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174 H. Spindola-Franco, S. Segal, B. G. Fish, and M. A. Greenberg
https://t.me/med1917
ment must be initiated once the diagnosis is suspected in
order to prevent blindness. The histopathologic findings
will not be masked if the biopsy is performed within 1
week. Rarely, surgical excision of an expanding aneurysm
or replacement of the aortic valve with a composite graft
may be necessary.
FIGURE 16-11. Periaortic neoplasm in a 19year-old man with neurofibromatosis. The T1weighted spin-echo magnetic resonance imaging
(MRI) in an axial plane shows the neoplasm encasing all of the mediastinal structures. The superior vena and the aorta are widely separated by
tumor interposition. No cleavage plane is identified between the mass and the vascular structures to permit surgical debulking.
FIGURE 16-12. Magnetic resonance imaging (MRI) studies in
a 16-year-old boy who had balloon angioplasty (BAP) for correction of a juxtaductal coarctation of the aorta. The fast field
echo (cine gradient) MRI was performed to exclude aneurysm
formation, dissection, or recoarctation at the site of the BAP.
None of these sequelae was present.
■ Periaortic Pathology
The aorta may be secondarily involved by extrinsic pathology. Neoplasms, abscesses, and hematomas can be
suspected by chest roentgenogram. MRI and CT permit
precise preoperative evaluation (Fig. 16-11).
■ Congenital Diseases of the Aorta
and Its Branches
Of the congenital thoracic diseases, coarctation of the
aorta and pseudocoarctation of the aorta (buckled aorta)
are the most common. Coarctation of the aorta is diagnosed in infants as well as in children and adults. In
infants, it can cause acute congestive heart failure and
often is associated with other cardiac defects such as
bicuspid aortic valve, mitral valve pathology, ventricular
septal defect, patent ductus arteriosus, endocardial fibroelastosis, and complex intracardiac disorders. In older
children and adults, it is found in some patients during
evaluation for hypertension and stroke.
Imaging
Treatment
High-dose steroids will control inflammation and prevent
progression of all manifestations of the disease. Treat-
The roentgenogram of the chest may show a classic “three
sign,” whereas a barium esophagogram may show a “reverse three sign,” or “E sign.” Subtle signs include an
inconspicuous aortic arch with a prominent descending
aorta and a prominent left subclavian artery. Rib notch-
Diseases of the Thoracic Aorta 175
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B
A
FIGURE 16-13. Congenital coarctation of the aorta and se-
vere valvular and peripheral pulmonic stenosis in a 12-year-old
boy treated by stenting procedures. The PA and lateral chest
roentgenograms (A,B) show a stent in the aortic arch and in
the thoracic aorta, and also one in each pulmonary artery.
Coronal T1 magnetic resonance imaging (MRI) before the
stenting procedure (C) demonstrates severe stenosis of the
pulmonary valve (arrow) and marked hypoplasia of the left and
right pulmonary artery. Severe biventricular hypertrophy is also
evident. Fast field echo
(gradient echo)
in the left anterior
oblique plane (D) demonstrates severe coarctation of the aorta
with turbulence
(signal void)
just distal to the narrowing.
C
D
176 H. Spindola-Franco, S. Segal, B. G. Fish, and M. A. Greenberg
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ing, formerly one of the classic signs of coarctation of the
aorta, is now rarely notedbecause diagnosisand treatment
occur earlier.
Pseudocoarctation is an important finding on plain
chest roentgenograms caused by a buckled aorta. An
acute bend in the aorta is noted at the site of the ligamentum arteriosum. A bicuspid aortic valve may be associated
but this occurs less frequently than with coarctation of
the aorta. Depending on the severity of the kink, no
pressure gradient may be noted or a small pressure gradient may be found. Although a barium esophagogram
may show two indentations in the esophagus similar to
the reverse three sign or E sign noted with coarctation of
the aorta, an MRI is definitive and is indicated if a pseudocoarctation cannot be differentiated from a mediastinal mass on plain films of the chest.
