aortic dissection review of literature

1. CASE PRESENTATION &
REVIEW OF LITERATURE

2.  52 yr old male from Theog
 Date & time of presentation in casualty-
7th May 2014/9:20 pm
 Chief complaints: Back pain since 7th May 2014/7:30
pm

3.  HOPI- Patient was apparently asymptomatic till
about 2 hours ago when he was travelling to
Theog on his motorcycle when he started having
back pain: localised to interscapular region,
sudden in onset, severe in intensity, stabbing in
nature, radiating to the front of chest, no
aggravating or relieving factors
no h/o any associated sweating
no h/o presyncope/syncope
no h/o LOC/weakness of any limb
no h/o SOB/palpitations
no h/o fever/cough
no h/o any recent trauma/lifting heavy weights

4.  PAST HISTORY- no h/o similar episodes in past
not a k/c/o HTN/DM/CAD
 PERSONAL HISTORY-
smoker with a SI=360(12*30)
occasional alcoholic
non vegetarian
no h/o any illicit drug abuse
engineer in PWD deptt.
 FAMILY HISTORY-
no family history of HTN/DM/CAD
no h/o any sudden death in family

5. Examination
 GPE: conscious , restless, oriented to T/P/P
BP
PR(right radial) 74/min regular, good volume
P-/I-/Cy-/Cl-/LAP-/JVP-/PE-
No radio-radial/radio-femoral delay
No pulsus paradoxus
Kussmaul sign negative
no local tenderness on chest/back
Rt arm 190/110 Lt arm 172/100
Radial Femoral Popiliteal Post
tibial
Dors
pedis
Rt +++ ++ ++ ++ +
Lt ++ ++ ++ ++ +

6.  Respiratory: trachea central, b/l symmetrical, both
sides moving equally, b/l VBS with no added sounds
 CVS- precordium normal
S1 S2 normal no added sounds
 P/A- soft, slight tenderness in epigastrium,
G-/R-/RT-
 CNS- HMF/motor/sensory /CN/speech-NAD
plantars- b/l flexor response

7.  Fundus examn-
no e/o hypertensive retinopathy
 ECG-
normal axis, HR 74/min, no e/o any chamber
hypertrophy
 CXR PA view(portable): NAD
 Troponin-T : negative

8. Provisional diagnosis
 ? AORTIC DISSECTION
 ??CAD:ACS:USA

9.  RBS 138 mg%
 S.Na+ 141
 S.K+ 3.7 meq/l
 S.Cl- 111
 Urea 69
 Creatinine 2.3 mg%
 Urine for RBC- no RBC seen
 TLC 8400/ mm3
 Hb 10.9 g/dl

10.  CECT AORTIC ANGIOGRAPHY:
flap in the aorta dividing it into true and false lumens
just after the origin of the left subclavian artery upto
the level of aortic bifurcation
“STANFORD Type B Aortic Dissection with multiple
hepatic and renal cysts ?ADPKD”

13. Final diagnosis
 Stanford type B aortic dissection with
?AKI ?Acute on CKD with
?ADPKD

14. Course
 Patient was managed with antihypertensives( NTG
infusion and I/V beta blockers) and analgesic support
(morphine).
 Consultation taken from Cardiology and CTVS
departments for any intervention.
 As the patient was still in severe pain despite analgesics
and had started experiencing signs of vital organ
damage, we were advised referral to higher centre.
 Due to inavailability of stent at the higher centre the
intervention was delayed for 2 days. Eventually
endovascular intervention done on 3rd day after referral.
 Patient collapsed on the 4th day after referral.

15. Review of Literature

16.  Acute aortic dissection is the most common
catastrophic event affecting the aorta with an
estimated annual incidence of approximately 5 to 30
per million.
 The early mortality rate: 1-2% per hour reported in
the first several hours after dissection occurs
 Twice more common in men than in women
 Aortic dissection is more common in blacks than in
whites and is less common in Asians than in whites.
 MC age group: 50-60 years (ascending)
60-70 years (descending)
 Patients with Marfan syndrome present earlier,
usually in the third and fourth decades of life.
The International Registry of Acute Aortic Dissection (IRAD): new insights into
an old disease.

