Chapter 11 – Blood Vessels: Aneurysms and Dissection Flashcards

1
Q

What is aneurysm?

A

An aneurysm is a localized abnormal dilation of a blood vessel or the heart ( Fig. 11-17 ); it can
be congenital or acquired.

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2
Q

What is true aneurysm?

A

When an aneurysm involves an intact attenuated arterial wall or thinned ventricular wall of the heart, it is called a true aneurysm

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3
Q

Give example of true aneurysm.

A

Atherosclerotic, syphilitic, and
congenital vascular aneurysms, and ventricular aneurysms that follow transmural myocardial
infarctions are of this type

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4
Q

What is a false aneurysm?

A

a false aneurysm (also called pseudo-aneurysm) is a

  • *defect in the vascular wall leading** to an extravascular hematoma that freely communicates with
  • *the intravascular space (“pulsating hematoma”)**
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5
Q

Give example of False Aneurysm.

A

Examples include a ventricular rupture after
myocardial infarction that is contained by a pericardial adhesion, or a leak at the sutured
junction of a vascular graft with a natural arter
y

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6
Q

What are arterial dissection?

A

An arterial dissection arises when blood enters
the arterial wall itself, as a hematoma dissecting between its layers.

Dissections are often but
not always aneurysmal (see also below)

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7
Q

Dissections are always aneurysmal.

T or F

A

FALSE

Dissections are often but
not always aneurysmal

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8
Q

Both true and false aneurysms as well as dissections
can rupture, often with catastrophic consequences

T or F

A

True

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9
Q
A

FIGURE 11-17 Aneurysms.

  • A, Normal vessel.
  • B, True aneurysm, saccular type. The wall focally bulges outward and may be attenuated but is otherwise intact.
  • C, True aneurysm, fusiform type. There is circumferential dilation of the vessel, without rupture.
  • D, False aneurysm. The wall is ruptured, and there is a collection of blood (hematoma) that is bounded externally by adherent extravascular tissues.
  • E, Dissection. Blood has entered (dissected) the wall of the vessel and separated the layers. Although this is shown as occurring through a tear in the lumen, dissections can also occur by rupture of the vessels of the vaso vasorum within the media.
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10
Q

Aneurysms are generally classified by what?

A

shape and size

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11
Q

What are Saccular aneurysms?

A

spherical outpouchings (involving only a portion of the vessel wall); they vary from 5 to 20
cm in diameter and often contain thrombus

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12
Q

What are Fusiform aneurysms ?

A

Fusiform aneurysms involve diffuse, circumferential

  • *dilation of a long vascular segment**; they vary in diameter (up to 20 cm) and in length, and can
  • *involve extensive portions of the aortic arch,** abdominal aorta, or even the iliac arteries.

These
types are not specific for any disease or clinical manifestations.

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13
Q

Arteries are dynamically remodeling tissues that maintain their integrity by constantly
synthesizing, degrading, and repairing damage to their ECM constituents.

So how does aneurysm can occur?

A

Aneurysms can occur
when the structure or function of the connective tissue within the vascular wall is compromised.
Although we cite here examples of inherited defects in connective tissues, weakening of vessel
walls is important in the common, sporadic forms of aneurysms as well

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14
Q

What is important in the pathogenesis of commom. sporadic forms of aneurysms?

A

weakening of vessel
walls is important in the common, sporadic forms of aneurysms as well

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15
Q

Pathogenesis of Aneurysms

A
  • The intrinsic quality of the vascular wall connective tissue is poor
  • The balance of collagen degradation and synthesis is altered by local inflammatory infiltrates and the destructive proteolytic enzymes they produce.
  • The vascular wall is weakened through loss of smooth muscle cells or the inappropriate
    synthesis of noncollagenous or nonelastic ECM.
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16
Q

Give examples of intrinsic quality of the vascular wall connective tissue is poor

A
  • Marfan syndrome
  • Loeys-Dietz syndrome
  • Ehlers-Danlos syndrome

MEL you are so Poor

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17
Q

What is defective in Marfan syndrome that leads to intrinsic quality of the vascular wall connective tissue is poor?