Treatment
Treatment in infants requires stabilization with prostaglandin E
gery to correct the defect. The left subclavian artery often
is used as a roof patch (also called a subclavian flap) to use
native tissue in the repairrather than exogenous material.
The left subclavian artery is ligated and divided distally. Its
proximal portion is incised longitudinally to match a longitudinal split along the coarcted segment. The subclavian artery then is opened, turned down, and sutured
to the two sides of the split aortic isthmus and coarcted
segment forming a roof, thus enlarging the lumen of the
aorta. Excision and end-to-end anastomosis or a prosthetic patch may be necessary in other persons. In infants,
balloon angioplasty generally is not performed in native
coarctation because of the risk of aortic rupture at the site
of the ductus arteriosus. If restenosis occurs, balloon
angioplasty can be used safely as a secondary repair.
Coarctation of the aorta in children and adults is often an
isolated defect but may be associated with aortic and
mitral pathology. It also may be associated with aneur ysmal dilatation of the aortic root. Complications include
Berry aneurysm and subarachnoid hemorrhage, aortic
dissection, and infective endocarditis with mycotic aneurysm. Coarctation of the aorta also may present with congestive heart failure. In children and adults, some physicians prefer balloon angioplasty for treatment (Fig.
16-12), whereas some centers treat native coarctation in
persons of any age by surgical means. In the unusual cases
in which balloon angioplasty fails to dilate a coarcted segment, a stent
the vessel (Fig. 16-13). Persons who have severe dilatation
of the aortic root will require replacement of the aortic
root and aortic valve at the time of the coarctation repair.
A prosthetic conduit between the ascending and the descending aorta, or between the left subclavian artery and
the descending aorta, also may be used.
(PGE1) and cardiac inotropes, followed by sur-
1
32
may be deployed to maintain patency of
■ Postoperative Complications
Common thoracic procedures include aortic valve replacement, coronary artery bypass grafting, placement of
a valved conduit for aortic dissection, placement of intravascular stents, surgical repair, and balloon angioplasty
of coarctation of the aorta. The most common complications following these procedures include mediastinal or
paravalvular leakage, infection, dissection, and true and
false aneur ysms. Complications should be suspected in
the presence of a wide superior mediastinum, retrosternal obliteration of the clear space, pleural effusions, or
an unusual cardiac silhouette.
REFERENCES
1. Spindola-Franco H, Fish BG. Abnormalities of the aortic arch and
pulmonary arteries—vascular rings and slings. In: Elliot LP, ed.
Cardiac imaging in infants, children, and adults. Philadelphia: JB Lippincott, 1991:344–368.
2. Spindola-Franco H, Fish BG. Left heart obstruction. In: SpindolaFranco H, Fish BG, eds. Radiology of the heart: cardiac imaging in
infants, children, and adults. New York: Springer-Verlag, 1985: 540–
583.
3. Wolfe WG, Moran JF. The evolution of medical and surgical management of acute aortic dissections. Circulation 1977;56:503–505.
4. Lindsay J Jr. Aortic dissection. In: Lindsey and Hurst, eds. The Aorta.
New York: Grune and Stratton, 1979:239.
5. DeBakey ME, Henly WS, Cooley DA, Morris GC Jr, Crawford ES,
Beall AC. Surgical management of dissecting aneurysms of the
aorta. J Thorac Cardiovasc Surg 1965;49:130.
6. Dailey PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway
NE. Management of acute aortic dissections. Ann Thorac Surg
1970;10:237–247.
7. O’Gara PT, DeSanctis RW. Acute aortic dissection and its variants:
toward a common diagnostic and therapeutic approach. Circulation
1995;92:1376–1378.
8. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating athero-
31
sclerotic ulcers of the thoracic aorta: natural history and clinic
pathologic correlation. Ann Vasc Surg 1986;1:15–23.