17.  Two main hypothesis:
first- primary tear in aortic intima -> blood in the aortic
lumen penetrates into the diseased media leading to
dissection -> creation of true and false lumen
second- primary rupture of vasa vasorum -> hemorrhage
in the aortic wall -> subsequent intimal disruption ->
intimal tear -> dissection

18.  The pressure of the pulsatile blood within the aortic
wall after dissection leads to the extension of
dissection.
 Usually propagate in antegrade direction.
 Arterial pressure and shear forces may lead to
further tears in the intimal flap producing exit sites or
additional entry sites for blood flow into the false
lumen.
 Distension of the false lumen with blood causes the
intimal flap to compress the true lumen, narrowing its
caliber and distorting its shape, which leads to
malperfusion

20. Classification

21.  Most ascending aortic dissections begin within a few
centimeters of the aortic valve and most descending
dissections have their origin just distal to the the left
subclavian artery.
 Approx 65% intimal tears in ascending aorta, 30% in
descending aorta, <10% in aortic arch, and approx 1% in
abdominal aorta.
 The treatment depends on the site with emergency
surgery recommended for acute type A dissections and
initial medical management for type B dissections.
 Also classified according to its duration: acute <2
weeks
chronic >2
weeks
 The morbidity and mortality rates of acute dissection are
highest in the first 2 weeks , especially within the first 24

22. Causes
•Approximately 75% of all pts have HTN
•Cystic medial degeneration is the chief
predisposing factor in aortic dissection. Cystic
medial degeneration is an intrinsic feature of
several hereditary defects of connective tissue,
most notably Marfan and Ehlers-Danlos
syndromes, and is also common among patients
with bicuspid aortic valve. In fact, Marfan
syndrome accounts for 5 percent of all aortic
dissections.
•Pregnancy can be a risk factor for aortic
dissection, particularly in patients with an
underlying anomaly such as Marfan syndrome.
An estimated 50% of all cases of aortic dissection
that occur in women younger than 40 years are
associated with pregnancy. Most cases occur in
the third trimester or early postpartum period.
Wilson SK, Hutchins GM. Aortic dissecting aneurysms:
causative factors in 204 subjects. Arch Pathol Lab Med 1982

23. Clinical manifestations
 The most common initial symptom of acute aortic
dissection is pain, which is found in up to 96 percent of
cases, whereas the large majority of those without pain
are found to have chronic dissections.
 The pain is typically severe and of sudden onset and is as
severe at its inception as it ever becomes, in contrast to
the pain of myocardial infarction, which usually has a
crescendo-like onset and is not as intense. In fact, the
pain of aortic dissection may be all but unbearable in
some instances and force the patient to writhe in agony,
fall to the ground, or pace restlessly in an attempt to gain
relief.
 Several features of the pain should arouse suspicion of
aortic dissection. The quality of the pain as described by
the patient is often morbidly appropriate to the actual

24.  Another important characteristic of the pain of aortic
dissection is its tendency to migrate from its point of
origin to other sites, generally following the path of
the dissection as it extends through the aorta.
However, such migratory pain is described in as few
as 17 percent of cases.
 Spittell and colleagues found that when the location
of chest pain was anterior only (or if the most severe
pain was anterior), more than 90 percent of patients
had involvement of the ascending aorta. Conversely,
when the chest pain was interscapular only (or when
the most severe pain was interscapular), more than
90 percent of patients had involvement of the
descending thoracic aorta (i.e., DeBakey type I or
III).
 The presence of any pain in the neck, throat, jaw, or
face strongly predicted involvement of the ascending
aorta, whereas pain anywhere in the back,Spittell PCet al. Clinical features and differential diagnosis of aortic dissection:
experience

25.  Less common symptoms at initial evaluation, occurring
with or without associated chest pain, include congestive
heart failure (7 percent), syncope (13 percent),
cerebrovascular accident (6 percent), ischemic peripheral
neuropathy, paraplegia, and cardiac arrest or sudden
death.
 Patients may have abdominal pain and on occasion,
develop severe nausea and vomiting related to
abdominal visceral involvement. These symptoms may
delay diagnosis and increase mortality rate.
 Painless aortic dissection was reported in 6% of the
patients in one study and was more commonly
associated with diabetes, prior aortic aneurysm, and prior
cardiac surgery.
Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysms of the aorta: a review of
505 cases. Medicine 1995; 37:217–279

