ANEURYSMA AORTAE

An aortic aneurysm is a general term for an

enlargement (dilation) of the aorta to greater
than 1.5 times normal size. While the cause of an
aneurysm may be multifactorial, the end result
is an underlying weakness in the wall of the
aorta at that location. The aneurysm may
occasionally cause pain, which is a sign of
impending rupture.
When rupture occurs, massive
internal hemorrhage results, and, unless treated
immediately, shock and death can occur within
minutes to hours.

Signs and symptoms

Figure A shows a normal aorta. Figure B shows a

thoracic aortic aneurysm (which is located behind the
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heart). Figure C shows an abdominal aortic aneurysm

located below the arteries that supply blood to the
kidneys.
Most intact aortic aneurysms do not produce
symptoms. As they enlarge, symptoms such as
abdominal pain and back pain may develop.
Compression of nerve roots may cause leg pain or
numbness. Untreated, aneurysms tend to become
progressively larger, although the rate of enlargement
is unpredictable for any individual.
The diagnosis of an abdominal aortic aneurysm can be
confirmed at the bedside by the use of ultrasound.
Rupture may be indicated by the presence of free fluid
in the abdomen. A contrast-enhanced abdominal CT
scan is the best test to diagnose an AAA and guide
treatment options
AORTIC DISSECANS
Aortic dissecans ditandai oleh adanya robekan Lpisan intimal dinding
aorta yang diawali oleh suatu proses degenerasi, atau disertai nekrosis
kistik dari pada lapisan tunika media. Darah akan mengalir melalui
robekan yang memisahkan lapisan tunika intima dengan lapisan tunika
media atau lapisan tunika adventitia yang kemudian membentuk false
lumen atau lumen palsu.

Aortic dissection may be fatal without early diagnosis

and appropriate medical, surgical, or endovascular
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treatment. The presenting symptoms and signs are so

myriad and nonspecific that dissection may be
overlooked initially in up to 40% of cases. In addition,
the diagnosis is established only postmortem in a
substantial number of cases.1 Few other conditions
demand such prompt diagnosis and treatment, because
the mortality rate of untreated dissection approaches
1%/h during the first 48 hours, 80% at 14 days, and
90% at three months.
Classification schemes for aortic dissection are based
on anatomic involvement of the aortic dissection
(Figure 1).2 In the DeBakey classification, type I
dissections originate in the ascending aorta and extend
to at least the aortic arch; type II dissections involve
the ascending aorta only; and type III dissections begin
in the descending aorta, usually just distal to the left
subclavian artery. In the Stanford classification, type A
dissections involve the ascending aorta, and type B
dissections are those that do not involve the ascending
aorta. Ascending dissections require emergency
surgical repair, whereas medical therapy is usually the
initial strategy for acute type B dissections. Ascending
aortic dissection is most common in the 50- to 60-year
age range, whereas descending dissections occur more
commonly in older individuals. Because acute aortic
dissection is much less common than other conditions
associated with chest or back pain, a high index of
suspicion is important in making this diagnosis
Clinical Manifestations
The symptoms of aortic dissection may be highly
variable and may mimic much more common
conditions. Thus, a high index of suspicion must be
maintained, especially when risk factors for dissection
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are present or signs and symptoms suggest this

possibility. The vast majority of patients with acute
dissection have sudden, severe chest, back, or
abdominal pain, which may be maximal at its onset.
The pain may be migratory or may radiate from chest
or back to the abdomen or to the lower extremities.
However, in some instances, the pain resolves and
symptoms may be referable to other complications
such as heart failure from acute aortic regurgitation,
neurological deficits, syncope, or vascular
insufficiency
Coarctation of the aorta
From Wikipedia, the free encyclopedia

Sketch showing heart with coarctation of the aorta. A: Coarctation (narrowing) of the aorta. 1:Inferior vena cava,
2:Right pulmonary veins, 3: Right pulmonary artery, 4:Superior vena cava, 5:Left pulmonary artery, 6:Left pulmonary
veins, 7:Right ventricle, 8:Left ventricle, 9:Pulmonary artery, 10:Aorta

Schematic drawing of alternative locations of a coarctation of the aorta, relative to the ductus arteriosus. A: Ductal
coarctation, B: Preductal coarctation, C: Postductal coarctation. 1: Aorta ascendens, 2: Arteria pulmonalis, 3: Ductus
arteriosus, 4: Aorta descendens, 5: Truncus brachiocephalicus, 6: Arteria carotis communis sinistra, 7: Arteria
subclavia sinistra

Illustration depicting Coarctation of the Aorta.

