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B
FIGURE 16-1. Type I dissection of the aorta in a 74-year-old
man. The dynamic spiral computed tomography (CT) shows
the characteristic flap in a type I dissection involving the
ascending aorta (A) and the proximal aortic arch (B). The
brachiocephalic vessels were not involved. Calcification of
the wall of the aorta is noted. Transesophageal echocardiogram in a different patient with a type I dissection showing the
flap in the descending aorta (C). On the real-time image, the
flap oscillates in the lumen of aorta. The true lumen is closest
to the transducer and the false lumen is farther away. The
echogenicity beyond the aorta represents extravasated blood
C
in the mediastinum.
A B
Diseases of the Thoracic Aorta 165
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atherosclerosis, trauma, syphilis, idiopathic kyphoscoliosis, and congenital heart defects, such as coarctation
and pseudocoarctation of the aorta. Approximately 2,000
new cases of aortic dissection are diagnosed each year in
the United States.
3,4
The male-to-female ratio is approximately 2:1, with a peak incidence in the sixth and seventh
decades of life.
Two major classifications of aortic dissection are widely
used. The older classification, introduced by DeBakey et
al., divides aortic dissections into type I, which includes
those involving the ascending and descending aorta (Fig.
16-1); type II, which involves the ascending aorta only;
and type III, which involves the descending aorta (Fig.
5
16-4).
A mnemonic for this classification is “BAD”: type I
⫽ both aortas, type II ⫽ ascending aorta and type III ⫽
descending aorta. Another classification, introduced by
Dailey et al., and often called the Stanford classification,
divides aortic dissection into two groups. Dailey’s type A
includes proximal dissections as well as those distal dissections that extend retrograde to involve the arch and ascending aorta. Type B includes dissections of the distal
aorta without proximal extension.
6
Important variants of aortic dissection are caused by
penetrating ulcers and by intramural hemorrhage (IMH)
(Fig. 16-5).
7
Penetrating ulcers result from erosion of
atherosclerotic plaque with eventual violation of the inter-
A
nal elastic lamina.
8
Penetrating ulcers occur most often in
persons who have extensive atherosclerotic disease, but
not in persons with Marfan syndrome or other diseases of
connective tissue. Ulcers affect the mid-portion to distal
portion of the descending thoracic aorta almost exclusively and do not result in valvular, pericardial, or
neurovascular complications that occur with aortic dissection. The ulcer has a nipple-like configuration extending
B
FIGURE 16-2. Findings on chest roentgenography in a man with Marfan syndrome. A: Frontal view. B: Lateral view. Marked
dilatation of the root of the aorta produces a double density within the cardiac silhouette (pseudo left atrial enlargement). The
normal angle formed between the ascending aorta and the base of the heart is effaced by the dilated ascending aorta. The aorta
also displaces the main pulmonary artery superiorly and laterally, producing a bulge in the pulmonary artery segment simulating
pulmonary artery dilatation. In the lateral film, the dilated aortic root obliterates the retrosternal clear space. Thus, the lateral film
shows that the double density noted on the frontal view is due to the dilatation of the aortic root rather than enlargement of the
left atrium. Note that the dilatation of the root of the aorta does not extend into the aortic arch. Mild left ventricular enlargement
is present (same patient as in Fig. 16-3). (Courtesy of Spindola-Franco H, Fish BG, eds. Radiology of the heart: cardiac imaging
in infants, children, and adults. New York: Springer-Verlag, 1985:203.)
FIGURE 16-3. Aortic insufficiency in an asymptomatic patient with Marfan syndrome. The aortogram. A: Lateral view. B:
Shallow left anterior oblique (LAO) view shows that the root of
the aorta is dilated symmetrically and bulbous, with effacement
of the semilunar sinuses. Aortic insufficiency is present. In (B)a
arrows
tear is demonstrated in the anterolateral wall (
was not detected on the lateral film, which emphasizes the
requirement to look carefully for tears, using multiple views as
necessary. This example is a “silent aortic dissection” (same
patient as in Fig. 16-2). (Courtesy of Spindola-Franco H, Fish
BG, eds. Radiology of the heart: cardiac imaging in infants,
children, and adults. New York: Springer-Verlag, 1985:204.)