9. Gore I. Pathogenesis of dissection aneurysm of the aorta. Arch
Pathol 1952;53:142–153.
10. Nienaber CA, von Kodolitsch Y, Petersen B, et al. Intramural hemorrhage of the thoracic aorta: diagnostic and theraputic implications. Circulation 1995;92:1465–1472.
11. Yamada T, Tada S, Harada J. Aortic dissection without intimal tear:
diagnosis with MR imaging and CT. Radiology 1988;168:347–352.
12. Wilson SK, Hutchins GM. Aortic dissecting aneurysms: causative
factors in 204 subjects. Arch Pathol Lab Med 1982;106:175–180.
13. Laissy JP, Blanc F, Soyer P, et al. Thoracic aortic dissection:diagnosis
with transesophageal echocardiography versus MR imaging. Radiol-
ogy 1995;194:331–336.
14. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of
thoracic aortic dissection by noninvasive imaging procedures. N
Engl J Med 1993;328:1–9.
15. Bansal RC, Chandrasekaran K, Ayala K, Smith DC. Frequency and
explanation of false negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol
1995;25:1393–1401.
16. Anagnostopoulos CE, Prabhakar MJS, Kittle CF. Aortic dissections
and dissecting aneurysms. Am J Cardiol 1972;30:263–273.
17. Kato N, Hirano T, Takeda K, Nakagawa T, Mizumoto T, Yuasa H.
Diseases of the Thoracic Aorta
https://t.me/med1917
177
Treatment of acute aortic dissections with expandable metallic
stents: experimental study. J Vasc Intervent Radiol 1994;5:417–423.
18. Marty-Ane CH, SerreCousine O, Laborde JC, Costes V, Mary H,
Senac JP. Use of a balloon-expandable intravascular graft in the
management of type B aortic in an animal model. J Vasc Inter vent
Radiol 1995;6:97–103.
19. Marty-Ane C, Serres-Cousine O, Laborde JC, Costes V, Alauzen M,
Mary H. Use of endovascular stents for acute aortic dissection: an
experimental study. Ann Vasc Surg 1994;8:434–442.
20. Williams DM, Andrews JC, Marx MV, Abrams GD. Creation of
reentry tears in aortic dissection by means of percutaneous balloon
fenestration: gross anatomic and histologic considerations. J Vasc
Intervent Radiol 1993;4:75–83.
21. Gaubert JY, Moulin G, Mesana T, et al. Type A dissection of the
thoracic aorta: use of MR imaging for long-term follow-up. Radiology
1995;196:363–369.
22. Cohen AM, Crass JR, Thomas HA, Fisher RG, Jacobs DG. CT evidence for the “osseous pinch” mechanism of traumatic aortic injury. AJR Am J Roentgenol 1992;159:271–274.
23. Marsh DG, Strum JT. Traumatic aortic rupture: roentgenographic
indications for angiography. Ann Thorac Surg 1976;21:337–340.
24. Simeone JF, Deren MM, Cagle F. The value of the left apical cap in
the diagnosis of aortic rupture. Radiology 1981;139:35–37.
25. Williams DM, Dake MD, Bolling SF, Deeb GM. The role of intravascular ultrasound in acute traumatic aortic rupture. Semin Ultrasound
CT MRI 1993;14:85–90.
26. Williams DM, Simon HJ, Marx MV, Starkey TD. Acute traumatic
aortic rupture: intravascular US findings. Radiology 1992;182:247–
249.
27. Williams DM, Andrews JC, Chee SS, Marx MV, Abrams GD. Canine
model of acute aortic rupture: treatment with percutaneous delivery of a covered Z stent—work in progress. J Vasc Intervent Radiol
1994;5:797–803.
28. Lande A, Berkman YM. Aortitis: pathologic, clinical and arteriographic review. Radiol Clin North Am 1976;14:219–240.
29. Ueda H, Morooka S, Ito I, Yamaguchi H, Takeda T, Saito Y. Clinical
observation of 52 cases of aortitis syndrome. Jpn 1969;10:277–288.