Coarctation of the aorta, or aortic coarctation,

is a congenital condition whereby
the aorta narrows in the area where the ductus
arteriosus (ligamentum arteriosum after
regression) inserts. Aortic coarctation is
considered when a section of the aorta is
narrowed to an abnormal width. The word
coarctation means narrowing. Coarctations are
most common where the aorta the major artery
leading away from the heart arches toward the
abdomen and legs. The aortic arch may be small
in babies with coarctations. Other cardiac defects
may also occur when coarctation is present,
typically occurring on the left side of the heart.
When a patient has a coarctation, the left
ventricle has to work harder. Since the aorta is
narrowed, the left ventricle must generate a much
higher pressure than normal in order to force
enough blood through the aorta to deliver blood
to the lower part of the body. If the narrowing is
severe enough, the left ventricle may not be
strong enough to push blood through the
coarctation, thus resulting in lack of blood to the
lower half of the body. Physiologically its
complete form is manifested as Interrupted aortic
arch
Buerger's disease:
Buerger's disease is a type of vasculitis in which there
is inflammation of the arteries and veins of the hands
and/or feet. Buerger's disease, also
called thromboangiitis obliterans, results in the
development of clots (thrombosis) in the arteries of
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the hands and/or feet and can lead to serious

complications if not treated promptly
Buerger's disease interferes with circulation leading
to ischemia of cells and tissues. In ischemia, cells are
unable to reproduce normally, recover effectively from
injury, and fight infection
Symptoms of Buerger's disease include pain in the
hands and/or feet and the development of sores or
lesions that do not heal. If Buerger's disease is left
untreated, gangrene (tissue death) can occur. For more
information on symptoms and complications, refer
to symptoms of Buerger's disease
The cause of Buerger's disease is smoking and the use
of chewing tobacco. It is theorized that tobacco
triggers an autoimmune reaction, in which the body's
immune system mistakes healthy tissues as potentially
dangerous invaders into the body and attacks them.
This causes inflammation and the development
of clots in the arteries and veins of the hands and feet
that are characteristic of Buerger's disease
Making a diagnosis of Buerger's disease includes
completing a thorough medical history, tobacco use
history, and a physical examination.
Diagnosis of Buerger's disease is based on medical
history and examination combined with ruling out a
variety of other diseases and conditions, such
as Raynaud's phenomenon and other types of
vasculitis. A test called an angiogram may be
performed to assist in diagnosis of Buerger's disease.
An angiogram is an imaging test that creates a picture
of the arteries and can reveal the artery damage and
blockages in the hands and feet that are typical of
Buerger's disease
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The only effective treatment for Buerger's disease is to

quit smoking (smoking cessation) and to abstain from
the use of all tobacco products, such as chewing
tobacco. At this time, there are no medications that are
effective in treating Buerger's disease
Peripheral Arterial Occlusive Disease
Peripheral Arterial Occlusive Disease, Peripheral
Arterial Disease, Peripheral Vascular Disease,
Arterial Insufficiency, Claudication, Vascular
Claudication, Aortoilliac Occlusive Disease, Leriche's
Syndrome, Iliac Artery Stenosis, Iliofemoral Occlusive
Disease, Femoropopliteal Occlusive Disease,
Femoropopliteal Stenosis, Femoral Arterial Stenosis,
Intermittent Claudication
Prevalence
A.

Overall: 7-12 million affected in U.States

B.

Age over 60 years: 3 to 6%

C.

Age over 70 years: 10 to 18%

Risk Factors
A.

Age over 60

B.

Cerebrovascular Disease

C.