). The tear
166 H. Spindola-Franco, S. Segal, B. G. Fish, and M. A. Greenberg
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FIGURE 16-4. Complications of DeBakey type III aortic dissection in a patient who presented with acute abdominal pain.
The left anterior oblique (LAO) plane of a T1-weighted spinecho image shows two flaps distal to the left subclavian artery.
One false lumen is confined to the distal aortic arch and proximal descending aorta. The other extends into the abdomen,
compromising the superior mesenteric artery (
mia of the gut caused acute abdominal pain in this patient.
Angiography was not successful because the catheter could
not be advanced into the lumen of the aorta.
arrow
). Ische-
beyond the intima and is surrounded by hematoma. The
process may be contained spontaneously or may progress
to false aneurysm formation or aortic rupture (Fig. 16-6).
IMH may result from rupture of aortic vasa vasorum.
IMH differs from classic dissection in that hematoma
forms within the aortic wall, but an intimal tear is not
present.
10,11
Intramural hemorrhage may be the first
stage in the development of aortic dissection, the second
FIGURE 16-5. Angiogram and magnetic resonance imaging
(MRI) in a patient with intramural hemorrhage (IMH). A: Subtraction film from the left anterior oblique (LAO) view of an
aortogram. B: T1-weighted spin-echo pulse sequence MRI in
the sagittal plane. In (A) the aortic lumen is normal with no
intimal flap or leakage, whereas in (B) the high signal intensity
and increased thickness of the aortic wall indicate intramural
hemorrhage. The increased signal intensity indicates a subacute process. Acute hemorrhage would be isointense and may
not be separated from the wall of the aorta. Blood isalso present
in the mediastinum, considered a typical feature of IMH.
A
9
B
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A B
C
stage being an intimal tear that allows blood to flow into
the false lumen, extending the plane of dissection.
Complications of IMH are the same as with aortic dissection, but they are significantly less common with IMH
than with aortic dissection.
Clinical features
Aortic dissection often presents with severe chest pain
(anterior or posterior) with a tearing character. Pain is
maximal atonset and changes inlocation as the dissection
propagates. Painless (“silent”) dissection is rare (Fig. 16-
3). Acute complications include aortic insufficiency and
congestive heart failure. Aortic insufficiency occurs in up
to 50% of patients who undergo type A dissection secondary to either wideningor distortion of the aortic annulus,
causing failure of coaptation of the valve leaflets, or torn
leaflets. Congestive heart failure may result from sudden
onset of severe aortic insufficiency. Syncope as a present-
FIGURE 16-6. Acute perforation of an atherosclerotic ulcer in a 54year-old man with sudden onset of severe chest pain. Frames from a
dynamic spiral CT scan. A: The lowest slice, the ascending aorta is
dilated, but no dissection is noted. B: 1 cm higher, a jet of contrast exits
the aortic lumen into the mediastinum. C: 1 cm above (B), a collection
of contrast is noted just under the aortic arch. The surrounding fat is
dense (“dirty fat sign”), indicating infiltration with blood. These findings
are consistent with rupture of an atherosclerotic plaque. Soon after the
scan, the patient became more unstable and was taken to the operating
room. At surgery, an aortic dissection and a hemopericardium were
found, indicating that propagation of the pathologic process had occurred, accounting for the sudden deterioration after the scan.
ing symptom may be associated with rupture into the peri-
12
cardial cavity and cardiac tamponade. Physical findings
with aortic dissection include shock with normal to elevated blood pressure and pseudohypotension or pulse
deficits secondary todissection of the brachiocephalic vessels. Myocardial infarction occurs in a small percentage of
patients with proximal dissection, secondary to involvement of the coronary arteries. Neurological findings and
renal and mesenteric infarctions occuras a result of occlusion of related vessels. Leftventricular hypertrophyis commonly noted on electrocardiography. Aortic dissection
should be suspected in patients with chest pain and no
electrocardiographic signs of myocardial ischemia.
Imaging modalities
On chest roentgenography, the characteristic findings of
aortic dissection are a widened aortic contour and a “calcium sign” consisting of a greater than 5 mm separation
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H. Spindola-Franco, S. Segal, B. G. Fish, and M. A. Greenberg
of the calcification of the aortic arch from its outer contour. A left pleural effusion may be present, indicating
leakage into the pleural space. The trachea may be deviated. Importantly, the chest roentgenogram may be normal in aortic dissection.