30. Lupi-Herrera E, Sanchez-Torres G, Marcushamer J, Mispireta J,
Horwitz S, Espino-Vela J. Takayasu’s arteritis: clinical study of 107
cases. Am Heart J 1977;93:94–103.
31. Anjos R, Qureshi SA, Rosenthal E, et al. Determinants of hemodynamic results of balloon dilation of aortic recoarctation. Am J
Cardiol 1992;69:665–671.
32. O’Laughlin MP, Perry SB, LockJE, Mullins CE. Use of endovascular
stents in congenital heart disease. Circulation 1991;83:1923–1939.
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S.I. Wahl and P. S. LakritzThoracic Outlet and Upper Extremi ties
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17
■■■
Thoracic Outlet and Upper Extremities
SAMUEL I. WAHL AND PHILLIP S. LAKRITZ
■ Indications for Arteriography and
Venography of the Thoracic Outlet and
Upper Extremities
Indications for arteriography of the thoracic outlet and
upper extremities include the evaluation of upper extremity ischemia, trauma, aneurysms, vasculitides, and
arteriovenous malformations. Venography of the thoracic
outlet and upper extremities are used routinely in the
evaluation of thoracic outlet obstruction, superior vena
cava (SVC) syndrome, and hemodialysis access shunts.
Techniques of upper-extremity arteriography
Vascular access for upper-extremity arteriography can be
achieved by using a 4 or 5 Fr diagnostic catheter using
the Seldinger technique via a transfemoral approach.
Additionally, access can be achieved either from an axillary or from a brachial artery approach if the transfemoral approach is not technically feasible. The axillary
approach has fallen out of favor because of the potential
for brachial plexus injury caused by an access site hematoma. The reported frequency of brachial plexus injury
has been between 0.4 and 9.5%. The axillary approach
has been replaced by the brachial artery approach.
Headhunter-type catheter may be used to catheterize the
brachiocephalic vessels in younger patients, but catheterization may be accomplished more easily by using a
Simmons-type catheter in older patients who have tortuous vessels.
The examination should begin with thoracic arch aor-
tography. A complete arteriographic examination of the
1
upper extremities necessitates evaluation of the entire
vasculature from the origins of the brachiocephalic and
left subclavian arteries to the level of the digital arteries.
It is imperative that the arteries of the entire extremity be
evaluated thoroughly because abnormalities of the inflow
arteries may result in distal clinical symptoms. Furthermore, as many as 15% of patients have an aberrantly high
origin of the radial artery arising from the axillary artery,
a finding that may be overlooked if evaluation of the
more proximal vessels is neglected (Fig. 17-1). Less frequently, the ulnar artery has an aberrantly high origin
arising from the brachial artery.
Arterial spasm may be encountered during arteriography of the upper extremity but usually subsides spontaneously or after the intraarterial injection of medications
such as tolazoline, phentolamine, or nitroglycerin. These
vasodilators also enhance blood flow to the distal extremity, improving digital artery visualization.
ture of the upper extremity is a critical factor influencing
vascular tone and blood flow to the hand and digits.
Decreased skin temperature may result in spastic narrowing of blood vessels, whereas temperature elevation improves blood flow. It is well known that artificial temperature elevation with the use of heating pads or warm water
improves visualization of distal arteries of the upper extremity and hand.
A
dilatation, such as general anesthesia, stellate ganglion
blockade, and oral alcohol, have fallen into disuse.
Attention must be given to secondary signs that indicate the presence of vascular disease such as opacification
of collateral vessels or retrograde filling of the vertebral
artery as a result of a proximal subclavian artery or brachiocephalic artery stenosis. These secondary findings
4
Older techniques of promoting vaso-
2
3
The tempera-
5
179
180 S. I. Wahl and P. S. Lakritz
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FIGURE 17-1. High origin of the left radial artery (arrow) from
the brachial artery.
are important because less complete views of the upper
extremities may fail to uncover significant underlying
disease.
