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CHAPTER
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33 Carotid Endarterectomy
Wesley S. Moore
Historical Background
The development of surgery for carotid artery disease required
three important advances: (1) recognition of the relationship
between atherosclerotic disease of the carotid bifurcation and
stroke, (2) premorbid identification of carotid bifurcation disease,
and (3) the vascular surgical techniques necessary to remove
carotid bifurcation atherosclerotic plaque.
For many years, the relationship between carotid artery disease
and stroke was overlooked because autopsy protocol did not
include harvesting the cervical vessels. Therefore, the only pathology observed in hemispheric stroke was thrombus in the intracranial vessels, most commonly the middle cerebral artery (MCA).
One of the earliest observations of the relationship of cervical
carotid artery disease with stroke was made in 1856 by Savory, who
described a patient with left monocular blindness, right hemiplegia, right dysesthesia, and an occluded left internal carotid artery
(ICA) at the carotid bifurcation.
by Gowers in 1875.
relationship between carotid artery disease, transient ischemic
attacks (TIAs), and stroke.
tion disease prior to death awaited the work of Moniz, who in 1927
reported on the technique of carotid angiography. This, for the
first time, provided the opportunity to identify carotid artery occlusive disease in the living patient.
used cerebral angio graphy to evaluate the intracranial circulation. In 1951, Fisher reemphasized the importance of the cervical
carotid artery, pointing out that prior to occlusion, a stenosis was
present that might be amenable to surgical correction.
The surgical phase for treating carotid artery disease began in
1951. Carrea et al. from Buenos Aires resected the diseased segment
of an ICA and restored flow by anastomosing the external carotid
artery (ECA) to the distal ICA. They waited until 1955 for sufficient
follow-up before reporting the case.6 Probably the first successful
carotid endarterectomy (CEA) was performed by DeBakey
et al. in 1953, but it was not reported until 1959, with a long-term
follow-up reported in 1975.7 The publication that led to rapid
incorporation of carotid artery surgery into clinical practice was
the operation reported by Eastcott et al. in 1954. They described
a case of a woman who was experiencing hemispheric TIAs,
with an associated stenosis of the bulb of the carotid artery. They
resected the carotid artery bifurcation and restored flow by a direct
anastomosis between the common and distal ICAs with a successful
outcome and cessation of symptoms. This report led to an explosion
of interest in the treatment of carotid bifurcation disease.
2
It was not until 1914 that Hunt described the
1
A similar observation was made
3
The ability to identify carotid bifurca-
4
In spite of this, clinicians solely
5
8
Pathology of Carotid Bifurcation Disease
The most common lesion of the carotid artery bifurcation is an
atherosclerotic plaque involving the bulb of the ICA. This localization of plaque is predictable and provides the opportunity for
treatment with CEA. The plaque can be calcific, fibrous, or composed of atherosclerotic elements of mixed consistency. Plaques
can expand slowly or, with intraplaque hemorrhage, rapidly. Other
pathological lesions causing carotid artery stenosis include fibromuscular dysplasia (FMD), Takayasu's arteritis (TA), radiation arteriopathy, and (rarely) aneurysms of the cervical ICA.
Pathogenetic Mechanisms of Stroke
and Transient Ischemic Events
The pathogenetic mechanism for ischemic events is primarily thrombotic or atheroembolic (also see Chapter 30). If the
occlusive plaque in the carotid bulb progresses to critical flow
reduction, the ICA will proceed to thrombotic occlusion. The
pace of the occlusive process is important. If this process occurs
slowly, collateral circulation may develop from the contralateral
carotid and vertebral arteries. In addition, the ipsilateral ECA can
be a source of collateral blood flow by flow reversal through the
ophthalmic artery to the siphon of the ICA. Under these circumstances, thrombosis of the ICA may be a silent event. On the other
hand, if plaque expansion occurs rapidly or if collateral circulation is inadequate, there will be thrombotic propagation beyond
the ophthalmic branch of the ICA into the middle cerebral artery,
causing hemisphere infarction and neurological deficit.
In addition to thrombotic occlusion of the ICA, the more common mechanism for ischemic events is rupture of the intimal
cover of the atherosclerotic plaque, permitting the discharge of
soft atherosclerotic debris into the blood flow stream. These fragments are carried distally to the intracranial branches, fostering
either permanent branch occlusion and cerebral infarction or, with
fragmentation and thrombolysis of the embolus, a temporary and
reversible neurological deficit or TIA. Following plaque rupture
and a primary wave of embolization, a defect is left in the plaque
that on angiographic inspection resembles an ulcer. This ulcer or
plaque defect can be the source of continual embolization, or it
can be the nidus for platelet aggregate and thrombotic material
to reside. Since there is no attachment of this material within the
ulcer crater, pulsatile blood flow can dislodge the material residing
with the ulcer crater, leading to a secondary wave of embolization.
Clinical Evaluation
Clinical evaluation of patients with cerebrovascular disease
(carotid artery disease) is discussed in Chapter 30.
Preoperative Imaging
The noninvasive examination of choice for patients with suspected
carotid artery disease is a carotid duplex ultrasound scan using
modern equipment in a validated vascular laboratory (also see
Chapter 12). This study identifies lesions in the carotid artery, classifies the severity of stenosis, and provides information regarding
plaque consistency. The opportunity to examine flow velocity and
pulse wave velocity analysis provides information about other
portions of the circulation, including proximal lesions at the level of
the aortic arch and distal intracranial lesions. In many centers, the
duplex scan serves as the definitive preoperative study.9 Additional
studies such as magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), computed tomographic angiography
(CTA), or catheter-based contrast angiography are reserved for
special circumstances.9 Use of MRA or CTA in conjunction with
duplex ultrasound of the carotid artery is considered when the
results of duplex ultrasonography are difficult to interpret or inconsistent with the clinical presentation.
Magnetic resonance angiography is used frequently because it
does not require ionizing radiation. When contrast is added, the
images are often clear and resemble those obtained via catheterbased intraarterial angiography, providing a sensitivity and specificity of 88% and 84%, respectively, for diagnosing a 70% to 99%
stenosis.
intracranial vascular anatomy, and when combined with MRI, can
identify areas of cerebral infarction or other intracranial pathology.
The major limitation of MRA is that it tends to overestimate percent
stenosis of lesions in the carotid bifurcation (also see Chapter 13).
This phenomenon occurs because turbulent blood blow, such as
occurs at carotid bulb stenosis, results in signal dropout and void,
giving the impression of a high-grade carotid stenosis.