26. Physical findings
 Hypertension is seen in 70 percent of patients with
distal aortic dissection but in only 36 percent with
proximal dissection.
 Hypotension, on the other hand, occurs much more
commonly among those with proximal than those with
distal aortic dissection (25 and 4 percent,
respectively).
True hypotension is usually the result of cardiac
tamponade, acute severe aortic regurgitation,
intrapleural rupture, or intraperitoneal rupture.
Dissection involving the brachiocephalic vessels may
result in pseudohypotension, an inaccurate
measurement of blood pressure caused by
compromise or occlusion of the brachial arteries.
 An interarm blood pressure differential greater than 20

27.  Acute, severe aortic regurgitation may result in signs
suggestive of congestive heart failure: dyspnea,
orthopnea, bibasilar crackles, or elevated jugular
venous pressure.
 Other cardiovascular manifestations include findings
suggestive of cardiac tamponade (eg, muffled heart
sounds, hypotension, pulsus paradoxus, jugular
venous distention, Kussmaul sign). Tamponade must
be recognized promptly.
 Patients with right coronary artery ostial dissection
may present with acute myocardial infarction,
commonly inferior myocardial infarction. It remains
essential that when evaluating patients with acute
myocardial infarction, particularly inferior infarctions,
one carefully considers the possibility of an

28.  Neurologic deficits are a presenting sign in up to 20%
of cases. The most common neurologic findings are
syncope and altered mental status
 Extension of aortic dissection into the abdominal
aorta can cause other vascular complications.
Compromise of one or both renal arteries occurs in
about 5 to 8 percent and can lead to renal ischemia or
frank infarction and, eventually, severe hypertension
and acute kidney injury.
 Mesenteric ischemia and infarction—occasional and
potentially lethal complications of abdominal
dissection—occur in 3 to 5 percent of cases.
 In addition, aortic dissection may extend into the iliac
arteries and cause diminished femoral pulses (12

29.  Additional clinical manifestations of aortic dissection
include the presence of small pleural effusions, seen
more commonly on the left side.
 The physical findings most typically associated with aortic
dissection—pulse deficits, the murmur of aortic
regurgitation, and neurological manifestations—are more
characteristic of proximal than of distal dissection.
Reduced or absent pulses in patients with acute chest
pain strongly suggests the presence of aortic dissection.
Such pulse abnormalities are present in about 30 percent
of proximal aortic dissections and occur throughout the
arterial tree, but occur in only 15 percent of distal
dissections, where they usually involve the femoral or left
subclavian artery.

30. DIAGNOSIS
 CHEST X RAY: Although chest radiography may help support
a diagnosis of suspected aortic dissection, the findings are
nonspecific and rarely diagnostic.
 The most common abnormality seen on a chest radiograph
in cases of aortic dissection is widening of the aortic
silhouette, which appears in 81 to 90 percent of cases. Less
often, nonspecific widening of the superior mediastinum is
seen. If calcification of the aortic knob is present, separation
of the intimal calcification from the outer aortic soft tissue
border by more than 1.0 cm—the “calcium sign”—is
suggestive, although not diagnostic, of aortic dissection.
Pleural effusions are common, typically occur on the left
side, and are more often associated with dissection involving
the descending aorta.
 Up to 12 percent, have chest radiographs that appear
unremarkable. Therefore, a normal chest radiograph can

32.  ECG-Electrocardiographic findings in patients with aortic
dissection are nonspecific.
 One third of electrocardiograms show changes consistent
with left ventricular hypertrophy, whereas another one third
are normal.
 In acute thoracic aortic dissection, the ECG changes can
mimic those seen in acute cardiac ischemia. In the
presence of chest pain, these signs can make
distinguishing dissection from acute myocardial infarction
very. Keep this in mind when administering thrombolytics to
patients with chest pain.
 The incidence of abnormal ECG findings is greater in
Stanford type A dissections than in other types of
dissections. ST segment elevation can be seen in Stanford
type A dissections because the dissection interrupts blood
flow to the coronary arteries. In one study, 8% of patients
with type A dissections had ST segment elevation, whereas
no patients with type B dissections had ST segment
elevation. More commonly, the ECG abnormality is ST
segment depression.
 If the dissection involves the coronary ostia, the right

33.  D-dimer:
 In a series comparing 94 consecutive patients with
aortic dissection and 94 controls, a d-dimer of >400
ng/ml had a sensitivity of 99 percent and a specificity
of 34 percent. Moreover, D-dimer levels correlated with
the anatomical extent of the dissection and with in-
hospital mortality.
 This suggests that D-dimer levels may be useful as a
screening test in the emergency department, with
elevated levels prompting at least clinical
consideration, if not diagnostic investigation, of
possible aortic dissection.