TEE (Fig. 16-1) and MRI are both very sensitive in the
diagnosis of aortic dissection.
13,14
Advantages of TEE include the availability of this modality at the bedside, enabling diagnosis in acutely unstable patients. TEE is useful
in proximal and distal dissections. A disadvantage is its
inability to delineate the branches of the aortic arch
accurately. In addition, TEE is an invasive procedure.
If available, MRI is the procedure of choice in persons
with aortic dissection who are relatively stable and can
tolerate a longer procedure (Fig. 16-4). The advantages
of MRI include its ability to determine the exact extent
and site of origin of the dissection and its anatomic relationships with neighboring organs. MRI also allows the
diagnosis of associated aortic insufficiency and leakage.
By using MRI, thrombus or flow in the false lumen can be
detected. Cine MRI allows visualization of the oscillations
of the flap separating the false lumen from the true
lumen, which is a hallmark of aortic dissection.
Spiral and ultrafast CT are extremely useful in the
acute assessment of aortic dissection when MRI is not
available or when the patient cannot tolerate the time
required by the MRI examination (Fig. 16-1). Ultrafast
CT is available in only a few centers, whereas spiral CT
has replaced standard CT in many centers and often is
staffed through the night. The shorter time taken to
perform a CT study compared with the time taken by
MRI should be weighed against the radiation exposure
involved and the requirement to administer angiographic contrast medium. One limitation of CT relates to
difficulty in timing the injection to enhance the false
lumen.
MRI, spiral CT, TEE, and angiography are all complementary, and each has an ability to identify aortic dissection; however, angiography cannot detect IMH (Fig. 16-
15
5).
Atherosclerotic ulcers are detected by angiography,
but the hematoma surrounding a penetrating ulcer may
be missed. For this reason, angiography is not the primary diagnostic modality for these entities but should be
used when the others are not definitive.
Treatment
Without treatment, aortic dissection is a lethal disease.
Death occurs as a result of progression of the dissection,
which causes damage to vital structures. Ninety percent
of untreated patients die within one year, with the highest
mortality occurring during the first week after the on-
16
set.
Initial treatment for all patients includes beta-blockers and aggressive control of hypertension to prevent
progression. Proximal dissections are surgically repaired
early or even emergently because of the risk of catastrophic consequences such as acute aortic insufficiency, cardiac tamponade, and neurologic complications with even
minimal progression. On the other hand, distal dissections may be treated medically unless they show signs of
rupture, impending rupture, or renal or mesenteric compromise. Chronic dissections, which present 2 weeks or
longer after onset, also may be treated medically because
they already have passed the most dangerous period,
suggesting a nonlethal outcome. Surgery of proximal
dissections commonly consists of placement of a composite graft containing a prosthetic valve. The native ascending aorta is wrapped around the graft. The coronary
arteries are reimplanted using a button of native aorta to
facilitate the anastomosis. Conduit grafts also may be
used to replace the aortic arch and descending aorta.
Recently interventional procedures have become available as alternatives to surgery for dissections in the descending aorta.
17–19
Placement of a self-expandable covered stent (Gianturco stent) to cover the proximal entry
site reestablishes the true lumen by compressing the false
lumen so that thrombosis of the residual false lumen is
promoted. The catheter is inserted by way of the femoral
artery into the true lumen, and the intraluminal prosthesis is deployed slightly proximal to the entry site of the
dissection. The diameter of the device should be slightly
larger than the aortic diameter to prevent migration.
Another treatment option currently being explored is the
percutaneous creation of a reentry tear in an aortic dissection, which decompresses the false lumen of a dissection, thereby limiting its progression.
20
Long-term follow-up is necessary for patients treated
medically and surgically. Blood pressure must be controlled at the lowest level tolerated. Follow-up chest roentgenograms are essential to detect changes that suggest
late complications such as false aneurysms and leakage
into the pleural space. Serial imaging studies are also
essential to detect complications or progression. Currently, MRI is considered the procedure of choice.
21
■ Thoracic Aortic Aneurysms
Aneurysms of the thoracic aorta are localized, sac-like
dilatations of the aortic wall. All layers of the aortic wall
are involved. They may be saccular, in which only part of
the circumference is involved, or fusiform, if all or almost
all of the circumference is involved. Fusiform aneurysms
are four times more common than saccular aneurysms,
which are found chiefly in the ascending aorta.