9
Magnetic resonance angiography permits imaging of the
415
416
Computed tomography (CT) and CTA are also quite helpful in
identifying intracranial lesions. Computed tomography angiography is accurate in identifying and quantifying intracranial and
extracranial carotid stenosis (also see Chapter 14). The sensitivity
and specificity of CTA for determination of carotid artery stenosis
are 95% and 99%, respectively.
CH
ning are exposure to ionizing radiation and the requirement for a
33
large volume of iodinated contrast material, which can be nephro-
10
The major drawbacks of CT scan-
toxic or cause allergic reaction in patients sensitive to iodine.
Intraarterial contrast angiography is considered the gold standard for identifying and quantifying arterial stenoses. Major
disadvantages of this invasive procedure include arterial injury,
occlusion, and embolization resulting in cerebral infarction. In
the Asymptomatic Carotid Artery Study (ACAS), angiography was
associated with a 1% stroke rate.
11
In addition, it requires ionizing
radiation and iodinated contrast material. This technique is now
rarely indicated prior to carotid endarterectomies. It does have a
role for preprocedure imaging as a part of carotid angioplasty/
stenting.
Techniques of Carotid Endarterectomy
An arterial canula is placed for continuous blood pressure monitoring and periodic sampling of blood gases. Carotid endarterectomy can be performed under either local or general anesthesia.
General anesthesia is more comfortable for the patient. It affords a
quiet operative field and allows the surgeon to concentrate without distraction by patient movement or discomfort. It also allows
optimal airway control, ventilation, and oxygenation.
The patient is positioned supine on the operating table. A cushion is placed under the shoulders to allow for mild neck extension,
and the head is rotated away from the side of incision.
When the carotid artery is clamped for the endarterectomy
procedure, the surgeon has several choices regarding the assurance of adequate blood flow to the ipsilateral cerebral hemisphere. About 90% of patients tolerate temporary clamping of
the carotid artery because adequate collateral circulation is provided through the circle of Willis. For patients with inadequate
collateral circulation, a temporary shunt is required to maintain
adequate cerebral perfusion during endarterectomy to avoid
periprocedural cerebral infarction. These observations have
led to two forms of practice: routine shunting of all patients or
selective shunting based upon intraoperative monitoring. The
argument for routine shunting is that special monitoring is not
required. The argument in favor of selective shunting is that there
are complications unique to the use of an internal shunt. These
include intimal damage with shunt placement and embolization
of air or atheromatous debris through the shunt to the intracranial
circulation, resulting in a cerebral infarction. In addition, when a
shunt is in place, it is difficult to see the end of the endarterectomized segment, thus opening the possibility of leaving a residual
intimal flap that can lead to thromboembolism and possibly postoperative carotid occlusion. Therefore, since only 10% of patients
undergoing CEA require a shunt, there is little reason to expose
the majority 90% who do not require a shunt to its potential
complications.
There are several acceptable methods for monitoring the adequacy of cerebral perfusion. The first method that was described
was measurement of ICA backpressure in patients undergoing
CEA under local anesthesia. With clamping of the common carotid
artery (CCA) and ECA, the residual pressure in the carotid artery
determines the perfusion in the middle cerebral artery. One study
found that the conscious response to clamping correlated with
the ICA backpressure.
no neurological deficit was 25 mmHg. This observation was subsequently validated in patients undergoing operation with general
anesthesia.
13,14
The next method, and one that is most commonly
used today, is continuous electroencephalographic (EEG) monitoring. This method is sensitive, easy to use, and has the advantage of providing continuous monitoring rather than a single
12
The minimum pressure associated with
observation. Other methods used to monitor cerebral perfusion
include assessment of the somatosensory evoked response and
transcranial Doppler (TCD) interrogation.
There are two possible incisions that can be used. Some surgeons use an oblique incision in a skin crease, with the thought
that the resulting scar will be more cosmetic in appearance. More
proximal or distal exposure, when required, is quite difficult to
obtain with this incision. The alternative is an incision placed
along a line connecting the suprasternal notch with the mastoid
process. The surgeon can begin with a relatively short incision
over the carotid bifurcation and extend it proximally or distally
if necessary. The incision is deepened through the platysma layer.
The sternocleidomastoid muscle is mobilized until the jugular
vein is identified. The common facial vein and any accessory
facial veins are divided between ligatures. The vein is allowed to
retract laterally, and the carotid artery will be found immediately
below the vein. Care must be taken to identify the vagus nerve
because its relationship within the carotid sheath can be quite
variable. The CCA is circumferentially mobilized within the perivascular plane of Leriche. Mobilization is continued distally until
the carotid bifurcation, ICA, and ECA are fully mobilized. The ICA
should be exposed far enough so that circumferentially normal
artery is encountered. If additional exposure is required, the nerve
to the carotid sinus can be divided. This will allow the carotid
bifurcation to drop inferiorly and permit more distal mobilization
of the ICA. In the case of a high carotid bifurcation or long extension of the plaque in the ICA, more extensive exposure of the
ICA can be obtained by mobilizing or, if necessary, dividing the
posterior belly of the digastric muscle. Finally, exposure of the ICA
to the base of the skull can be obtained by dividing the styloid
process. This is very rarely required.
Once the arteries are sufficiently mobilized, intravenous (IV)
heparin is administered. The dose varies from 2500 units to 5000
units depending upon the size of the patient and the nature of preoperative antiplatelet agents administered. The internal, external,
and common carotid arteries are then clamped. A longitudinal
arteriotomy is made in the CCA and extended through the plaque
distal to normal ICA. During this time, the EEG monitor is observed.
If no EEG changes indicative of brain ischemia appear with clamping, the surgeon proceeds with the endarterectomy procedure. If
there are EEG changes with clamping, an internal shunt is placed.
The exception for selective shunting occurs in patients who have
had a prior stroke on the side of operation; shunt placement can
lessen the risk of stroke in the ischemic penumbra that surrounds
the area of infarction.
Once the decision is made concerning the shunt, the surgeon
proceeds with endarterectomy. Endarterectomy of the external
carotid is blind. There should be a feathered endpoint in the ICA.
The endarterectomy is carried to the clamp, which serves as the
endpoint. The plaque should be cleared in the common carotid
artery, and the proximal endpoint may require sharp division. Once
the plaque is removed, the carotid artery is irrigated with heparinized saline, and any loose bits of medial debris are carefully
removed. The segment between the ICA endarterectomy and
normal intima is carefully inspected to ensure that the intima is
adherent to the media at that level. If an intimal flap is present, it is
carefully removed back to a point of adherence.
