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CARDIOMYOPATHY
265
Section IV: Decision making
The greatest challenge of working up and treating •
a cardiomyopathy is to include it in the differential
diagnosis list and then to make the proper disposition
for the patient.
To sort out the etiology in the ED, obtain the •
best history possible and a thorough physical
examination.
EKG and chest X-ray studies are appropriate ED •
tests, while an echocardiogram can usually can
wait until after ED evaluation.
Disposition should be predicated on the initial •
evaluation and risk factors for an adverse outcome.
Close interaction with a cardiologist or internist who
can follow the patient can aid in the disposition.
References
Heart Disease and Stroke Facts1 . Dallas: American Heart
Association; 2006.
La Vecchia L, Mezzena G, Zanolla L, et al. Cardiac tro-2
ponin I as diagnostic and prognostic marker in severe heart
failure. J Heart Lung Transplant. 2000;19:644–652.
The test of choice in the workup of cardiomyo-
pathy is an echocardiogram (ECHO). An ECHO
can be used to differentiate between the types of
cardiomyopathy, as well as other cardiac diseases.
An ECHO showing dilatated chambers and diffuse
hypokinetic muscle is consistent with a dilatated
cardiomyopathy. Focal hypokinesis is found in
ischemic cardiomyopathy. Hypertrophy of cardiac
muscles, incomplete emptying of the ventricle, and
outfl ow tract obstruction can be seen in hypertro-
phic cardiomyopathy.
7
Disposition of patients with cardiomyopathy
The decision to admit or discharge a patient with
cardiomyopathy depends on the severity of the symp-
toms, concern for deterioration, and ability of the
patient to obtain adequate follow up. If the patient
is in extremis, the ideal location for admitting the
patient is to an ICU with a cardiologist involved in
the patient’s care. Stable patients should be admitted
to the hospital with telemetry and close monitoring.
If a patient is to be discharged, close follow up with
a cardiologist should be arranged prior to the patient
leaving the ED.
Table 18-1. Etiologies of cardiomyopathy.
Congenital
• Autosomal dominant, X-linked
Infectious
• Viral: coxsackivirus, cytomegalovirus, or human immunodefi ciency virus (HIV)
• Mycobacteria, Staphylococcus species
• Parasites (Chagas disease, toxoplasmosis, trichinosis)
Metabolic diseases
• Diabetes mellitus, hypothyroidism, thyrotoxicosis, acromegaly, Cushings disease, pheochromocytoma
• Nutritional defi cits
Systemic disorders
• Systemic lupus erythematosus, hemochromatosis, amyloidosis, sarcoidosis
Cardiac disorders
• Myocardial ischemia, valvular diseases, hypertension
Neuromuscular dystrophies
• Duchenne muscular dystrophy, Friedreich’s ataxia, myotonic dystrophy, X-linked cardioskeletal myopathy
Pregnancy
Autoimmune
• Kawasaki disease
Idiopathic
Toxic
• Alcohol, cocaine, doxirubicin, antiretrovirals, steroids, heavy metals
CHAPTER 18
266
Azevedo VM, Albanesi Filho FM, Santos MA, Castier 6
MB, Tura BR. How can the echocardiogram be use-
ful for predicting death in children with idiopathic
dilated cardiomyopathy? Arq Bras Cardiol. 2004;82:
505–514.
Egan D, Bisanzo M, Hutson H. Emergency department 7
evaluation and management of peripartum cardiomyo-
pathy. J Emerg Med.2009;36:141–147.
Sasson Z. Hypertrophic cardiomyopathy 3 Cardiol Clin.
1988;6:233–288.
Arbustini E, Morbini P, Pilotto A, Gavazzi A, Tavazzi 4
L. Genetics of idiopathic dilated cardiomyopathy. Herz.
2000;25:156–160.
Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. 5
Does this dyspneic patient in the emergency department have
congestive heart failure? JAMA. 2005;294:1944–1956.