Aneurysms may be congenital or acquired. Congenital
aneurysms are rare and mostly affect the sinuses of Valsalva. Causes of acquired thoracic aortic aneurysms include atherosclerosis, syphilis, trauma, cystic medial necrosis, arteritis, and infection (mycotic). Atherosclerotic
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aneurysms are the most common, and their incidence is
increasing as a consequence of increasing longevity of the
population. They are more common beyond the aortic
arch. Syphilitic (luetic) aneurysms are most common in
the ascending aorta. Posttraumatic aneurysms occur in a
small number of persons who survive chest trauma.
These are found mainly in the most proximal portion of
the descending aorta, resulting from a small tear. Mycotic
aneurysms, also called infected aneurysms, are rare and are
caused by sepsis in the wall of the aorta or any vessel.
Infection can cause fusiform, saccular, or even false aneurysms. They can perforate into adjacent venous structures, resulting in arteriovenous fistulae.
Annuloaortic ectasia is a specific subgroup of aortic
aneurysm affecting the root of the aorta and the aortic
annulus (Figs. 16-2 and 16-3). This entity is typical of
Marfan syndrome and other conditions associated with
cystic medial necrosis. Persons with annuloaortic ectasia
should be investigated for other stigmata of Marfan syndrome. The ectasia is often progressive, leading to aortic
insufficiency, congestive heart failure, dissection and rupture of the ascending aorta, sometimes resulting in sudden death. A diameter greater than 7 cm is associated with
a high incidence of aortic dissection, and usually this
measurement in itself constitutes sufficient grounds for
replacement of the aortic root and the aortic valve with a
valved conduit. The coronary arteries are reimplanted
into the conduit. Cystic medial necrosis with dilatation of
the aortic root also occurs in Ehlers-Danlos syndrome,
osteogenesis imperfecta, homocysteinuria, Larsen syndrome, and Cogan syndrome.
Clinical features
Presenting features relate to the size and location of
the aneur ysm. Small aneurysms may be asymptomatic
whereas large aneurysms produce symptoms by directly
compressing adjacent structures. Wheezing, cough, dyspnea, stridor, hemoptysis, recurrent pneumonitis, intrapulmonary hemorrhage, and superior vena cava syndrome
all may result from large thoracic aneurysms. As with aortic dissection, acute aortic insufficiency may result in
acute congestive heart failure. Collapse and sudden death
may be caused by rupture of an aortic aneurysm. Most
patients, however, die of associated disease unrelated to
the aneurysms (e.g., coronary artery disease). Patients
with mycotic aneurysms have other signs of infection,
such as high fever. Other features that differentiate mycotic aneurysms from uninfected aneurysms include tenderness, lack of calcification, and early vertebral erosion.
bulge (Fig. 16-7). The differential diagnosis includes an
uncoiled aorta (atherosclerotic elongated aorta), kinking or
buckling of the aorta (pseudocoarctation), and poststenotic
dilatation (aortic stenosis). A localized aneurysm may be
confused with a mediastinal mass. Calcification occurs
much less commonly in thoracic aneurysms than in aneurysms involving the abdominal aorta.
Axial or spiral CT, MRI, TEE, and angiography are all
definitive in the diagnosis of aneurysms of the thoracic
aorta. If available and not contraindicated (e.g., pacemaker, hemodynamic instability), MRI is the procedure
of choice. No radiation is involved, and no intravenous
contrast needs to be administered.
Treatment
Survival is related to the size of the aneurysm. Aneurysms
larger than 6 to 7 cm in diameter and those causing
symptoms by compression are more likely to rupture
than smaller ones. Surgical excision is indicated in aneurysms greater than 7 cm in the ascending or descending
aorta and in smaller aneurysms if they produce symptoms.
■ Aortic Trauma
Injuries to the thoracic aorta may be blunt or penetrating.