The arteriotomy is closed with a patch (typically Dacron) to
prevent stenosis and accommodate any restriction from intimal hyperplasia that might occur with primary closure. Patch
closure is associated with a lower incidence of postoperative
thromboembolic complication and recurrent carotid steno-
15
sis.
Before the arteriotomy is completely closed, the vessels
should be “backbled” and flushed to remove any debris. Upon
completion of closure, flow is restored first to the ECA and then
the ICA. At this time, it is important to verify the quality of the
endarterectomy by intra operative duplex ultrasound scanning
or a completion angiogram. The latter permits accurate visualization of the carotid artery bifurcation and the intracranial
portion of the repaired ICA to detect any anatomical problems
or residual stenosis. If an intimal flap is seen in the ICA, the
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patch is removed and the arteriotomy extended beyond the
flap, thereby reducing the risk of postoperative thromboembolism. A new patch is used to close the arterio tomy. More commonly, an endpoint problem is found in the ECA, which can
lead to postoperative thrombosis of the ECA and then in retrograde propagation of thrombus to the ICA, embolism, and
16
stroke.
When a problem is identified, the ECA is clamped both
at its origin and distally. A transverse arteriotomy is made
just distal to the residual lesion, and the remaining plaque
is removed. The transverse arteriotomy is closed with interrupted polypropylene sutures, and flow is restored. The neck
incision is then closed. Closure consists of a running absorbable suture in the platysma layer and a running absorbable
subcuticular suture for cosmetic skin closure.
Postoperative Management
A brief postoperative neurological assessment is performed in the
operating room following extubation. If no neurological deficits are
noted, the patient is transferred to the recovery room for monitoring.
Once the patient is fully awake, the blood pressure controlled, and
the neck free of hematoma, the patient is transferred to a regular
hospital room for overnight observation. Postoperative blood pressure monitoring and treatment is important. Patients often become
hypertensive after awakening from anesthesia. Regulation of blood
flow is impaired on the side of endarterectomy for approximately
3 to 6 weeks, so the ipsilateral cerebral hemisphere is vulnerable
to elevated postoperative blood pressure. Uncontrolled hypertension can result in excessive perfusion pressure, the consequences
of which range from headache to seizures and lead to intracerebral bleeding resulting in major stroke or death. Hypotension and
bradycardia occur from baroreceptor activation caused by stimulation of the nerve to the carotid sinus. This can easily be treated
by injecting the nerve with 1% lidocaine. Following recovery from
anesthesia, hypotension is a rare occurrence.
If the patient is stable overnight and does not have a new
neurological complication, he or she can be discharged the
following morning. The patient is instructed to resume usual medications, including an antiplatelet agent.
The first postoperative visit should occur in approximately
3 weeks, at which time a carotid duplex ultrasound scan is performed to assess the result of endarterectomy and establish a
new baseline for further follow-up. Additional carotid ultrasound
examinations are recommended at 6 months and then 1 year from
the time of operation.
Complications of Carotid Endarterectomy
The mortality rate reported in large surgical trials of CEA is approximately 1% and is usually cardiovascular in nature.
ity rate is similar to that observed in a general vascular surgical
practice.
etiology of postoperative stroke is embolism of thrombus or atheromatous debris.
permanent nerve palsy is noted in 1%.
18
The risk of stroke is approximately 2.6%.19 The principal
20
Cranial nerve injury occurs in up to 7% of patients, although
21
Several cranial nerves
lie within the operative field, including the vagus (X), hypoglossal
(XII), and (less commonly) glossopharyngeal (IX). The mandibular
branch of the facial nerve (VII) may be at risk if the surgical incision is made anterior to the ear instead of on a line connecting the
mastoid process and the suprasternal notch.
Despite achieving hemostasis prior to wound closure, hematomas may develop. These are usually evident within the first 4 hours
following operation. Patients with expanding hematomas should
return to the operating room for evacuation and restitution of
hemostasis. A bleeding source after hematoma evacuation usually
is not found. Judicious use of heparin, particularly if the patient
is on more than one antiplatelet agent, is important. Heparin
reversal with protamine is associated with risk of anaphylaxis.
17
This mortal-
Prevention may be the best strategy. Irrigating the wound with a
dilute antibiotic solution and observing for bleeding sites (to be
controlled with ligature or electrocoagulation) may be the best
strategy.
Wound infection is rare because patients undergoing CEA
receive prophylactic antibiotics. If a wound infection occurs,
the patient should be hospitalized and treated with an IV antibiotic therapy regimen. A deep wound infection may affect a
prosthetic patch and threaten the integrity of the carotid artery.
Clinical Trials of Carotid Endarterectomy
Prospective randomized trials comparing CEA to medical management involve either symptomatic or asymptomatic patients. They
serve as the basis for current CEA recommendations in appropriately selected patients.
Symptomatic Carotid Endarterectomy Trials
The North American Symptomatic Carotid Endarterectomy Trial
(NASCET) was a multicenter prospective randomized trial carried out in the United States and Canada. The trial was divided into
two cohorts; one involved patients with carotid artery stenosis of
70% to 99%, and the other involved patients with stenosis of 50% to
69%. The high-grade (70%-99%) stenosis component of the study
was stopped after only 18 months because stroke morbidity and
mortality for CEA was 9%, compared with 26% for best medical
management.
22
erate stenosis, went to completion. It demonstrated a 5-year event
rate after CEA of 15.7%, vs. 22.2% for medical management.23 The
European Carotid Endarterectomy Trial (ECST) was conducted
during the same time as NASCET. It recruited a population similar to the high-grade stenosis portion of NASCET, with similar
findings. Stroke morbidity and mortality after CEA was 10.3%, vs.
16.8% for medical management.
Symptomatic Trial was started after the other two trials were ongoing. It was stopped after 189 patients were entered as the results
of the North American and European trials were reported. Despite
the small number of patients, the rate of stroke and crescendo TIA
after only 12 months’ follow-up was 7.7% for surgery and 19.4%
for medical management.25 Based on these trials, CEA is recommended for symptomatic patients with greater than 50% stenosis.
Asymptomatic Carotid Endarterectomy Trials
The Veterans Affairs Asymptomatic Carotid Endarterectomy Trial
enrolled 444 asymptomatic men with carotid artery stenoses
greater than 50% as documented by angiography. These were randomized to CEA plus best medical management, or best medical
management alone. At the end of 5 years, the primary event rate of
TIA, stroke, and death was 8% for surgery, vs. 20.6% for medical
management.
26
domized trial that compared CEA plus best medical management
to best medical management alone. At the end of 5 years, the primary
event rate of stroke or death was 5.1% for CEA and 11% for medical
management.