SECTION FOUR
Vascular Emergencies
269
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Aortic dissection
Keith A. Marill
1
& David F. M. Brown
2
1
Assistant Professor, Division of Emergency Medicine, Harvard Medical School, Attending
Physician, Department of Emergency Medicine, Massachusetts General Hospital, Boston
Massachusetts, USA
2
Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital,
Associate Professor, Harvard Medical School, Boston, Massachusetts, USA
19
Section I: Case presentation
A 76-year-old woman came to the emergency depart-
ment (ED) complaining of anterior chest pain that
radiated to the back. She had a multiyear history of
hypertension. The pain began abruptly while watch-
ing television, and she reported it as 10/10 on a pain
scale. She also reported left fl ank pain, diaphoresis,
and nausea. She had one episode of vomiting when the
pain fi rst came on. There was no dyspnea. The pain
was nonpositional and nonpleuritic. There was no
fever, cough, or sputum. In addition to hypertension,
she had mild chronic obstructive pulmonary disease
(COPD). She was a one pack per day smoker for the
prior 40 years, and drank alcohol occasionally.
On physical examination, she was diaphoretic and
in moderate distress. She was moving around on the
stretcher, and appeared unable to get comfortable.
The vital signs were: blood pressure 180/110 mmHg,
heart rate 100 beats/min, respirations 20 breaths/
min, temperature 37ºC (98.6ºF), oxygen saturation
95% on room air. The head was normal, the neck
was without bruits, and the carotid pulses were nor-
mal. The chest was clear to auscultation, and there
was no chest wall tenderness. The cardiac examina-
tion revealed a normal S1 and S2 with an S4. There
were no systolic or diastolic murmurs and no rubs or
heaves. The abdomen was soft and nontender; there
were no masses or bruits. The back had no tenderness
over the spine, but there was left costovertebral angle
tenderness. The extremities were notable for 1⫹ bilat-
eral ankle edema and symmetric pulses. The capillary
refi ll was brisk. The neurological examination was
without any focal fi ndings.
The patient was treated with fentanyl for pain, and
intravenous labetalol was started. The blood pres-
sure improved to 150/90 mmHg, and then declined to
120/70 mmHg. The pulse rate dropped to 80 beats/
min. She was taken to radiology for a CT scan. While
in the CT scanner, the blood pressure further dropped
to 60 mmHg by palpation. The CT revealed a Type
A thoracic aortic dissection and a pericardial effu-
sion was seen. She was taken directly to the operating
room, and underwent emergent surgical repair.
Section II: Case discussion
Dr Peter Rosen: Did this patent describe ever having
chest pain before?
Dr David Brown: She had no prior history of a chest
pain syndrome, and no known coronary artery disease.
PR: Was she diabetic?
DB: No
Dr Shamai Grossman: Was the pain truly sudden in
onset, or did it begin abruptly and gradually worsen?
CHAPTER 19
270
matter, pulmonary embolus. Acute myocardial isch-
emic pain tends to increase over time whereas, in
my experience, patients with aortic dissection can
often tell you exactly what they were doing when the
chest pain started because it was so intense. In addi-
tion, the pain is often sharp or tearing, rather than
pressure-like. However, in acute myocardial ischemia
the chest pain can also be sharp or tearing, and still
represent MI rather than dissection. Next, I look for
a history of hypertension, which is the principal risk
factor for aortic dissection, and is frequently present
in those patients who present with dissection, unless
the patient has a connective tissue disorder.
PR: I think those are the less diffi cult-to-diagnose dis-
sections, as these patients tend to be younger and have
some of the physical stigmata of a Marfan’s syndrome,
such as height and a family history. Seventy-six-year-
old patients, or even patients a little younger with a
history of hypertension, are the cases in which it is the
most diffi cult to diagnose a dissection.
DB: Another clue is the presence of two separate vas-
cular lesions separated by distance in the body. For
example, an MI or chest pain with a stroke, chest
pain with a cold foot, chest pain with what might be
interpreted as fl ank pain or renal colic, or concomi-
tant abdominal pain with mesenteric ischemia would
be much more suggestive of aortic dissection than of
myocardial ischemia.
PR: We were always taught to look for differential
blood pressures, but I honestly don’t know anyone
who does. Is there value in trying a left versus right
arm pressure routinely? I think that most of us accept
the pressures that are given to us by the nursing staff,
and they are almost always unilateral.
DB: I fi nd that blood pressure asymmetry is not very
helpful, especially in a population that has had long-
standing hypertension, and is likely to have atherosclero-
sis outside of their coronary arteries. A differential blood
pressure in two extremities may be related to a fi xed
obstructive atherosclerotic lesion, which has nothing
to do with the patient’s presentation. Similarly, patients
could have a dissection without impairment of fl ow to
an extremity. Therefore, one should be cautious of being
falsely reassured by symmetric blood pressures.