Upper-extremity arterial contrast injections can be
quite painful; however, the degree of discomfort has been
decreased since the introduction of digital subtraction
angiography (DSA), which allows for the use of more
dilute and lower volumes of contrast media compared
with cut-film angiography. Newer, low-osmolar contrast
agents tend to be better tolerated than the standard highosmolar agents.
6
Disease entities
Conditions resulting in upper-extremity arterial insufficiency may be attributable to abnormalities extending
from the inominate or subclavian arteries to the digital
arteries. The etiologies of critical ischemia of the upper
extremity are quite variable, involving both small- and
large-vessel arteridites, trauma, atherosclerosis, and vascular complications secondary to thoracic outlet obstruc-
7
tion.
tributed to the perpendicular origin of the left subclavian
artery from the aortic arch.
8
In upper-extremity claudication, multiple segmental
occlusions may be identified (Fig. 17-2). Less frequently,
embolization may occur, resulting in distal ischemia of
the upper extremity.
9
Most emboli arise from a cardiac
source, such as emboli resulting from atrial fibrillation or
endocarditis.
3,10–12
Emboli may be secondary to atherosclerosis, frequently within the subclavian artery, or as
the result of arterial injury secondary to trauma (Fig.
17-3). In up to one third of cases, digital ischemia may
be due to embolic occlusion and may mimic primary
distal disease of the upper extremities. Therefore, evaluation of the proximal vessels during angiography is imperative.
3
The goal of arteriography in the setting of embolic occlusion is to demonstrate arterial reconstitution distal to
the site of occlusion so that proper management may be
planned, such assurgical embolectomy, surgicalbypass, or
transcatheter thrombolysis. Catheter-directed thrombolysis is frequently the initial treatment of choice.
13
Trauma
Indications for arteriography for the evaluation of trauma
include diminished or absent distalpulses, thepresence of
a bruit, pulsatile or expanding hematoma, hemothorax,
electrical trauma. Trauma to the vessels of the thoracic
outlet and upper extremities is classified by the mechanism of injury as penetratingor nonpenetrating. Both types of
injuries are potentially limb threatening.
Penetrating trauma from either gunshot or knife
wounds is frequently encountered in the emergency setting. Penetrating trauma may lead to direct intimal injury, vessel transection with or without extravasation of
blood and formation of pseudoaneurysms (Fig. 17-4),
dissection, occlusion, spasm, arteriovenous fistula formation (Fig. 17-5), and arterial displacement by hematoma.
Slow antegrade flow of blood may be identified angiographically and is often due to spasm induced by the
trauma itself or to compartment syndrome.
14
Atherosclerosis
Manifestations of atherosclerosis of the upper extremities
vary widely and usually involve proximal rather than distal arteries.
Raynaud’s phenomenon. The left upper extremity is
more commonly the symptomatic extremity. This is at-
1
Symptoms include claudication, ulcers, and
FIGURE 17-2. Atherosclerosis in long-standing diabetes; extensive stenotic and occlusive disease of the medium and
small vessels of the forearm and wrist.
Thoracic Outlet and Upper Extremities 181
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FIGURE 17-3. A: High brachial artery embolic occlusion in a patient with atrial fibrillation and
acute onset of ischemic left upper extremity pain. Note the smaller filling defect in the humeral
circumflex branch (arrow). B: Distal emboli in the proximal right radial and ulnar arteries evident
by “tram track” filling defects. Patency was reestablished after transcatheter thrombolysis.
BA
Repetitive blunt trauma may result in pathologic
changes in the vessel, including intimal tears or pseudoaneurysms with mural thrombus formation. In turn, this
thrombus may result in distal embolization and consequent ischemia. Therefore, prompt diagnosis is critical to
minimize morbidity.