11
randomized 1560 patients to immediate CEA and 1560 patients
to medical management. At the end of 5 years, the primary event
rate for immediate CEA was 6.4%, compared with 11.8% in patients
randomized to medical management.
Cardiology/American Heart Association (ACC/AHA) guidelines
give a class IIa recommendation for CEA for asymptomatic patients
with carotid artery stenosis greater than 70%.
Carotid Endarterectomy Compared to Carotid
Angioplasty/Stenting
Carotid artery angiography and stenting is described in detail in
Chapter 32. Several clinical trials have compared CEA with carotid
artery stenting (CAS).
21
The second part of the study, for patients with mod-
24
The Veterans Administration
21
The ACAS trial was a multicenter prospective ran-
The Asymptomatic Carotid Stenosis Trial (ACST)
19
The American College of
417
CH
33
CARoTid EndARTERECTomy
418
The Stenting and Angioplasty with Protection in Patients at
High Risk for Endarterectomy (SAPPHIRE) trial was a prospective
multicenter randomized trial of symptomatic and asymptomatic
patients considered high risk for surgery due to coexisting medical
morbidity or a hostile neck; 156 patients were randomized to CAS,
and 151 were randomized to CEA. The primary composite end-
CH
point included death, stroke, and myocardial infarction (MI). The
33
30-day rates of death and stroke were no different between the two
procedures, but with MI added to death and stroke, the composite
endpoint rate for CAS was 5.8%, vs. 12.6% for CEA. These differences
persisted for 1 year, but by 4 years, there was no difference between
the two groups regarding event-free survival.
27,28
The Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3 S) trial was a prospective multicenter trial carried out in France. A total of 527 patients with
greater than 60% stenosis were randomized to CEA (262) or CAS
(265). The study was stopped early because the death and stroke
rate at 30 days was 3.9% for CEA and 9.6% for CAS. The study patients
were followed for 4 years, at which time the death and stroke rates
were 6.2% for those treated with CEA and 11.1% for those treated
with CAS.
29,30
The Stent-Protected Angioplasty versus Carotid Endarterectomy
for Symptomatic Stenosis (SPACE) trial, carried out in Germany,
Austria, and Switzerland, was a prospective multicenter randomized trial of symptomatic patients with high-grade carotid stenoses. The hypothesis was that CAS was not inferior to CEA. Twelve
hundred patients were randomized, but the study was stopped
because a futility analysis was performed indicating that the primary hypothesis could not be proved. At the time the study was
stopped, the death and stroke rate for CAS was 7.7%, vs. 6.5%
for CEA. Of note, by 2 years, the recurrent stenosis rate was 10.7% for
CAS and 4.6% for CEA.
31
The International Carotid Artery Stenting Study (ICSS) compared CEA with CAS. It involved 50 academic centers in the United
Kingdom, Europe, Australia, New Zealand, and Canada. A total of
1713 patients with high-grade carotid stenoses were randomly
allocated to CEA (858) or CAS (855). The primary outcomes
were stroke, death, or procedural MI analyzed at 120 days following the procedure. The incidence of the combined endpoints of
death, stroke, and MI in the CAS group was 8.5%, vs. 5.2% for CEA.
Subgroup analyses of the patients who underwent pre- and postprocedure MRI found that 50% of the CAS group had at least one
new area of cerebral infarction, vs. 17% of the CEA group.
The Carotid Revascularization Endarterectomy versus Stenting
(CREST) trial was a multicenter prospective randomized trial of
symptomatic and asymptomatic patients with hemodynamically
significant carotid stenoses; it was carried out in 108 centers in the
United States and Canada. Between the years 2000 and 2008, 2502
patients were randomized; 47% were asymptomatic, and 53% were
symptomatic. The initial analysis occurred after the last group
of patients had at least 1 year of follow-up, and median followup was 2.5 years. The primary composite endpoint was periprocedural death, stroke in any distribution, and MI, which occurred
in 4.5% of patients randomized to CEA and 5.2% randomized to
CAS. The differences were not significant. The combined rate of
death and stroke was 2.3% for CEA and 4.4% for CAS. There was
a higher nonfatal MI rate in the CEA group. The study identified
age as an important differentiating factor between CEA and CAS.
Older patients did better with CEA, and younger patients did better
with CAS. The inflection point occurred at age 70.
33
Based on these
studies, the ACC/AHA guidelines give a class IIa recommendation
for CEA over CAS for older patients.
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16. Moore WS, Martello JY, Quinones-Baldrich WJ, et al: Etiologic importance of the intimal flap
of the external carotid artery in the development of post carotid endarterectomy stroke,
Stroke 21:1497–1502, 1990.
17. Halliday A, Harrison M, Hayter E, et al: 10-year stroke prevention after successful carotid
endarterectomy for asymptomatic stenosis (ACST-1): a multicentre randomised trial,
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18. Finks JF, Osborne NH, Birkmeyer JD: Trends in hospital volume and operative mortality for
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19. Halliday A, Mansfield A, Marro J, et al: Prevention of disabling and fatal strokes by successful
carotid endarterectomy in patients without recent neurological symptoms: randomised
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20. Spencer MP: Transcranial Doppler monitoring and causes of stroke from carotid
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21. Brott TG, Halperin JL, Abbara S, et al: ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/
SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial
carotid and vertebral artery disease. A report of the American College of Cardiology
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of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis,
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23. Barnett HJ, Taylor DW, Eliasziw M, et al: Benefit of carotid endarterectomy in patients
with symptomatic moderate or severe stenosis. North American Symptomatic Carotid
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24. European Carotid Surgery Trialists’ Collaborative Group: MRC European Carotid Surgery
Trial: interim results for symptomatic patients with severe (70%-99%) or with mild
(0%-29%) carotid stenosis, Lancet 337:1235–1243, 1991.
25. Mayberg MR, Wilson SE, Yatsu F, et al: Carotid endarterectomy and prevention of cerebral
ischemia in symptomatic carotid stenosis. Veterans Affairs Cooperative Studies Program
309 Trialist Group, JAMA 266:3289–3294, 1991.
26. Hobson RW 2nd, Fields WS, Weiss DG, et al: Efficacy of carotid endarterectomy for
asymptomatic carotid stenosis. The Veterans Affairs Cooperative Study Group, N Engl J Med
328:221–227, 1993.
27. Yadav JS, Wholey MH, Kuntz RE, et al: Protected carotid-artery stenting versus endarterectomy in high-risk patients, N Engl J Med 351:1493–1501, 2004.
28. Gurm HS, Yadav JS, Fayad P, et al: Long-term results of carotid stenting versus endarterectomy in high-risk patients, N Engl J Med 358:1572–1579, 2008.