Blunt trauma may be associated with a sudden high-speed
deceleration on impact, such as a motor vehicle accident
or severe fall or explosion. Abrupt deceleration creates
shearing forces ata point where a highly mobile portion of
the aorta joins a relatively fixed segment. The most common site is the aortic isthmus (the portion of the aorta
between the left subclavian artery and the ligamentum
arteriosum), which is attached to the relatively fixed segment at the site of insertion of the ligamentum arteriosum. The secondmost frequent site is the ascending aorta,
just above theaortic valve. Tears of the ascending aorta are
associated withsignificantly higher mortality than those in
the isthmic region. Recently, an “osseous pinch mechanism” was described in which the spine and manubrium/clavicle/first rib may play a role during acute deceleration injury.
interventions such as cardiac catheterization or balloon
dilatation of coarctation of the aorta. The tear of the aorta
may be small, resulting in a localized aneurysm or false
aneurysm, or it may be circumferential, resulting in transection of the aorta.
22
Aortic trauma also may result from
Imaging modalities
Most aneurysms are easily detectable on chest roentgenography, appearing as a dilated aorta or as a localized
Clinical features
A high index of suspicion is needed because severe injuries of the central nervous system, visceral injury, and
multiple fractures may overshadow the diagnosis. The
170 H. Spindola-Franco, S. Segal, B. G. Fish, and M. A. Greenberg
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A B
FIGURE 16-7. Aneurysmal dilatation of the aorta
in a 67-year-old man noted on chest roentgenogram. A: Frontal. B: Lateral. The magnetic resonance imaging (MRI) and computed tomography
(CT) scan showed no dissection. C: The aorto-
gram in the left anterior oblique (LAO) view was
performed at the time of coronary angiography.
The ascending aorta measures 5 cm above the
sinotubular junction. The coronary ostia are unobstructed. Mild aortic insufficiency was noted. The
aortic arch and descending aorta also were aneurysmally dilated (not shown). The patient was
C
syndrome of “acute coarctation” (upper-extremity hypertension, low pressure in the lower extremities, systolic
noted. An aortic insufficiency murmur is heard with significant tears of the ascending aorta.
monitored medically.
murmur over the precordium or in the interscapular
region, and a palpable radial-femoral pulse lag) is diagnostic. Other signs of aortic trauma include hoarseness,
cough, or dysphagia from compression of the adjacent
recurrent laryngeal nerve, trachea, or esophagus. Additionally, swelling of the lower neck and paraplegia may be
Imaging modalities
The roentgenogram of the chest is essential in the diagnosis of trauma even in the absence of classic clinical
features. Signs include a widened mediastinum, oblitera-
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tion of the aortic arch (knob), a rightward tracheal shift,
depression of the left mainstem bronchus, displacement
of the nasogastric tube to the right, displacement of the
right or left paraspinal line, and opacification of the
space between the descending aorta and the pulmonary
23
artery.
A pleural effusion, especially one that obliterates
the left thoracic apex (apical cap sign) is an important
24
sign.
An aortic transection also can occur in the absence
of these signs. The portable technique and other factors
occuring during the course of acute trauma may obscure
the findings. Bone fractures, pulmonary contusion,
pneumothorax, and pneumoperitonium indicate severe
thoracic trauma, and should result in a suspicion of aortic
trauma.
Despite the advent of sophisticated noninvasive imaging modalities such as spiral CT and MRI, angiography
remains the diagnostic procedure of choice when aortic
transection is suspected. MRI can provide a complete
diagnosis in patients with aortic trauma, but it requires a
lengthy procedure and may not be practical for critically
ill patients who are instrumented with multiple invasive
monitoring and life support devices. High-speed CT may
be a useful primary imaging modality. Abdominal CT can
be performed concurrently. Associated hemorrhage and
hematoma, which might be missed by both chest roentgenography and angiography, may be detected by CT
scanning or MRI. It is important to note that traumatic
rupture of the aorta can be missed on CT scanning unless
a linear lucency inside the aortic lumen caused by the
torn edge of the aortic wall is noted or a dissection is
present. Irregularity of the intima of the opacified aortic
lumen and periaortic or intraluminal hematoma are
other confirmatory findings on CT scanning, but these
may not be diagnostic. Mediastinal hematoma usually is
caused by tearing of small vessels, which requires no
treatment. Immediate angiography with digital subtraction should follow if the CT scan is not definitive and the
patient is stable. If a patient cannot be moved, TEE may
be performed at the bedside to exclude transection of
the aorta. In the future, intravascular ultrasound may
play an important role.
25,26
Treatment
Surgery should be performed as soon as possible once
aortic transection is diagnosed. The repair consists of
resection of the torn edges and interposition of a graft.