Coronary Artery Disease

D.

Diabetes Mellitus

E.Hypercholesterolemia
F. Tobacco abuse (risk persists >5 years after
cessation)
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1. Cigarette smoking 20 per day: 2.11 relative

risk
2. Cigarette smoking 11-20 per day: 1.75
relative risk
G.

Systolic Hypertension

H.

Hyperhomocysteinemia

I. Increased Body Mass Index (Obesity)

J. C-Reactive Protein increased
K.
Chronic Kidney Disease with GFR rate <60
ml/min/1.73m2
Symptoms
A.

Presentations
1. Classic Claudication: 10% of cases
2. Atypical Leg Pain: 50% of cases
3. Asymptomatic: 40% of cases

B.

Classic Claudication
1. Cramp-like leg muscle pain with Exercise,
better with rest
a. Calf pain typical (pain may occur in
thigh, buttock)
2. Pain worse with exertion
3. Pain relieved within 10 minutes rest
4. Pain relieved with rest and dependent position

C.

Critical limb ischemia (1% of presentations)

1. Tissue loss or gangrene
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2. Chronic rest pain

D.
Timing of symptoms related to degree of
stenosis
1. Exertional pain: 70% arterial pain
2. Nocturnal pain: 70 to 90% arterial stenosis
3. Ischemic rest pain: 90% arterial stenosis
A.
Vascular Exam (Arterial Bruits or diminished
pulses)
1. Abdominal aorta bruit
2. Femoral artery pulse
3. Dorsalis pedis pulse
4. Posterior tibial pulse
5. Carotid Artery pulse and bruit (for
comorbid Carotid Stenosis)
B.

Neurologic Exam
1. Critical in determining acute limb ischemia
degree (see Rutherford Classification below)
2. Extremity Motor Exam
3. Extremity Sensory Exam

VIII. Signs
A.
Most reliable signs of Peripheral Vascular
Disease (Sensitivity, Specificity assumes
ABI<0.9)
1. Posterior tibial artery doppler Ultrasound

10

a. All 3 components present rules-out

Peripheral Arterial Disease
b. Only 1 of 3 components present is
strongly suggestive of PAD (Positive
Likelihood Ratio = 7.0)
2. Dorsalis pedis and posterior tibial pulse
absent
a. Test Sensitivity: 63%
b. Test Specificity: 99%
3. Femoral artery bruit
a. Test Sensitivity: 29%
b. Test Specificity: 95%
4. Atypical Skin Color (pale, red, blue) of
extremity
a. Test Sensitivity: 35%
b. Test Specificity: 87%
B.

Local Signs of Peripheral Vascular Disease

1. Dry, scaly, shiny atrophic skin
2. Skin hairless over lower extremity (e.g. shin)
3. Dystrophic, brittle Toenails
4. Non-healing ulcers or other lower extremity
wounds
5. Decreased skin temperature (cool feet)
6. Decreased Capillary Refill Time
7. Distal extremity color change with position
a. Skin rubor when leg dependent
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b. Skin pallor when leg elevated >1 minute

i. Color returns within 15 seconds in
mild cases
ii. Delay >40 seconds suggests severe
ischemia
IX. Signs: Acute Limb Ischemia (5 P's)
A.

Pain

B.

Pulselessness

C.

Pallor

D.

Paresthesias

E.Paralysis
X. Signs: Occlusion Location
A.

Inflow Disease: Aortoilliac Occlusive Disease

1. Also known as Leriche's Syndrome
2. Bilateral leg diminished pulses throughout
3. Slow Wound Healing legs
4. Impotence

B.