29. Mas JL, Chatellier G, Beyssen B, et al: Endarterectomy versus stenting in patients with
symptomatic severe carotid stenosis, N Engl J Med 355:1660–1671, 2006.
30. Mas JL, Trinquart L, Leys D, et al: Endarterectomy versus Angioplasty in Patients with
Symptomatic Severe Carotid Stenosis (EVA-3S) trial: results up to 4 years from a randomised,
multicentre trial, Lancet Neurol 7:885–892, 2008.
31. Ringleb PA, Allenberg J, Bruckmann H, et al: 30 day results from the SPACE trial of StentProtected Angioplasty versus Carotid Endarterectomy in symptomatic patients: a
randomised non-inferiority trial, Lancet 368:1239–1247, 2006.
32. Bonati LH, Jongen LM, Haller S, et al: New ischaemic brain lesions on MRI after stenting or
endarterectomy for symptomatic carotid stenosis: a substudy of the International Carotid
Stenting Study (ICSS), Lancet Neurol 9:353–362, 2010.
33. Brott TG, Hobson RW 2nd, Howard G, et al: Stenting versus endarterectomy for treatment
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PA RT IX
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AORTIC DISSECTION
CHAPTER
34 Pathophysiology, Clinical
Evaluation, and Medical
Management of Aortic Dissection
Bradley A. Maron, Patrick T. O'Gara
Acute aortic dissection is an uncommon but life-threatening
emergency that requires prompt diagnosis, rapid triage, and immediate medical, endovascular, or surgical treatment. A unified effort
across several international centers over the past 15 years has led
to the establishment of a detailed registry that describes major
aspects of presentation, management, and outcomes of patients
with acute aortic dissection.
given new clinical insights into an old disease and spawned
additional multicenter efforts to explore its genetics and pathobiology. Although gains have been made in the delivery of
life-saving care to patients with acute aortic dissection, hospital
mortality rates remain distressingly high. Enhanced awareness of
risk factors for aortic dissection, presentation features, diagnostic
pathways, and medical, endovascular, and surgical treatment strategies is a critical first step toward improving outcomes.
Epidemiology
Published figures on the incidence of aortic dissection likely underestimate the actual occurrence rate, since misdiagnosis of this condition is common and the percentage of acute aortic dissection
patients who expire before hospital presentation cannot be accurately estimated.
event. Analysis of the Swedish National Cause of Death Register
between 1987 and 2002 estimated the incidence of thoracic aortic aneurysm or dissection to be 16.3 per 100,000 men and 9.1 per
100,000 women; others have reported acute aortic dissection to
affect 30 in 1 million individuals per year.
myocardial infarction (AMI) is 140-fold more common.
the International Registry of Aortic Dissection (IRAD) indicate that
the mean age of patients at presentation with aortic dissection is
63 years, with men accounting for 63% of cases.
2
Nevertheless, acute aortic dissection is a rare
Classification
1
This longitudinal experience has
3
By comparison, acute
1
Data from
1
dissection originates in the descending thoracic aorta beyond the
origin of the left subclavian artery and terminates above (type IIIA)
or extends below (type IIIB) the level of the diaphragm.
there is no single universally accepted classification system, the
Stanford classification scheme is most often used in practice today
and will be used throughout this chapter. The terms communicating
and noncommunicating refer to the presence or absence, respectively, of blood flow between the true and false lumens of the aorta.
Aortic dissection is acute if presentation occurs within 14 days
of the onset of symptoms and chronic if more than 2 weeks
have elapsed. Morbidity and mortality are highest within the
acute phase; patients who have survived without treatment for
2 weeks are self-selected for better short- and intermediate-term
outcomes.
In practice, diagnosis of aortic dissection depends on demonstration with imaging of an intimal flap with separation of true and
false lumens. In type A dissection, the true lumen is usually displaced along the inner curvature of the aortic arch and continues
caudally along the medial aspect of the descending thoracic aorta.
Aortic branch vessel blood flow may derive from either the true or
false lumen; alternatively, flow may be sluggish or absent within the
false lumen, or branch vessels may be completely occluded at or
near their origins.
5
Although
Pathogenesis
Forces that weaken the medial layer of the aorta increase the probability of dilation, aneurysm formation, and dissection (
Acquired and genetic diseases that mediate this process are discussed later. In classic acute aortic dissection, the initiating event
is an intimal tear through which blood rapidly surges distally into
the media under systolic pressure, splitting the layers of the aortic
wall and creating an intimal flap that separates the true from the
false lumen.
Box 34-1).
Classifying aortic dissection according to anatomical location and
time from onset of symptoms helps stratify risk and guide selection
of initial treatment strategy (Fig. 34-1). The Stanford classification
system designates dissections that involve the aorta proximal to
the brachiocephalic artery (i.e., root and ascending aorta) as
type A, and those that do not as type B.4 This distinction is clinically important because dissection involving the ascending aorta
is a key determinate of early death and major morbidity. Location
of the intimal tear does not influence Stanford dissection type.
In the older DeBakey classification scheme, a type I dissection
originates within the ascending aorta and extends for a variable
distance beyond the take-off the innominate artery. A DeBakey
type II dissection is confined to the ascending aorta, and a type III
Intimal Tear
Contemporary imaging modalities or autopsy findings identify
the primary entry tear in approximately 90% of cases. It is most
frequently located a few centimeters above the level of the aortic
valve along the greater curvature of the aorta in cases of type A
dissection and accounts for nearly 60% of all cases. Compared
with other locations in the ascending aorta, the proximal few centimeters of the greater curvature are exposed to relatively greater
hemodynamic, shear, and torsional force. A pivot region located
in the descending thoracic aorta just beyond the insertion of the
ligamentum arteriosum where the relatively mobile arch meets
the fixed descending thoracic aorta is the second most common
419
420
De Bakey Type IIType I Type III
CH
34
Stanford
De Bakey
Type I Originates in the ascending aorta, propagates at least to the aortic arch and often beyond it
Type II
Type III
Stanford
Type A
Type B
Acute: Presentation 2 weeks following symptom onset
Chronic: Presentation 2 weeks following symptom onset
distally
Originates in and is confined to the ascending aorta
Originates in the descending aorta and extends distally down the aorta or, rarely, retrograde
into the aortic arch and ascending aorta
All dissections involving the ascending aorta, regardless of the site of origin
All dissections not involving the ascending aorta
Box 34-1 Aortic Dissection Predisposing Factors
Genetic
Marfan's syndrome (MFS)
Ehlers-Danlos' syndrome (EDS)
Familial thoracic aortic aneurysm disease (FTAAD)
Bicuspid aortic valve (BAV) disease
Aberrant right subclavian artery
Aortic coarctation
Noonan's syndrome
Turner's syndrome
Polycystic kidney disease
Loeys-Dietz's syndrome
Acquired
Hypertension
Iatrogenic
Pregnancy
Inflammatory aortitis
Cocaine, (?)chronic amphetamine use
Type A Type B
The dissecting hematoma usually propagates in an anterograde direction, although retrograde extension can occur. By this
mechanism, as many as 20% of dissections that originate in the
distal arch or descending thoracic aorta may involve the ascending aorta.