34.  Myocardial muscle creatine kinase isoenzyme, myoglobin,
and troponin I and T levels are elevated if the dissection
has involved the coronary arteries and caused myocardial
ischemia. The lactate dehydrogenase level may be
elevated because of hemolysis in the false lumen.
 Measurement of the degradation products of plasma fibrin
and fibrinogen can facilitate the diagnosis of acute aortic
dissection. In symptomatic patients, aortic dissection with
a patent false lumen should be considered if the plasma
fibrin degradation product (FDP) level is 12.6 μg/mL or
higher; the possibility of dissection with complete
thrombosis of the false lumen should be considered if the
FDP level is 5.6 μg/mL or higher.
 A smooth muscle myosin heavy-chain assay is performed
in the first 24 hours. Increased levels in the first 24 hours
are 90% sensitive and 97% specific for aortic dissection.
Levels are highest in the first 3 hours. A cutoff of 2.5 has a

35.  Once suspected on clinical grounds, it is
essential to confirm the diagnosis of aortic
dissection both promptly and accurately.
The modalities currently available for this
purpose include
Aortography
Contrast-enhanced CT
MRI
TTE or TEE

36.  Aortography-The diagnosis of aortic dissection is based
on direct angiographic signs, including visualization of
two lumina or an intimal flap (considered diagnostic) or
on indirect signs (considered suggestive), such as
deformity of the aortic lumen, thickening of the aortic
walls, branch vessel abnormalities, and aortic
regurgitation. Prospective studies have found that for the
diagnosis of aortic dissection, the sensitivity of aortography
is 88 percent and the specificity is 94 percent.

37.  Contrast-enhanced CT scanning- In contrast-
enhanced CT scanning, aortic dissection is diagnosed
by the presence of two distinct aortic lumina, either
visibly separated by an intimal flap or distinguished by
a differential rate of contrast opacification. Several
series have found that spiral CT scanning has both a
sensitivity and specificity for acute aortic dissection of
96 to 100 percent.
 CT is helpful in identifying the presence of thrombus in
the false lumen and in detecting pericardial effusion.
 The use of CT angiography permits assessment of
branch vessel compromise in both the thoracic and
abdominal segments.

40.  MRI-
Magnetic resonance imaging has both a sensitivity and
a specificity of approximately 98 percent. Intravenous
administration of gadolinium yields a magnetic
resonance angiogram, which defines the patency of
aortic branch vessels. Still, MRI does have a number
of disadvantages. MRI provides only limited images of
branch vessels (unless gadolinium is used) and does
not consistently identify the presence of aortic
regurgitation. In most hospitals, magnetic resonance
scanners are not readily available on an emergency
basis.

41.  Echocardiography is well suited for the evaluation of
patients with suspected aortic dissection because it is
readily available in most hospitals, it is noninvasive
and quick to perform, and the full examination can be
completed at the bedside.
 The echocardiographic finding considered diagnostic
of an aortic dissection is the presence of an undulating
intimal flap within the aortic lumen that separates the
true and false channels. Reverberations and other
artifacts can cause linear echodensities within the
aortic lumen that mimic aortic dissection. To
distinguish an intimal flap definitively from such
artifacts, the flap should be identified in more than one
view, it should have motion independent of that of the
aortic walls or other cardiac structures, and a
differential in color Doppler flow patterns should be

42.  Transthoracic echocardiography has a sensitivity of 59
to 85 percent and a specificity of 63 to 96 percent for
the diagnosis of aortic dissection. Such poor sensitivity
significantly limits the general usefulness of this
technique.
 The results of large prospective studies have
demonstrated that the sensitivity of TEE for aortic
dissection is 98 to 99 percent, whereas the sensitivity
for detecting an intimal tear is 73 percent.
TEE detects both aortic regurgitation and pericardial
effusion in 100 percent of cases. The specificity of
TEE for the diagnosis of aortic dissection is less well
defined but is likely in the range of 94 to 97 percent.