SG: On the other hand, I fi nd that the one of the sim-
plest way to almost immediately make this diagnosis is
DB: The pain began suddenly while she was watching
TV. It was immediately at its most intense point.
PR: How well controlled was her hypertension?
DB: She took one medication daily, and was moder-
ately compliant.
PR: Had there been any episodes of hypertensive
urgency or clear lack of blood pressure control?
DB: No.
PR: Did she also complain of a headache or weakness
in either of her arms or legs?
DB: No, the only other complaint was left fl ank pain.
PR: Aortic dissection is a disease process that if you
don’t think about its possibility, you’ll never fi nd it.
What would lead you away from considering that
chest pain is from coronary artery disease, and lead
you to start thinking about dissection?
SG: There are a couple of clues that push me away
from coronary artery disease and more toward other
diagnoses. First, I would assess the description of the
pain. Sudden onset of symptoms in a patient who has
never had any pain before, and as well as sudden onset
pain that is already at its worst and radiates to the
back, all would make me think that perhaps that this
isn’t coronary ischemia in etiology. Next, I’d consider
how the patient appears. Is the patient in extremis?
Is there an appearance of serious illness? If not, then
I start to think that perhaps this may be something
more ordinary. If the patient starts to look sick, then I
would have to start looking for something that would
explain this. If the EKG is normal, then aortic dissec-
tion would jump to the top of my differential list.
PR: The cases that I’ve encountered of aortic dissection,
in which the patient wasn’t in extremis, all had signifi -
cant pain. However, in these cases it was impossible
to distinguish that pain from the pain of a myocardial
infarction (MI). Helpfully, their EKGs were relatively
normal. When the patient presents with the sequelae
of aortic dissection, with symptoms of a stroke or an
abdominal process, it can be an even more subtle diag-
nosis. Do you have any other clues that you use to
trigger the concern about dissection?
DB: Again, pain that is most severe at its onset is
much less typical of acute myocardial ischemia,
and more suggestive of aortic dissection, or for that
AORTIC DISSECTION
271
patients who do truly have thromboembolic stroke.
It helps to identify the smaller group of patients who
have other entities causing the neurologic defi cits, but
who could be injured by thrombolytic therapy.
PR: Is there an association between dissection and
drugs of abuse? Can methamphetamine cause a
hypertensive burst that triggers a dissection? When
we see stroke in those patients, is it more likely to be
vasospasm in the cerebral area?
SG: Clearly, amphetamines can give you hypertension,
and profound hypertension potentially could trigger a
dissection in someone who has underlying disease. A
number of case reports have similarly suggested that
the use of amphetamines, like cocaine, enhance nora-
drenaline release, and that by causing surges in blood
pressure, the amphetamine participates in the patho-
genesis of aortic dissection.
1
PR: Are there other physical fi ndings beyond pulse
differential and multiorgan involvement that would
help you think of aortic dissection? What about the
presence of cardiac murmurs?
DB: For a Type A or for Debakey Type 1 or 2 dissec-
tions, patients may present with acute aortic regur-
gitation, but those patients are usually in so much
heart failure that it is diffi cult to hear the diastolic
murmur. If I did hear a diastolic murmur consistent
with aortic regurgitation, it would increase my con-
cern for aortic dissection. However, I don’t think
there’s any particular pathognomonic fi nding on car-
diac examination that would be extremely helpful.
PR: We used to think that you had to do angiogra-
phy to fi nd the exact anatomic location of the lesion
for the surgeon, but this is rarely done today as CT
angiography has become the diagnostic method of
choice. Is there any utility in bedside ultrasound in
the ED to help you with this diagnosis?
SG: A transthoracic echocardiogram will show a
dissection about 60% of the time. A transthoracic
ECHO is relatively easily available, depending on
the time of day and depending on the institution, but
still not as universally available as a CTA. If you’re
going to use ultrasound to look for a dissection, ide-
ally you should use a transesophageal echocardio-
gram (TEE). A TEE has a sensitivity very similar to
that of a CTA. The issue with TEE is that it is diffi cult
to obtain in a timely fashion, while the less sensitive
by feeling a patient’s pulses. If they are asymmetric, I
have invariably found that the patient is having a dis-
section. This is a very simple thing to do, particularly in
a case when symptoms don’t make sense. Here, aortic
dissection should be in the back of your mind, and you
should be checking for symmetry of pulses, which you
can often do while you are talking to the patient.