9
In rare cases, a second tear may occur, resulting in a
three-channel dissection
Blood within the false lumen may reenter the true lumen
anywhere along the length of the dissection. Reentry may be
protective because of spontaneous decompression of the false
lumen that may reduce the risks of rupture and/or development of
malperfusion syndromes.
Aortic Rupture and End-Organ Malperfusion
Aortic rupture, defined as tearing in the vessel wall that results in
extravascular hemorrhage, most commonly occurs with trauma
(e.g., motor vehicle collision) but may occur as a complication of
the primary dissection.
ing in cardiac tamponade occurs in type A dissection, whereas
11
rupture into the left pleural space is usually encountered with type
entry site for intimal tears, which will then propagate as a type B
dissection (30% of cases). Arch entry occurs in 7% of cases. The
abdominal aorta is the least common site for entry (3% of cases),
despite the high prevalence of intima media ulcers in patients with
atherosclerotic disease in this segment.
6–8
B dissection. Dissection-mediated end-organ ischemia or infarction
occurs from (1) mechanical compression of aortic branch vessels
by false lumen hematoma, (2) extension of the dissection plane
across the ostium of the branch vessel, or (3) dynamic vessel inlet
obstruction caused by an oscillating intimal flap. Compromise of
FIGURE 341 Aortic dissection
type according to De Bakey and
Stanford classification systems.
(From Nienaber C, Eagle KA: Aortic
dissection: new frontiers in diagnosis and
management. Part I: from etiology to
diagnostic strategies. Circulation 108:628–
7
635, 2003.)
10
(Fig. 34-2).
Rupture into the pericardial space result-
421
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CH
34
PATHOPHYSIOLOGY, CLINICAL EVALUATION, AND MEDICAL MANAGEMENT OF AORTIC DISSECTION
FIGURE 342 Three-channeled aortic dissection. A, Computed
tomographic image demonstrates three-channel descending aortic
dissection in Marfan syndrome patient. B, Schematic representation
of dissection is provided: region 1 represents thrombosed false
lumen, region 2 is true lumen significantly diminished in size, and
region 3 designates contrast-enhanced false lumen. (From Yoshida S,
Shidoh M: Three channeled aortic dissection. Postgrad Med J 79:532,
2003.)
AO
LV
FIGURE 343 Aortic dissection intimal flap prolapsing into left ventricle.
Horizontal plane transesophageal echocardiographic image captures prolapse
of intimal flap (arrows) from a proximal Stanford type A aortic (AO) dissection into
left ventricular (LV ) cavity. (From Rosenszweig BP, Goldstein S, Sherid M, et al: Aortic
dissection with flap prolapse into the left ventricle. Am J Cardiol 77:214–216, 1996.)
A B
coronary, brachiocephalic, mesenteric, renal, spinal, and iliac
circulations can occur and result in a myriad of clinical presentations. Occlusion of the left ventricular (LV) outflow tract by an
intimal flap has been reported (
Fig. 34-3).
False Lumen Thrombosis
Thrombosis of blood within the false lumen may seal the entry tear,
thus eliminating communication with the true lumen and interruption of false lumen expansion. Partial thrombosis of the false
lumen, however, has been identified as a risk factor for long-term
death in patients with type B dissection.
with partial thrombosis within the false lumen may lead to further
extrinsic compression of the true lumen and impairment of blood
flow to critical organs. Alternatively, it has been proposed that
partial thrombosis of the false lumen is associated with worse
clinical outcomes by promoting vascular inflammation, hypoxia,
and/or neovascularization with weakening of adjacent vascular
structures and an increased risk for aortic rupture.
Persistent patency of the false lumen is also associated with
a higher risk of long-term complications such as late rupture or
false aneurysm formation requiring operative intervention.
Although native aortic aneurysm disease is often a risk factor for
dissection, a dissection need not result in aneurysm formation.
The term “dissecting aneurysm” is an inaccurate anachronism, and
12,13
Elevation of pressure
13–17
12,15–17
1
2
these diseases are not synonymous, a distinction that is particularly
important when considering their natural histories and treatments.
Predisposing Genetic Factors
As is true for aneurysms, any process that leads to destruction
or degeneration of the major supporting elements of the aortic
media (elastin, collagen, smooth muscle cells [SMCs]) can predispose to development of dissection. The histopathological term
medial degeneration refers to noninflammatory destruction or
fragmentation of elastic lamellar units, dropout of SMCs, and accumulation of mucopolysaccharide ground substances (not always
in distinct cystic spaces), which characterize the final common
pathway for a variety of processes that affect the integrity of the
aortic media (
Marfan's syndrome (MFS) is the most common inherited connective tissue disorder, with an estimated prevalence of 1 case per
3000 to 5000 individuals irrespective of racial, ethnic, or geographic
considerations.
and incompatible with normal longevity. Half of patients in whom
aortic dissection occurs at younger than 40 years of age have a history of MFS.
a critical component of the microfibrils that help form cellular
adhesions in the extracellular matrix (ECM), are largely responsible
for disease expression.
of MFS and may be present in numerous other conditions.
Marfan's syndrome disease expression is heterogenous, but
the presence of an aortic root aneurysm (aortic diameter z score
≥2) and ectopia lentis are sufficient to make the diagnosis even
in the absence of a family history
absence of either of these two clinical features, the revised Ghent
nosology for MFS outlines a scoring system based on the presence of FBN1 mutation and/or other key systemic features of MFS
to make the diagnosis (
MFS include positive wrist sign (entire distal phalanx of adducted
thumb extends beyond ulnar border of the palm), positive thumb
sign (tip of thumb covers entire fingernail of fifth finger when
wrapped around contralateral wrist), pectus excavatum, pneumothorax, dural ectasia, hindfoot deformity, and protrusio acetabuli.
Other clinical features less strongly associated with MFS include
mitral valve prolapse, various abnormal facial features, and thoracolumbar kyphosis.