Outflow Disease
1. Iliofemoral Occlusive Disease
a. Unilateral leg diminished pulses
throughout
b. Buttock Claudication may be present
2. Femoropopliteal Occlusive Disease
a. Thigh and calf Claudication
12

b. Normal femoral pulses in groin

Raynaud's Disease
What is Raynaud's disease?
Raynaud's disease is a problem with small blood
vessels in the skin. During an attack of Raynaud's,
these blood vessels get narrower, which means that
less blood flows to the skin. The skin first turns white,
then blue. Then the skin turns red as the vessels relax
and blood flow is better again. Hands and feet are most
commonly affected, but Raynaud's disease can affect
other areas, such as the nose and ears.
Women between the ages of 15 and 50 are most likely
to have the problem, but it can affect anyone.
How does it occur?
For most people, an attack is usually triggered by
emotional stress or exposure to cold. For example,
reaching into a refrigerator may trigger an attack.
There are 2 forms of Raynaud's disease.
Most people who have Raynaud's disease have the
milder primary form. Its cause is not known.

Secondary Raynaud's disease is caused by

another disease or condition. It is a more serious
problem. Connective tissue diseases are the most
common cause. Medical conditions that may
cause secondary Raynaud's include:
o

Scleroderma (a thickening and hardening of

the skin and other body tissues). Most people
who have scleroderma have Raynaud's.

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Systemic lupus erythematosus (a chronic

inflammation of the skin and organ systems
also called lupus).
Rheumatoid arthritis (a chronic inflammation
and swelling of tissue in the joints).
Blood flow reduction (problems that slow or
stop blood flow in a vessel, such as
inflammation and hardening of the arteries).
Pulmonary hypertension (high blood pressure
in the lungs).
Sjgrens syndrome (a disease in which
immune cells attack and destroy the glands
that make tears and saliva).
Polymyositis (a chronic disease that causes
inflammation and weakness of the muscles).
Dermatomyositis (a form of polymyositis
with skin symptoms).
Carpal tunnel syndrome (a painful disorder of
the hand and wrist caused by pressure on a
nerve in the wrist).

Smoking and drugs can also cause secondary

Raynauds disease. Examples of drugs that might
cause it are beta blockers used to treat high blood
pressure, ergotamine medicines used for migraine
headaches, anticancer drugs, nonprescription cold
medicines, and narcotics.
Also, injuries from frostbite, surgery, or some jobs
may cause Raynaud's disease. Some workers in
the plastics industry who are exposed to vinyl
chloride develop a scleroderma-like illness and
have Raynaud's disease. Regular use of machinery
14

such as chain saws, jackhammers, and vibrating

drills can hurt blood vessels.
What are the symptoms?
Symptoms include:
changes in skin color (pale to blue to red)

changes in skin temperature (the area feels

cooler).

It is common for the area to throb or feel numb, tingly,

or painful as it warms up again or as stress is relieved.
How is it diagnosed?
Your healthcare provider will ask about your medical
history and examine you. You may have blood tests.
Depending on your history and exam, your provider
may check for diseases or other conditions that cause
secondary Raynaud's.
How is it treated?
Most healthcare providers recommend trying nondrug
treatments and self-help measures first, as described
below in the section on taking care of yourself.
Several kinds of medicines may be used to treat severe
Raynaud's symptoms. They all improve circulation.
Types of drugs that might be prescribed are calcium
channel blockers, alpha blockers, and vasodilators.
Nitroglycerin paste, which is put on the fingers, helps
improve your circulation and heal any sores on the
skin (caused, for example, by cuts or bug bites).
Drugs that help at first may get less effective over
time. Women of childbearing age should know that the
medicines used to treat Raynaud's disease might affect
the baby. If you are pregnant or are trying to become
15

pregnant, talk with your healthcare provider before

taking these medicines.
If you are taking a new medicine that seems to be
causing Raynaud's disease or making your existing
Raynauds disease worse, let your provider know. You
may need to change your medicine or dosage.