15
This type of injury is seen in athletes in whom repetitive motion is the underlying cause
of injury. These patients may develop signs and symptoms
of acute ischemia of the hand and digits. Some may
progress to tissue breakdown evident by skin ulceration
and gangrene.
8
The angiographic appearance may be
similar to that seen in atherosclerosis with multiple segmental arterial occlusions.
12
Raynaud’s phenomenon
Raynaud’s phenomenon is an idiopathic vasospastic condition of the small vessels of theextremities characterized by
episodic digital ischemia provoked by cold, emotion, and
FIGURE 17-4. Stab wound to the axilla with transection and
pseudoaneurysm of the proximal right brachial artery but with
continued distal flow.
FIGURE 17-5. Traumatic arteriovenous fistula involving the
right sublavian artery and brachiocephalic vein following a
gunshot wound. Note the bullet fragments.
182 S. I. Wahl and P. S. Lakritz
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other sympathetic stimuli.16Patients with this condition,
most frequently women, develop trophic changes as a result of microcirculatory damage and prolonged local ischemia.
tremities than in the lower.
17
It is more often symptomatic in the upper ex-
1
Raynaud-type symptoms are
common in the general population, and in a minority of
these patients, it may be attributable to an underlying,
often reversible cause (primary Raynaud’s phenomenon
or Raynaud’s disease), or it may beattributable to a known
underlying systemic illness (secondary Raynaud’s phenomenon) such as systemic lupus erythematosis, scleroderma,
or rheumatoid arthritis. Other associated conditions include drug or chemical injury, occupational injury, occlusive arterial disease, and hyperviscosity diseases.
16,18
Symptoms of Raynaud’s phenomenon include pain,
paresthesias, pallor, cyanosis, and rubor. Small digital ulceration and or fissuring over the pads of the digits can
be seen in severe or recurrent attacks. Gangrene only
rarely occurs.
17,18
Primary Raynaud’s phenomenon typically presents
during the teenaged years in women who are otherwise
healthy, but symptoms may develop as late as the fourth
decade. It has been suggested that persons with this condition have a higher incidence of other vascular complications, such as migraine headache, hypertension, and
atypical angina.
18
Although angiography is not particularly useful in the
diagnosis or distinction of the various causes of Raynaud’s phenomenon, it does, however, have a role in the
evaluation of patients presenting with unilateral symptoms. Patients with unilateral symptoms frequently have
identifiable underlying upper-extremity pathology of
either the major or smaller vessels. An arteriographic
finding is stenosis of the subclavian artery. This is usually
a result of an extraluminal abnormality. Stenosis can lead
to poststenotic aneurysmal dilatation, which may in turn
lead to the development of mural thrombus and subsequent embolization with distal ischemic changes.
19
The typical angiographic findings of Raynaud’s phenomenon are those of spasm with slow antegrade flow
(Fig. 17-6) and poor opacification of the distal small
vessels. Angiography following the injection of vasodilators can lead to dramatic improvements in visualization
of small distal arteries.
1
Vasculitides
All the several categories of vasculitides are relatively rare
and affect the upper extremities. These conditions may
affect the arteries primarily or relate to a systemic disease
process; however, they all share the characteristic of arterial wall inflammation and often necrosis. Differentiation
of these vasculitides is best accomplished by a thorough
review of the clinical history, with particular attention to
the distribution of vessel involvement as well as the rapid-
FIGURE 17-6. Raynaud’s disease with slow antegrade flow.
Late angiographic exposure approximately 28 seconds after
contrast was injected in the midbrachial artery via transfemoral
catheterization after an intraarterial injection of 60 mg of
papvarine. No spasm is seen secondary to artificial vasodilatation, but occlusive disease of the digital arteries remains evident.
ity of onset. The pathogenesis and etiologies of these
vasculitides are poorly understood, but most investigators
agree that a relationship to immune complex and cellmediated mechanisms exists.