Using an
strated that fibrillin-1 is a key target for binding of transforming
growth factor (TGF)-β, a molecule involved in activation of
inflammatory, fibrotic, and metalloproteinase cell signaling
Fig. 34-4).
18–21
If untreated, aortic disease in MFS is progressive
22
Mutations in the gene encoding fibrillin-1 (FBN1),
20
Medial degeneration is not pathognomic
24
(Box 34-2A). Conversely, in the
Box 34-2B). Systemic features suggestive of
in vivo murine model of MFS, Dietz et al. demon-
3
23
422
CH
34
FIGURE 344 Cystic medial
degeneration. A, Hematoxylin and
eosin microscopic section of aorta
reveals fragmentation and loss of
elastin fibers with cyst-like structures
present within media. B, Movat
pentachrome stain emphasis medial
interlamellar cystic “drop out.” (From
Maleszewski JJ, Miller DV, Lu J, et al:
Histopathologic findings in ascending
AA
200 µm 200 µm200 µm
BB
aortas from individuals with LoeysDietz syndrome [LDS]. Am J Surg Pathol
33:194–201, 2009.)
Box 34-2A Revised Ghent Criteria for Diagnosis
of Marfan's Syndrome and Related
Conditions*
In the Absence of Family History
(1) Ao (z ≥2) and EL = MFS
(2) Ao (z ≥2) and FBN1 = MFS
(3) Ao (z ≥2) and Syst (≥7pts) = MFS
(4) EL and FBN1 with known Ao = MFS
EL with or without Syst and with an FBN1 not known with Ao or no
FBN1 = ELS
Ao (z <2) and Syst (≥5 with at least one skeletal feature) without
EL = MASS
MVP and Ao (z <2) and Syst (<5) without EL = MVPS
In the Presence of Family History
(5) EL and FH of MFS (as defined above) = MFS
(6) Syst (≥7 pts) and FH of MFS (as defined above) = MFS
(7) Ao (z ≥2 above 20 years old, ≥3 below 20 years old) + FH of MFS
(as defined above) = MFS
*In general, MFS is diagnosed in the presence of aortic root dilation/dissection and ectopia
lentis; aortic root dilation/dissection plus FBN1 mutation; aortic root dilation plus sufficient
systemic findings (Box 34-2B, ≥7 points); ectopia lentis plus FBN1 mutation previously
associated with aortic disease; or in an individual with a positive family history of MFS, the
diagnosis is made in the presence of ectopia lentis, or a systemic score ≥7 points, or aortic
root dilation.
†
Caveat: without discriminating features of Shprintzen-Goldberg's syndrome, Loeys-Dietz's
syndrome, or vascular Ehlers-Danlos' syndrome and after TGFBA1/2, collagen biochemistry,
COL3A1 testing if indicated. Other conditions/genes will emerge with time.
Ao, aortic diameter at the sinuses of Valsalva above indicated z-score or aortic root dissection;
EL, ectopia lentis; ELS, ectopia lentis syndrome; FBN1, fibrillin-1 mutation; FBN1 not known
with Ao, FBN1 mutation that has not previously been associated with aortic root aneurysm/
dissection; FBN1 with known Ao, FBN1 mutation that has been identified in an individual
with aortic aneurysm; MASS, myopia, mitral valve prolapse, borderline (z <2) aortic root
dilation, striae, skeletal findings phenotype; MFS, Marfan's syndrome; MVPS, mitral valve
prolapse syndrome; Syst, systemic score (see Box 34-2B); z, z-score.
†
†
†
†
Box 34-2B Scoring of Systemic Features
Wrist and thumb sign: 3 (wrist or thumb sign: 1)
Pectus carinatum deformity: 2 (pectus excavatum or chest asymmetry: 1)
Hindfoot deformity: 2 (plain pes planus: 1)
Pneumothorax: 2
Dural ectasia: 2
Protrusio acetabuli: 2
Reduced US/LS and increased arm/height and no severe scoliosis: 1
Scoliosis or thoracolumbar kyphosis: 1
Reduced elbow extension: 1
Facial features (3/5): 1 (dolichocephaly, enophthalmos, downslanting
palpebral fissures, malar hypoplasia, retrognathia)
Skin striae: 1
Myopia >3 diopters: 1
Mitral valve prolapsed (all types): 1
Maximum Total: 20 points; score ≥7 indicates systemic involvement.
US/LS, upper segment/lower segment ratio.
From Loeys BL, Dietz HC, Braverman AC, et al: The revised Ghent nosology for the Marfan's
syndrome. J Med Genet 47:476–485, 2010.
24
pathways.25 To investigate the possibility that angiotensin I (AT1)mediated TGF-β activation could represent a pharmacological target to modify development of aortic dilation in MFS, Habashi et al.
studied the effects of losartan, an AT1 receptor antagonist, on aortic aneurysm formation in transgenic mice encoding a cysteineto-glutamine substitution at position 1039 in the fibrillin-1 gene
C1039G/−
(Fbn1
). Mice with this fibrillin-1 mutation, the most common class of mutation associated with MFS, demonstrate significant and progressive aortic root dilation compared with wild-type
26
mice.
Treatment with losartan attenuated TGF-β signaling in the
aortic wall and resulted in full normalization of aortic wall thickness and a marked improvement in aortic wall architecture (i.e.,
a decrease in elastin fiber disruption) compared with placebo or
β-adrenergic receptor antagonist therapy with propranolol.
These landmark observations have advanced understanding of
the molecular basis of MFS and provided new targets for therapy. In
one small clinical trial in young MFS patients, initiation of losartan
resulted in a significant decrease in rate of growth of the aortic root
(mean change 0.46 ± 0.62 mm/yr vs. 3.5 ± 2.8 mm/yr prior to treatment; P < 0.001).
27
These findings were supplemented by Ahimastos
et al., who conducted a randomized placebo-controlled clinical
trial testing the effect of the angiotensin-converting enzyme inhibitor (ACEI) perindopril on aortic root diameter and aortic stiffness
in 17 MFS patients.29 At 24 weeks, circulating TGF-β levels and
central pulse wave velocities were lower and aortic root diameters
were smaller in perindopril-treated patients. Several larger randomized clinical trials directed at modulating TGF-β
signaling are ongoing (clinicaltrials.gov; NCT00683124, NCT00782327 NCT00429364,
NCT00723801).