DB: I think pulse asymmetry is important when it is
present, but doesn’t appear often enough to be very
helpful when it is not present.
PR: I encountered a case recently that horrifi ed me
because I was sure that I would have missed it. It was
a young man who presented with a seizure without
having a prior history of epilepsy, and then became
comatose with obvious signs of a one-sided stroke.
He did not have a history of IV drug abuse, so these
symptoms were unlikely to be induced by cocaine or
crystal methamphetamine. I assumed that he had some
sort of acute cerebral crisis. As he was comatose, after
he was intubated, a CT scan was obtained, but it was
normal. I am hard pressed to think of an acute onset
cerebral catastrophe, in a young patient, that would
have a normal acute CT scan. As it turns out, this
unfortunate young man’s symptoms were related to
a huge carotid and aortic dissection beginning in the
proximal aorta and extending to the internal carotid
artery. Do you think that this entity needs to be on
our differential diagnosis list for acute seizures?
DB: I would limit my concern for dissection to those
patients with seizures that are followed by acute localiz-
ing neurologic defi cits. Most of the time, these patients
simply have a Todd’s paralysis and recover, becoming
asymptomatic; nevertheless, I think it’s important to
exclude acute stroke in patients who have a localizing
neurologic defi cit after a seizure. This is an example
of when a CT angiogram of the head and neck is very
helpful in patients presenting with an acute stroke. In
our institution, a patient like this would initially have
a head CT without contrast, which would be negative.
To be considered a candidate for thrombolytic therapy
in our institution, he would then have a CT angiogram
(CTA) of the head and neck. In this case, we would have
discovered the dissection, and consequently avoided
the catastrophic mistake of giving thrombolytics to a
Type A aortic dissection. The CTA can be performed
on a patient on the same trip to the CT scanner, avoid-
ing delays in the time to thrombolytic therapy in those
CHAPTER 19
272
these concerns, the benefi ts of beta-blockade are
undisputed fi rst-line therapy. Their effect is to lower
the change in pressure over the change in time (dP/
dT), reducing both the blood pressure and even more
importantly lowering the heart rate, and in turn reduc-
ing the shear stress on the aorta. This then reduces
the risk that any of these complications will occur. If
you’re concerned about these complications, then con-
sider using a short-acting agent such as esmolol.
PR: This patient has a history of COPD; would that be
a relative contraindication to using beta-blockade?
SG: I would emphasize that it is a relative contrain-
dication rather than an absolute contraindication. I
would start this patient on a short-acting beta-blocker
so that if the patient develops some bronchospasm, I
would be able to shut it off abruptly. Clearly, beta-
blockade is the avenue of choice in beginning phar-
macologic therapy in this type of patient.
PR: So we’ve reduced the shear forces on the aorta,
obtained the diagnostic information that hopefully
gives us the extent of the dissection, and we’ve lined
up our surgical consultation for correcting the lesion
if it’s a Type A. When do you need to go the operating
room with a Type B dissection, if ever?
DB: Patients with Type B dissections are generally
managed medically, unless they develop limb or end-
organ ischemia. If a patient develops either a cold
extremity or acute impairment of circulation to the
mesentery or to one of the kidneys, taking that patient
to the operating room to at least fenestrate the aorta
and try to restore blood fl ow to the limb or organ
would be appropriate.
PR: Would you, therefore, consult your cardiac sur-
geon immediately with a Type B, as well as a Type A,
dissection?
DB: In our institution, the Type B dissections would
be managed by vascular surgery. In a patient with a
Type B dissection, we would involve cardiology and
vascular surgery. The patients without limb or end-
organ ischemia are admitted to the cardiology service
for medical management, and those with limb or end-
organ ischemia are admitted to the vascular service
for operative repair.
PR: Would you consider intubating these patients and
taking away the work of respiration so that you could
give them higher dosages of analgesia and sedation?
transthoracic echocardiogram is more readily avail-
able. Nevertheless, there are some scenarios where a
TEE may be your test of choice, such as in a patient
not able to have a CT angiogram because of contrast
dye load issues. In addition, in cases where a patient
needs to go to the operating room in a more emergent
fashion, the anatomy can be delineated intraopera-
tively with a TEE.