The distal circulation may be supported by a pump oxygenerator or by a conduit bypass. Late sequelae include
aneurysms that may require secondary surgical excision
to prevent dissection and rupture. Early animal trials that
may lead to the replacement of surgical treatment using
covered endovascular stents in selected subjects are ongo-
27
ing.
■ Penetrating trauma
Penetrating trauma to the aorta and its branches is caused
by puncture or laceration, most commonly a result of a
bullet or stab wound. These are likely to cause acute exsanguination and require immediate surgical exploration
with or without the findings on chest roentgenography of
a widened mediastinum, pleural effusions, and cardiomegaly (hemopericardium). Although signs of acute
penetrating trauma may be obtained by angiography or by
CT scanning, these patients are usually too unstable to
allow these studies.
■ Aortic Arteritis Syndromes
Aortitis is caused by an infectious or immunologic process
that affects any layer of the wall of the aorta. Aortitis may
manifest as aneurysmal dilatation (ectasia) or as segmental narrowing. The aneurysmal form is more common,
and fusiform aneurysms are more common than saccular
ones. Conditions that result in ectasia of the ascending
aorta frequently cause aortic insufficiency. These conditions include Takayasu’s arteritis, giant cell arteritis, syphilis, rheumatoid arthritis, ankylosing spondylitis, psoriatic
arthritis, ulcerative colitis, relapsing polychondritis, and
Reiter syndrome. Stenosing aortitis occurs in a few conditions, including Takayasu’s arteritis and radiation aortitis.
In most inflammatory diseases of the aorta, the media is
primarily involved, with occasional damage to the adventitia. Thickening of the intima is a reactive phenomenon.
Rheumatic fever and rheumatoid arthritis cause an inflammatory reaction and fibrinoid necrosis of all three
layers of the aorta, resulting in a true panaortitis.
28
Takayasu’s arteritis is a syndrome caused by a panarteritis and leads to narrowing and occlusion of the aorta and
its branches. Less commonly, the coronary ostia may be
involved. Localized areas of dilatation also mayoccur (Fig.
16-8). This syndrome usually occurs in young women, occasionally in children, and rarely in infants and middleaged individuals. The female-to-male ratio is 8.5:1, peaking in the teenage years.
The syndrome has been classified into four subtypes
according to the site of involvement. Type I (8%) involves
the aortic arch and brachiocephalic vessels. Type II (11%)
affects the thoracoabdominal aorta, especially the renal
arteries. Type III (65%) combines the features of both
types I and II. Type IV (45%) includes characteristics of
the first three types along with involvement of the pulmonary arteries.
29
Clinically, there are two recognized phases of the syndrome. The early, or systemic phase, is characterized by
the signs and symptoms of a generalized inflammatory
process, such as fever, anorexia, malaise, weight loss, night
172 H. Spindola-Franco, S. Segal, B. G. Fish, and M. A. Greenberg
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FIGURE 16-8. Abdominal aortogram in a 6-year-old girl with
Takayasu arteritis and severe systemic hypertension. Marked
aneurysmal dilatation of the abdominal aorta is noted with
minimal narrowing of the right and severe narrowing of the left
common iliac artery. Similar changes were found in the thoracic aorta on magnetic resonance imaging (MRI).
sweats, arthralgias, pleuritic pain, and fatigue. This phase
generally lasts from weeks to months and is followed by
the occlusive features of the late phase, which include
diminished or absent pulses (96%), bruits (94%), hypertension (74%), and congestive heart failure (28%). Angina or myocardial infarction may occur if coronary arteries are involved.
30
The etiology of Takayasu’s arteritis is probably autoimmune, although no specific cause has been identified.
Laboratory studies in the early phase are consistent with
an autoimmune etiology but are nonspecific and include
elevated erythrocyte sedimentation rate, low-grade leukocytosis, and mild anemia.
Imaging modalities
In the early phase, the chest roentgenogram is frequently
normal. In the late phase, nonspecific findings such as
cardiomegaly and congestive heart failure may be pre-
FIGURE 16-9. Aneurysmal dilatation of the aorta and severe
aortic insufficiency in a 31-year-old patient with giant cell arteritis. The frontal chest roentgenogram shows cardiomegaly with
moderate left ventricular dilatation. The left heart border is
elongated, and the cardiac apex projects below the left hemidiaphragm. The ascending aorta and the aortic arch are markedly dilated. Mild pulmonary venous hypertension is indicated
by equalization of the caliber of the upper and lower pulmonary
vessels. Microscopic examination of surgical specimens of the
aortic wall showed giant cell aortitis (same patient as in Fig.