Limited forms (i.e., forme frustes) of MFS that feature cardiovascular manifestations include mitral valve prolapse syndrome
(MVPS) (mitral valve prolapse, pectus excavatum, scoliosis, and
mild arachnodactyly) and the MASS phenotype (myopia, mitral
valve prolapse, borderline and nonprogressive aortic root dilation,
skeletal findings and striae). There is increasing awareness of familial thoracic aortic aneurysm disease (FTAAD), though candidate
genes affecting both matrix and SMC components have been identified in only 20% of such patients. Vascular-type Ehlers-Danlos'
syndrome (EDS) is associated with arterial rupture and dissection,
including the aorta.
24,28
Ehlers-Danlos' syndrome (1:5000 births) comprises a heterogeneous group of disorders characterized clinically by hypermobile
joints, hyperextensible skin, tissue fragility, and a predisposition to
spontaneous vascular rupture. Aortic involvement occurs in EDS
type IV, an autosomal dominant disorder attributed to structural
defects in the pro-α1 (III) chain of type III collagen, encoded by
the COL3A1 gene on chromosome 2q31.
30
FTAAD has been mapped to other genetic loci, including
16p13.11 (MYH11 gene), 5q13-14, and 11q23.2-q24, which are not
associated with abnormalities of fibrillin or collagen.
31,32
More
than five mutations in the fibrillin-1 gene have been identified in
patients with familial or spontaneous thoracic aortic aneurysm
and dissection, with histopathological changes characteristic of
medial degeneration, yet with no demonstrable abnormalities
AB
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of collagen or fibrillin in fibroblast culture.
33,34
Polymorphisms
encoding the gene vitamin K epoxide reductase complex subunit 1 (VKORC1), which results in under-carboxylation of specific matrix proteins, are associated with calcification of the
arterial wall. In patients carrying the C allele (CT or CC), a relative two-fold increase in the probability of developing aortic dissection has been observed.
gene that encodes for actin filaments in SMCs is linked to 14% of
patients with FTAAD.
35
A missense mutation in the ACTA2
36
As a consequence of this mutation, intracellular actin filament assembly is disrupted, promoting focal
areas of SMC disarray, decreased SMC contraction, and medial
degeneration of the aorta. This phenotype is felt to be associated with aortic wall weakening and increased predisposition
to dissection.
Bicuspid aortic valve (BAV) disease is the most common congenital cardiac anomaly in adults (4:1000 live births) and is often
accompanied by an aortopathy that is histologically similar but
less severe than that observed in patients with MFS. Similar pathological changes have been described in patients with aortic coarctation (many of whom have BAV disease), Noonan's syndrome,
Turner's syndrome, and polycystic kidney disease. Dilation of the
root and (more commonly) the ascending aorta is present in up to
40% of patients with BAV disease and is a risk factor for dissection
or rupture (
Fig. 34-5).
Acquired Disorders
Systemic hypertension is the most common treatable risk factor for
aortic dissection and is present in approximately 75% of patients.
Hypertension accelerates the normal aging process and leads to
intimal thickening, SMC apoptosis, fibrosis, loss of elasticity, and
compromise of nutritive blood supply. Decreased aortic compliance and vulnerability to pulsatile forces predispose to injury and
create a substrate for dissection.
Iatrogenic Dissection
In the IRAD registry, iatrogenic aortic dissection after cardiac surgery or catheterization accounted for 5% of the total reported.
Older age, hypertension, and severe peripheral vascular disease
are risk factors associated with procedure-related dissection.
Pain may be absent in iatrogenic dissection. Retrograde dissections created at the time of catheterization usually seal spontaneously on withdrawal of the catheter. Aortic atherosclerotic
plaques may prevent longitudinal propagation of a dissection.
Dissections arising from sites where the aorta has been incised or
37
38
cross-clamped may occur intraoperatively or at any time following
surgery. Deceleration injury from high-speed accidents results in
aortic transection with false aneurysm formation and rupture,
most commonly in the region of the aortic isthmus just beyond the
origin of the left subclavian artery. Transection results in a transmural tear that is different both pathologically and etiologically from
aortic dissection.
Dissection in Pregnancy
Aortic dissection as a complication of pregnancy is rare, although
by some estimates 50% of all dissections in women younger
than 40 occur during labor, delivery, or early after childbirth.
Histopathological changes affecting the aortic media of pregnant women have been described, including alterations in elastic
fibers and SMCs.
40
Both estrogen and relaxin are associated with
alterations in matrix metalloproteinase (MMP) homeostasis and
contribute to vascular remodeling and a susceptibility to injury
independent of the hemodynamic stress of labor and delivery. In
many cases, pregnancy unmasks primary conditions that predispose to aortic dissection (e.g., MFS). In those patients with preexisting MFS or BAV disease, aortic root size greater than 4.0 cm is a
contraindication to pregnancy, owing to increased risk for spontaneous rupture or dissection.
2
Drug Use and Other Acquired Conditions
Recent cocaine use, particularly among young men who smoke
tobacco, is an additional risk factor for aortic dissection.
38 patients with acute aortic dissection occurring over a 20-year
2
period in an urban center, 37% reported cocaine (in particular, crack cocaine) use within the preceding 24 hours (mean
12 hours). Chronic amphetamine use and/or dependence appear
to increase the probability of developing a thoracoabdominal
aortic dissection in those aged 18 to 49 years.42 Presumed mechanisms for aortic injury from cocaine and amphetamine use involve
oxidant stress–mediated endothelial dysfunction and extreme
catecholamine-induced shear forces, with abrupt hypertension
and tachycardia that collectively lead to weakening of the aortic
media and predisposition to tearing.
Inflammatory diseases of the aorta can lead to destruction of
ECM proteins and SMCs, with subsequent aneurysm formation
and/or dissection. Aortic dissection has been reported in patients
with Takayasu's disease, giant cell aortitis, Behçet's disease, relapsing
polychondritis, systemic lupus erythematosus (SLE), and the aortitis associated with inflammatory bowel disease.
tis, on the other hand, does not predispose to dissection, perhaps
2
Syphilitic aorti-
41
Among
423
CH
34
PATHOPHYSIOLOGY, CLINICAL EVALUATION, AND MEDICAL MANAGEMENT OF AORTIC DISSECTION
39
FIGURE 345 Bicuspid aortic valve
(BAV) with aortic dilation. Electrocardio-
gram (ECG)-triggered breath-hold
contrast-enhanced magnetic resonance
angiography (MRA) using a 1.5-T imager
demonstrates (A) bicuspid aortic va lve
(arrows) and (B) signi ficant dilation of
the root and proximal ascending aorta.
(From Arpasi PJ, Bis KG, Shetty AN, et al:
MR angiography of the thoracic aorta
with an electrocardiographically triggered
breath-hold contrast-enhanced sequence.
Radiographics 20:107–120, 2000.)
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