PR: Although the evidence suggests that TEE is accu-
rate, as you point out, it’s only as accurate as its avail-
ability. I have yet to work in an institution where it’s
readily available.
DB: We can get a TEE relatively easily, but it requires
a cardiologist who specializes in TEE to come in and
do the procedure, and this takes time. In addition,
the patients often need to be intubated, or at least
adequately sedated, to do this comfortably, and this
takes even more time. The CTA can be done in just a
few minutes in the CT suite in the ED. Therefore, it is
unusual, even at our tertiary care center, to reach for
a TEE as our fi rst choice for imaging.
PR: These patients’ pain is often dramatic in my expe-
rience, and undergoing CTA while you are in agonizing
pain may be one of the more sadistic things we make
patients endure. What is the best method of manage-
ment while you are trying to obtain a diagnosis?
SG: Assuming the patient is hypertensive, as the major-
ity of these patients are, the initial therapy should be
directed toward the hypertension. Treating the hyper-
tension may also lessen the discomfort. I would usually
start with a beta-blocker such as esmolol or labetolol.
As I start to bring down the blood pressure, I would
add some sort of opioid analgesia, such as morphine.
PR: Is there any danger to using blood-pressure-
lowering agents with various types of dissection? In
other words, if you have an arch dissection, the Type
A Stanford, are you in any therapeutic danger if you
lower the pressure as opposed to leaving it up? Is
there a therapeutic advantage to hypertension with a
proximal dissection?
DB: In other words, what happens if the patient has a
complication of the dissection that causes immediate
cardiogenic shock, such as with acute aortic regurgita-
tion, pericardial tamponade, or a dissection of one of
the coronary arteries, which one would only see with a
type A dissection and not a type B dissection? Despite
AORTIC DISSECTION
273
the patient in an emergent fashion. Often times this
means transporting the patient by air, but at a mini-
mum, with critical care and rapid transport.
PR: What packaging requests would you ask your
transferring physician to do? What level of blood pres-
sure would you try to reduce the patient to, and how
much diagnostic testing do you want the transferring
institution to do?
DB: Lowering the heart rate is really more important
than lowering the blood pressure, which is why the
fi rst drug to be reached for is a beta-blocker or a mixed
alpha- and beta-blocker. If the heart rate can be slowed
down, then one markedly reduces aortic wall stress.
If there is room to lower the blood pressure after the
heart rate has been slowed to the low 60s or high 50s,
then I would add an agent such as nitroprusside or a
very short acting vasodilatator, and be satisfi ed with
whatever blood pressure the patient could tolerate
from a mental status standpoint. A young patient may
tolerate very low blood pressures, but an older person
with fi xed atherosclerotic lesions in the cerebrovascu-
lar circulation will need a higher blood pressure.
PR: Would you be willing to accept a patient who clini-
cally appears to be having a dissection, but for whom
you haven’t gotten proof with a CTA or a transthoracic
echocardiogram?
DB: If you’re in an institution where obtaining a CTA
is easy, I think that the scan ought to be done, unless
the patient has complications that already make it
imperative to transfer the patient, such as an acute
stroke, ST elevation myocardial infarction, or acute
aortic regurgitation we think secondary to a dissec-
tion. However, for patients who simply have chest
pain radiating to the back, if we recommend transfer
for diagnostic imaging, we are going to be transferring
many patients from small hospitals to large ones who
don’t have an aortic dissection, and in the process use
up scarce resources at those larger hospitals.
PR: Should therapy be any different for a younger
patient with a vascular connective tissue disorder such
as Marfan’s or Ehlers-Danlos syndrome, since hyper-
tension is probably not triggering this dissection? Do
we manage these patients in any different fashion?
SG: I would manage these patients in very much the
same way. Remembering that these are often younger
patients should remind one to consider illicit drug use
SG: Intubating the patient may also lower your dP/dT
(wall stress). If the patient is headed to the operating
room anyhow, there is little downside, in my mind,
to intubation. Adding a vasodilatator like nitroprus-
side is also reasonable, as it may offer some additional
benefi t both from a pain management and a therapeu-
tic management perspective by further reducing the
stress on the vessel.
