
acute hemodynamic collapse, especially if a
larger volume fluid is remove and increase
BP more bleeding in pericardial space

Endovascular
and/or Surgical
Therapy

Medical
Therapy

Acute type A aortic dissection

Retrograde dissection into the ascending aorta

Acute type B aortic dissection complicated by

Visceral ischemia
Limb ischemia
Rupture or impending rupture
Aneurysmal dilation
Refractory pain

Uncomplicated type B aortic dissection

Uncomplicated isolated arch dissection

Intra Mural
Haematoma (IMH)
Haematoma
develops
in the media of the
aortic wall in the
absence of an FL and
intimal tear
10-25% AAS
CT and MRI
diagnosis

Penetrating Aortic Ulcer

(PAU)
Ulceration of an aortic atherosclerotic plaque
penetrating through the internal elastic lamina into the
media
An atherosclerotic lesion penetrates through the
internal elastic lamina into the media, often associated
with a variable degree of IMH formation
PAUs may lead to pseudoaneurysm formation, aortic
rupture, or late aneurysm
Aortic ulcers may be single or multiple and range from
5 to 25 mm in diameter and 4 to 30 mm in depth.
PAUs are more common in the thoracic and
abdominal aorta than in the arch or ascending aorta.

Management
Individualized
management
Prevent aortic rupture
and progression to acute
AD
Recurrent and refractory
pain, as well as signs of
contained rupture, such
as rapidly growing aortic
ulcer, periaortic
haematoma, or pleural
effusion

Traumatic Rupture
of The Aorta

Definition
Traumatic aortic rupture (TAR) is a lesion
due to blunt trauma involving the aortic
wall, from the intima to the adventitia
TAR can result from car and motorcycle
collisions, falls from a height or blast
injuries, airplane and train crashes, and
skiing and equestrian accidents

 A traumatic lesion may

be classified as :
(1)intimal haemorrhage
(2)intimal haemorrhage
with laceration
(3)medial laceration
(4)complete laceration of
the aorta
(5)false aneurysm
formation
(6)peri-aortic
haemorrhage

 The signs of aortic rupture are not

specific, and the pre- sence of coexisting
head, facial, orthopaedic and visceral
lesions dominates the physicians
attention
Dyspnoea and chest pain are prominent
symptoms, localized in the back in 20
76% of cases. Loss of consciousness and
hypotension are also frequent, as
generally reported in polytraumatized
patients, while generalized hypertension
is reported in about 17%

Diagnostic
The most important diagnostic imaging
modalities are chest X-ray, TEE, contrastenhanced CT, MRI and contrast
angiography

Management
TAI associated aortic ruptures in 24
hours
Immediate treatment ( within 24 hours)
Surgical therapy :
- Clamp and sew
- Bypass
Endovascular stent therapy

Trauma of the
Heart

Overview
Thoracic trauma is: 25% of vehicular
accidents deaths 10-70% due to blunt
cardiac rupture
Early transport times, prehospital CPR,
and successful endotracheal intubation
are positive factors for survival when
patient suffers pulseless cardiac injury in
the field

Tsai PI, et al. Traumatic heart disease. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Penetrating Cardiac Injury

(1)
Greatest risk: RV, LV (Anterior location)
Clinical spectrum: cardiac arrest with no vital signs to
asymptomatic with normal vital signs
Cardiac stab wounds: tamponade >>
Gunshot wounds: hemorrhage >>

Evaluation: ABC, FAST (pericardial fluid in unstable

patient transfer to operating room to address injury)
Indications for emergency department thoracotomy:
Salvageable postinjury cardiac arrest (witnessed arrest with
high likelihood of intrathoracic injury, esp. penetrating cardiac
wounds)
Severe postinjury hypotension due to tamponade, air
embolism, thoracic hemorrhage

Vital signs regained after resuscitative thoracotomy

transfer to operating room for definitive repair

Penetrating Cardiac
Injury (2)
Definitive treatment:
surgical exposure through
anterior thoracotomy or
median sternotomy
Goals of treatment: relief
of tamponade and control
of hemorrhage
Concomitant correction of
acidosis and hypothermia
and reestablishment of
effective coronary
perfusion by appropriate
resuscitation
Tsai PI, et al. Traumatic heart disease. In: Braunwalds Heart Disease. 10

th

Edition. 2015.

Tsai PI, et al. Traumatic heart disease. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Blunt Cardiac Injury (1)

Ranging from minor bruises of myocardium to
cardiac rupture
Caused by direct energy transfer to heart or
heart compression between sternum and
vertebral column
Manifested as septal rupture, free wall rupture,
coronary artery thrombosis, cardiac failure,
dysrhythmias, rupture of chordae tendineae or
papillary muscles
Clinically severe blunt cardiac trauma is
manifested as tamponade or hemorrhage into
pleural cavity, depends on pericardium status

Blunt Cardiac Injury (2)

Routine ABCs
FAST examination
12-lead ECG
TEE septal defects, valvular insufficiency
Treatment:
Normotensive, normal initial ECG, suspected blunt
cardiac injury: observation units
Abnormal ECG: admitted for monitoring and treated
accordingly
Initially seen in cardiogenic shock: evaluated and any
structural injury confirmed, best repaired by a
cardiothoracic surgeon

Tsai PI, et al. Traumatic heart disease. In: Braunwalds Heart Disease. 10 th Edition. 2015.

Miscellaneous Cardiac
Injury
Iatrogenic Cardiac Injury
External/open cardiac massage, central venous line insertion, cardiac
catheterization procedures, endovascular/cardiac interventions, percutaneous
pericardiocentesis, open pericardial window

Intracardiac Foreign Bodies

Can cause acute suppurative pericarditis, chronic constrictive pericarditis,
foreign body reaction, hemopericardium

Metabolic Cardiac Injury/Burns

Cardiac dysfunction in response to injury, associated with burns, electrical
injury, sepsis, SIRS, multisystem trauma

Electrical Injury
Immediate cardiac arrest, acute myocardial necrosis ventricular failure,
myocardial ischemia, dysrhythmias, conduction abnormalities, acute
hypertension+peripheral vasospasm, asymptomatic nonspecific abnormalities

Pericardial Injury
Traumatic pericardial rupture is rare, occurs mostly in left pleuropericardial
surface, motor vehicular accidents as main cause

Late Sequelae of Cardiac

Injury
Include valvular abnormalities and
intracardiac fistulas
Can be identified intraoperatively by
gross palpation of a thrill or with TEE
Incidence is as high as 56% follow-up
echocardiography 4 weeks after injury

Thank You