43.  In a setting in which all these imaging modalities
are available, CT should be considered first in the
evaluation of suspected aortic dissection in light of
its accuracy, safety, speed, and convenience.
 When CT identifies a type A aortic dissection, the
patient may be taken directly to the operating
room, where TEE can then be performed to
assess the anatomy and competence of the aortic
valve without unduly delaying surgery.
 However, in cases of suspected aortic dissection
in which aortic valve disease is suspected or the
patient is unstable, TEE may be the initial

44. Management
 Therapy for aortic dissection aims to halt
progression of the dissecting hematoma because
lethal complications arise not from the intimal tear
itself but rather from the subsequent course taken
by the dissecting aorta, such as vascular
compromise or aortic rupture. Without treatment,
aortic dissection has a high mortality rate.

45.  Aggressive medical treatment of aortic dissection was
first advocated by Wheat and colleagues in the 1960s.
The authors established reduction of systolic blood
pressure and diminution of the rate of left ventricular
ejection (dP/dt) as the two primary goals of
pharmacological therapy.
 Originally introduced for patients too ill to withstand
surgery, medical therapy is now the initial treatment for
virtually all patients with aortic dissection before
definitive diagnosis and furthermore serves as the
primary long-term therapy in a subset of patients,
particularly those with distal dissections.

46. Initial therapy
 Initial therapeutic goals include the elimination of pain
and reduction of systolic blood pressure to 100 to 120
mm Hg (mean of 60 to 75 mm Hg) or the lowest level
commensurate with adequate vital organ (cardiac,
cerebral, renal) perfusion. Beta-blocking agents should
be administered simultaneously, regardless of whether
pain or systolic hypertension is present. Pain, which
may itself exacerbate hypertension and tachycardia,
should be promptly treated with intravenous morphine
sulfate.
 For the acute reduction of arterial pressure, the potent
vasodilator sodium nitroprusside is effective. When
used alone, however, sodium nitroprusside can
actually cause an increase in dP/dt, which in turn may
potentially contribute to propagation of the dissection.
Therefore, concomitant beta-blocking treatment is

47.  To reduce dP/dt acutely, an intravenous beta blocker
should be administered in incremental doses until
evidence of satisfactory beta blockade is noted,
usually indicated by a heart rate of 60 to 80 beats/min
in the acute setting. Because propranolol was the first
generally available beta blocker, it has been used
most widely in treating aortic dissection.
 Labetalol, which acts as both an alpha- and a beta-
adrenergic receptor blocker, can be especially useful
in the setting of aortic dissection because it effectively
lowers both dP/dt and arterial pressure.
 The ultra-short-acting beta blocker esmolol may be
particularly useful in patients with labile arterial
pressure, especially if surgery is planned, because
use of this drug can be abruptly discontinued if
necessary.

48.  When contraindications exist to the use of beta
blockers—including severe sinus bradycardia, second-
or third-degree atrioventricular block, congestive heart
failure, or bronchospasm—other agents to reduce
arterial pressure and dP/dt should be considered.
Calcium channel antagonists, which are effective in
managing hypertensive crisis, are used on occasion in
the treatment of aortic dissection. The combined
vasodilator and negative inotropic effects of both
diltiazem and verapamil make these agents well suited
for the treatment of aortic dissection. Moreover, these
agents may be administered intravenously.
 Refractory hypertension may result when a dissection
flap compromises one or both of the renal arteries,
thereby causing the release of large amounts of renin.
In this situation, the most efficacious antihypertensive

49.  In the event that a patient with suspected aortic
dissection has significant hypotension, rapid
volume expansion should be considered, given the
possible presence of cardiac tamponade or aortic
rupture. Before initiating aggressive treatment of such
hypotension, however, the possibility of
pseudohypotension, which occurs when arterial
pressure is being measured in an extremity where the
circulation is selectively compromised by the
dissection, should be carefully excluded. If
vasopressors are absolutely required for refractory
hypotension, norepinephrine or phenylephrine is
preferred. Dopamine should be reserved for improving
renal perfusion and used only at very low doses, given
that it may raise dP/dt.