DB: If it‘s truly pain control that we’re after, then I
would treat that directly with intravenous narcotics.
I would not choose to intubate in the hope that the
reduction in need for blood fl ow to the diaphragm
would somehow relieve the patient’s pain. I would
reserve intubation for those who appear critically ill,
or who are otherwise going to need intubation for
other problems such as congestive heart failure com-
plicating an aortic dissection.
PR: It is not just pain alone that disturbs these patients,
but a tremendous anxiety and sense of impending
doom, which often seems very accurate. How often
is acute renal failure a problem, and is there anything
you can do to avert it while you are trying to deal
with the vessel itself?
DB: Acute renal failure is uncommon unless it’s an
acute complication of contrast in these patients who
undergo CTA. More commonly, the fl ow to the right
or left renal artery is impaired by propagation of the
dissection down the abdominal aorta, causing isch-
emia of a single kidney and a lot of pain. Sometimes
that pain may be misinterpreted as renal colic. But
losing fl ow to one kidney usually does not cause acute
renal failure, at least not during the time in which ED
management could effectively change.
PR: What does the emergency physician do who works
in remote rural areas or in more remote suburban
areas that don’t have cardiothoracic surgery or major
interventional cardiology?
SG: This is a patient who will require transfer to a
center where the surgery can be done, particularly if
it’s a Type A dissection. If it is a Type B, the patient
will often be transferred as well, usually to get a better
look at both the patient and at the imaging that was
done to make the diagnosis. Your job in the commu-
nity is to stabilize the patient as best you can, which
means again, stabilizing the blood pressure, reduc-
ing dP/dT, and to ensure that you are transporting
CHAPTER 19
274
aneurysm without dissection, and atherosclerotic ulcer-
ation that can cause a dissection into the descending
aorta. Aortic dissection is defi ned as acute if the symp-
toms began within the previous 14 days.
The incidence of the disease is approximately 3 in
100,000 people/year, and thus it is estimated that there
are 7,000–10,000 cases per year in the U.S.
2,3
Although
relatively rare, the importance of the disease is charac-
terized by its severity. If left untreated, mortality is at
least 1% per hour, and 50% within the fi rst 48 hours of
symptoms.
3,4
Even with appropriate treatment, overall
mortality remains approximately 27%.
5
The etiology, presentation, treatment, and progno-
sis of aortic dissection vary depending on whether the
dissection involves the ascending, descending, or both
areas of the aorta. For this reason, the commonly
used Stanford and DeBakey classifi cation schemes
are based on the geographic involvement of disease
(Figure 19-2). Regardless of the location of the intimal
tear, any dissection that involves the ascending aorta
is classifi ed as Stanford Type A. Dissection involving
only the descending aorta is classifi ed as Stanford
Type B. DeBakey Type I dissection involves both
the ascending and descending aorta, while Debakey
Type II, only the ascending aorta, and Type III, only
the descending aorta.
The approximate geographic distribution of dissec-
tions is as follows: 65% ascending, 20% descending,
and its association with aortic dissection. Cocaine
users might benefi t from benzodiazepines as an addi-
tional therapy. Beyond that, maximizing control of
the heart rate and blood pressure remains appropriate
in this patient population as well.
Case resolution
The patient underwent operative repair of a type A
aortic dissection and cardiac tamponade. She was ini-
tially unstable in the postoperative period, developing
mild renal insuffi ciency and suffered a small non-ST
elevation MI. She was discharged to a rehabilitation
facility on postoperative day ten.
Section III: Concepts
Epidemiology and pathophysiology
Aortic dissection is defi ned as a dissection of the wall of
the aorta with formation of a false lumen or hematoma
within the dissected layer. The aortic wall contains three
layers, with dissection generally occurring in the middle
(media) layer of the wall, usually emanating from a tear
in the intimal layer of the vessel (Figure 19-1). Related
variations from the typical mechanism of intimal tear
and media dissection include an intramural hematoma
with no evidence of intimal tear, dilated thoracic aortic
Figure 19.1 Pathologic specimen of
the inner aortic surface of a patient
who presented with a spontaneous
tear in the arch of the aorta (arrow).
The takeoff of the arch vessels were
uninvolved; however the lesion
dissected in a retrograde fashion
through the media layer to the
pericardial sac, causing pericardial
tamponade.