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Atherothrombosis

Atherosclerosis is a diffuse, systemic disease that affects the

coronary, cerebral, and peripheral arterial trees. Disruption of
atherosclerotic plaques leads to thrombus formation and
arterial occlusion. This unpredictable and potentially lifethreatening atherothrombotic sequence underlies clinical
events such as angina, myocardial infarction, transient
ischemic attacks, and stroke. One of the key components of a
clot is the platelet. Although it was previously thought that
platelets were relatively inactive cells that merely provided a
framework for the attachment of other cells and proteins to
mechanically stop bleeding due to injury, it is now known
that this is not the case. Platelets secrete and express a large
number of substances that are crucial mediators of both
coagulation and inflammation. This article reviews the
centrality of the platelet in atherothrombosis and briefly
looks at the efficacy of antiplatelet agents in preventing and
treating cardiovascular disease.
Atherothrombosis has essentially 5 phases.3 In the first
phase, endothelial dysfunction stimulates the deposition,
accumulation, and oxidation of low-density lipoprotein
cholesterol within the cells of the intima. The second and
third phases are the recruitment of inflammatory cells to the
endothelium and the growth of a plaque; during these phases,
smooth muscle cells migrate to the lesion and replicate, and
lipid-laden foam cells accumulate, held together by
extracellular matrix macromolecules such as collagen and
elastin. As these processes occur and the plaque matures, its
surface calcifies to form a fibrous cap. During the fourth
stage of atherothrombosis, the balance of smooth muscle cell
proliferation and removal changes, and breakdown outstrips
formation. The fibrous cap then ruptures, or the lesion
surface erodes, exposing the prothrombotic contents of the
17

plaque to the circulating blood. This triggers a dynamic

coagulatory response in which the platelet plays a primary
role, resulting in the formation of a platelet-rich thrombus
over the disrupted lesion (the fifth phase) and mechanical
disruption of the diseased artery. If blood flow is sufficiently
impeded, clinical manifestations (acute coronary syndromes,
ischemic stroke, and critical limb ischemia) result.

SUBCLAVIAN CORONARY STEAL SYNDROME

A 75-year-old man was transferred to our department from the local hospital because of
recurrent episodes of dyspnea and angina at rest, with significant 3.0-mV ST-segment
depressions in ECG leads V3 through V6. His medical history was significant for coronary
artery disease, 2-vessel coronary artery bypass grafts (1999), nondisabling stroke (2004),
type 2 diabetes mellitus, hypertension, and peripheral vascular disease. The patient also
complained of dizziness and weakness of the left hand. Clinical examination was
characterized by lack of radial pulse, and blood pressure could not be measured on the left
arm. The echocardiogram showed apex and inferior wall hypokinesis with slightly
diminished ejection fraction (50%).
Ultrasound examination revealed occlusion of the left internal carotid artery and reversed
flow through the left vertebral artery, confirmed by angiography (Figure 1). Symptomatic
vertebral-subclavian steal syndrome was diagnosed.

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Figure 1. Contrast injection into the brachiocephalic trunk and reversed flow through the
left vertebral artery in late phase. The figure is a composite of 2 images obtained during
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different phases of the same injection: early- and late-phase contrast filling.
Angiography of the left coronary artery showed the entire left internal mammary artery
(LIMA) graft (Figure 2) with reversed flow of contrast into the subclavian artery. The right
and circumflex coronary arteries were occluded, as well as the venous graft to the right
coronary artery. Contrast injection into the subclavian artery demonstrated critical 90%
stenosis in the proximal part of the subclavian artery, with a translesion pressure gradient
of 80 mmHg (Figure 3). Contrast selectively injected beyond the lesion merely showed the
proximal parts of the left vertebral artery and LIMA, indicating the presence of reversed
flow. Direct stenting of the subclavian artery was performed (Figure 4), and anterograde
flow through the left vertebral artery and LIMA was reestablished. Control coronary
angiography revealed only minor retrograde filling of the distal part of the LIMA,
indicating that the subclavian angioplasty had produced favorable results (Figure 5). At
discharge from the hospital, the patient was asymptomatic and the left radial pulse was
palpable. Although subclavian steal syndrome is rather rare, it can be manifested as acute
coronary syndrome among patients with LIMA grafts or vertebrobasilar insufficiency,
especially in the presence of concomitant internal carotid artery occlusion. Percutaneous
angioplasty is the preferred treatment option for those patients.

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Figure 2. Left lateral projection of the left anterior descending artery indicating reversed
flow through the LIMA.

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Figure 3. Critical stenosis of the proximal part of the left subclavian artery.

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Figure 4. The effect of stenting the left subclavian artery.

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