16-10). (Courtesy of Spindola-Franco H, Fish BG, eds. Radiology of the heart: cardiac imaging in infants, children, and
adults. New York: Springer-Verlag, 1985:200.)
sent. The authors observed abnormal dilatation of the
descending aorta. In addition, rib notching resulting
from acquired coarctation has been observed in severe
cases. Angiography, spiral CT, and MRI demonstrate
characteristic findings such as stenosis of the aorta and its
branches and poststenotic dilatation, saccular aneurysms,
and even occlusions. The aorta may present the typical
“rat-tail narrowing.” Echocardiography is helpful in assessing left ventricular function and in identifying the
presence of thrombus in the left ventricle.
Treatment
Treatment is directed at control of the initial inflammatory process using steroids. Congestive heart failure and
hypertension are treated with medical therapy. Surgical
intervention occasionally is required in severe cases. Endarterectomy or bypass surgery is used for obstructive lesions. Excision of aneur ysms, and rarely aortic valve replacement, may be necessary. Balloon angioplasty has
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173
been used in selected cases. Endovascular covered stents
for treatment of aneurysms, or a combination of stenting
and balloon dilatationfor selectedstenotic lesions, may be
useful.
■ Giant Cell Arteritis
Giant cell arteritis, also known as temporal arteritis, is a
granulomatous arteritis that involves medium-sized arteries in patients aged 50 years and older. The mean age of
onset is 69 years, and 64% of cases occur in women. The
aorta and its branches are involved in 15% of cases. The
etiology is unknown, but it may be infectious or autoimmune. The disease may manifest rapidly or it may have an
insidious course. The triad of severe headache, malaise,
and fever, along with aching and myalgias of the shoulder
and pelvic girdle musculature, neck, and proximal extremities, has been called polymyalgia rheumatica. The
symptoms of claudication, headache, visual changes, and
scalp tenderness are the result of arteritis. Claudication
can occur in muscle groups in which the vascular supply
is involved. Most commonly, muscles of mastication, deglutition, and the extremities are involved. Visual symptoms include diplopia, ptosis, and blindness, either partial or complete. Rarely, the aorta may be the first target,
mimicking Takayasu’s arteritis. Even more rarely, aortic
aneurysms, aortic insufficiency, and aortic dissection may
occur. Death can occur from heart failure, aortic rupture,
or dissection. Laboratory findings, such as an elevated
erythrocyte sedimentation rate, are nonspecific, reflecting an inflammatory process. A definitive pathologic diagnosis usually is established by examining multiple biopsies of the temporal arteries.
28
Imaging modalities
In patients with aortic involvement, chest roentgenography shows a widened mediastinum (Fig. 16-9). The left
ventricle may beenlarged if significant aortic insufficiency
is present. MRI is the procedure of choice to assess the
degree of aortic involvement and the presence of aortic
insufficiency. TEE may help to distinguish giant cell arterities from arteriosclerotic disease because irregularities of
the wall and pedunculated plaques noted with arteriosclerosis are not present in giant cell arteritis. CT is indicated
when signs of dissection are evident, and immediate diagnosis is necessary. Cardiac catheterization may be required before surgery to assess the extent of aortic insufficiency relative to the need for replacement of the aortic
valve (Fig. 16-10).
FIGURE 16-10. Aortogram in a 31-year-old man with giant cell arteritis and aortic insufficiency. A:Anteroposterior view. B: Lateral
view. The ascending and descending aorta are dilated. The arch is also dilated but to a lesser extent. The root of the aorta and the
semilunar sinuses also are dilated. The left ventricle opacifies densely because of severe aortic insufficiency. The coronary
arteries usually are dilated in patients with severe aortic insufficiency (same patient as in Fig. 16-9). (Courtesy of Spindola-Franco
H, Fish BG, eds. Radiology of the heart: cardiac imaging in infants, children, and adults. New York: Springer-Verlag, 1985:205.)
BA
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