20
Buerger’s disease (thromboangiitis obliterans)
Buerger’s disease is an inflammatory disorder characterized
by nonspecific inflammation and cellular infiltration occurring within the vessel wall. There is no direct association with atherosclerosis. Buerger’s disease is a painful
vasoocclusive disorder of young men in the third and
fourth decades of life involving predominately the small
and medium-sized arteries of the extremities. The disease
process typically begins in the smaller peripheral vessels
but may occur proximal to the level of the elbow. Additionally, veins and sometimes the adjacent nerves can become involved in the disease process.
afflicted present with signs and symptoms of distal arterial
ischemia or migratory superficial thrombophlebitis.
Peculiar to this disease is the clear association with tobacco use. With the cessation of smoking, signs and symptoms of the disease usually remit or become quiescent. If
smoking continues, however, the condition may progress,
necessitating amputation.
21
More commonly, however,
the disease tends to follow a self-limited course.
21
Clinically, those
22
8,21
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183
Angiography classically demonstrates the abrupt cutoff
of small arteries and the appearance of a dense network
of “corkscrew-” like collaterals. Although it is commonly
confused with atherosclerosis, its angiographic recognition depends on the absence of calcification and a distal
rather than a proximal distribution with segmental occlusions of the radial and ulnar arteries with preservation of
the interosseous artery.
8
Takayasu’s arteritis
Takayasu’s arteritis, also known as pulseless disease, is chronic
inflammatory obliterative arteritis and is seen predominately in young women.
yasu’s arteritis commonly involves systemic complaints of
night sweats, arthralgias, fever, malaise, and weight loss.
Although its cause remains unknown, it may have some
relationship to giant cell arteritis.
disease occurs, symptoms are referable to the involved
vascular territory. The brachiocephalic vessels are primarily affected but the aorta and its branches also may be
affected.
Although Takayasu’s disease predominately results in
arterial stenoses, dilatation may be seen as well.
angiographic changes of the disease may be localized narrowing or irregularity. Although the appearance is nonspecific, the distribution of disease is highly specific. The
left subclavian artery is the most commonly involved
8
The initial presentation of Taka-
20
If progression of the
23
The first
branch vessel of the aorta in about 45% of patients. Arterial occlusion is the second most common finding, and
often a characteristic “flame-shaped” appearance of the
occluded vessel is seen (Fig. 17-7). Occlusions of the main
branches of the aortic arch usually are associated with
extensive collateral circulation.
findings may be seen in temporal arteritis.
23
Similar angiographic
24
Subclavian steal
Subclavian steal is defined as the reversal of flow in the
vertebral artery secondary to a stenosis or occlusion of
the subclavian artery proximal to the origin of the vertebral artery or brachiocephalic artery. The stenosis or
occlusion results in decreased blood flow to the vessel
distal to the lesion. Blood flow to the affected extremity
may occur from the contralateral vertebral artery, via the
basilar artery, and then in a retrograde direction through
the ipsilateral vertebral artery and into the subclavian
artery distal to the stenosis (Fig. 17-8). Blood is therefore
“stolen” from the basilar circulation, resulting in basilar
insufficiency and subsequently the subclavian steal syndrome. Symptoms include vertigo, syncope, and extremity paresthesia.
A subclavian artery stenosis may cause myocardial ischemia if it is located proximal to an internal mammary
artery used for coronary arter y bypass graft. A stenosis or
occlusion of the subclavian artery also may jeopardize an
A
FIGURE 17-7. Takayasu’s arteritis in a young woman with severe bilateral upper extremity
claudication. A: Abrupt occlusion of the right brachiocephalic trunk with faint reconstitution of the
right subclavian artery via collateral circulation. Additionally, there are at least two high-grade focal
stenoses of the left subclavian artery proximal to the origin of the left vertebral artery (arrows) as
well as a mild stenosis at the origin of the left common carotid. Note sparing of the aorta;
atherosclerosis, in contrast, would involve the aorta as well as its proximal branches. B: Same
patient after extensive vascular resonstruction.
B
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