50.  When a patient with acute aortic dissection
complicated by cardiac tamponade is relatively
stable, the risks of pericardiocentesis probably
outweigh the benefits and every effort should be
made to proceed as urgently as possible to the
operating room for direct surgical repair of the
aorta with intraoperative drainage of the
hemopericardium.
 However, when patients have pulseless electrical
activity or marked hypotension, an attempt to
resuscitate the patient with pericardiocentesis is
warranted and may indeed be successful. A
prudent strategy in such cases is to aspirate only
enough pericardial fluid to raise blood pressure to

51. Definitive Therapy

52.  Definitive surgical therapy was pioneered by DeBakey and
colleagues in the early 1950s.
 The usual objectives of definitive surgical therapy include
resection of the most severely damaged segment of aorta,
excision of the intimal tear when possible, and obliteration of
entry into the false lumen by suturing of the edges of the
dissected aorta both proximally and distally. After the
diseased segment containing the intimal tear is resected,
typically a segment of the ascending aorta in proximal
dissections or the proximal descending aorta in distal
dissections, aortic continuity is then reestablished by
interposing a prosthetic sleeve graft between the two ends
of the aorta.
 One of the more promising avenues of investigation is the
use of endovascular techniques for treating high-risk
patients with aortic dissection. More recently, intraluminal
stent-grafts placed percutaneously by the transfemoral
catheter technique have been introduced as a potential
alternative to aortic repair. This procedure aims to close the
site of entry into the false lumen (intimal tear), decompress
and promote thrombosis of the false lumen, and relieve any

54.  When patients with type B aortic dissection are managed
medically, in addition to the reduction in dP/dt and heart
rate, a second goal is to monitor the patient vigilantly for
any evidence of branch arterial compromise, with the most
lethal consequence being mesenteric ischemia.
 Late follow-up of patients leaving the hospital with treated
aortic dissection shows an actual survival rate not much
worse than that of individuals of comparable age without
dissection. No significant differences are seen among
discharged patients when comparing proximal versus distal
dissection, acute versus chronic dissection, or medical
versus surgical treatment. Five-year survival rates for all
these groups (among discharged patients) are typically 75
to 82 percent.
 Thus, the initial success of surgical or medical therapy is
usually sustained on long-term follow-up. Late
complications include aortic regurgitation, recurrent
dissection, and aneurysm formation or rupture. The
presence of a persistently patent false lumen is one of the
strongest predictors of adverse late outcomes, including

55.  Long-term medical therapy to control hypertension
and reduce dP/dt is indicated for all patients who have
sustained an aortic dissection, regardless of whether
their in-hospital definitive treatment was surgical or
medical.
 Systolic blood pressure should be maintained at or
below 130 mm Hg. The preferred agents are beta
blockers or, if contraindicated, other agents with a
negative inotropic as well as a hypotensive effect,
such as verapamil or diltiazem. ACE inhibitors and
angiotensin receptor blockers are attractive
antihypertensive agents for treating aortic dissection
and may be of particular benefit in patients with some
degree of renal ischemia as a consequence of the
dissection. Pure vasodilators, such as dihydropyridine
calcium channel antagonists or hydralazine, may
cause an increase in dP/dt and should therefore be

56.  Follow-up evaluation of patients after aortic dissection
should include serial aortic imaging with CT, MRI, or
TEE.
 Patients are at highest risk immediately after
hospitalization and during the first 2 years, with the risk
progressively declining thereafter. It is therefore
important to have more frequent early follow-up; for
example, patients can be seen and imaged at 1, 3, and
6 months initially and then return every 6 months for 2
years, after which time they can often be re-imaged at
12-month intervals, depending on the given patient's
risk.

57.  In its natural evolution, without treatment, acute type A
aortic dissection reportedly has a mortality rate of about
1% per hour initially, with half of the patients expected
to be dead by the 3rd day, and almost 80% by the end
of the 2nd week.
 Death rates are lower but still significant in acute type
B aortic dissection: 10% minimum at 30 days, and 70%
or more in the highest-risk groups.
Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et
al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old
disease. JAMA 2000;283(7):897–903.

58. Atypical Aortic Dissection
 In aortic dissection as classically described, two
other diseases of the aorta are closely related,
intramural hematoma of the aorta and penetrating
atherosclerotic ulcer of the aorta. These two
conditions share with aortic dissection many of the
predisposing risk factors and initial symptoms, and
indeed, both may lead to either classic aortic
dissection or aortic rupture. In light of their clinical
similarities, it is appropriate to consider classic aortic
dissection and its variants collectively among the
“acute thoracic aortic syndromes,” a category
that also includes traumatic aortic transection and
rupture, contained rupture (pseudoaneurysm), or

59. Schematic of aortic dissection (left), penetrating ulcer (middle), and IMH (right).
Tsai T T et al. Circulation. 2005;112:3802-3813

63. Thanks
The tragedies of life are
largely arterial
— Sir
William Osler