A
Marfan syndrome,
for example ( Chapter 5 ), defective synthesis of the **scaffolding protein fibrillin** leads to
**aberrant TGF-β** activity and **progressive weakening of elastic tissue**; in the aorta, the consequence is **progressive dilation due to remodeling of the inelastic media**
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18
Q

What is defective in Loeys-Dietz syndrome that leads to intrinsic quality of the vascular wall connective tissue is poor?

A

another recently recognized cause of aneurysms; in this
disorder, mutations in TGF-β receptors lead to abnormalities in elastin and collagen I
and III.

Aneurysms in such individuals can rupture fairly easily (even at small size).

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19
Q

What is defective in Ehlers-Danlos syndrome that leads to intrinsic quality of the vascular wall connective tissue is poor?

A

altered collagen crosslinking
associated with vitamin C (ascorbate) deficiency
is an example of anutritional
basis for aneurysm formation.

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20
Q

What is an example of a nutritional

basis for aneurysm formation.

A

Ehlers-Danlos syndrome

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21
Q

How does MMP production contributes to aneurysm dev?

A

MMP production, especially by macrophages in atherosclerotic plaque or in vasculitis,
probably contributes to aneurysm development [56] ; these enzymes have the capacity
to degrade virtually all components of the ECM in the arterial wall (collagens, elastin,
proteoglycans, laminin, fibronectin).

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22
Q

What regulates the balance of collagen degradation and synthesis that is altered by local inflammatory
infiltrates and the destructive proteolytic enzymes they produce which contribute to the formation of aneurysm?

A
  • TIMP
  • MMP

Genetic predisposition to aneurysm formation in the setting of inflammatory
lesions (such as atherosclerosis) may be related to polymorphisms of MMP and/or TIMP
genes, or to the nature of the local inflammatory response that results in increased
production of MMP.

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23
Q

What factors contribute tovascular wall is weakened through loss of smooth muscle cellsor theinappropriatesynthesis of noncollagenous or nonelastic ECM.

A
  • Ischemia of the inner media occurs when there is atherosclerotic thickening of the intima, which increases the distance that oxygen and nutrients must diffuse.
  • Systemic hypertension can also cause significant narrowing of arterioles of the vasa vasorum (e.g., in the aorta), which can cause outer medial ischemia. Ischemia is reflected in “degenerative changes” of the aorta, whereby smooth muscle cell loss—or change in synthetic phenotype—leads to scarring (and loss of elastic fibers), inadequate ECM synthesis, and production of increasing amounts of amorphous ground substance (glycosaminoglycan).
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24
Q

Where is ischemia is reflected ?

A

in “degenerative changes” of the aorta,

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25
Q

Smooth muscle cell loss—or change in synthetic phenotype—leads to what?

A

leads to scarring (and loss of elastic fibers), inadequate ECM synthesis, and production of increasing amounts of amorphous ground substance (glycosaminoglycan).

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26
Q

What is cystic medial degeneration?

A

Ischemia is reflected in “degenerative changes” of the aorta, whereby smooth muscle cell loss—or change in synthetic phenotype—leads to scarring (and loss
of elastic fibers), inadequate ECM synthesis, and production of increasing amounts of
amorphous ground substance (glycosaminoglycan).

Histologically these changes are
collectively called cystic medial degeneration ( Fig. 11-18 ). These changes are
nonspecific and can be seen in a variety of settings, including Marfan disease and
scurvy.

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27
Q
A

FIGURE 11-18 Cystic medial degeneration. A, Cross-section of aortic media from a patient
with Marfan syndrome, showing marked elastin fragmentation and formation of areas devoid
of elastin that resemble cystic spaces (asterisks). B, Normal media for comparison, showing
the regular layered pattern of elastic tissue. In both A and B, elastin is stained black.

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28
Q

What are the two most important disorders that predispose to aortic aneurysms?

A
  • atherosclerosis and
  • hypertension
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29
Q

What is a greater factor in abdominal aortic aneurysms?

A

atherosclerosis

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30
Q

What is the most common condition associated with aneurysms of the ascending
aorta.

A

hypertension is the most common condition associated with aneurysms of the ascending
aorta.

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31
Q

What are Other conditions that weaken vessel walls lead to aneurysms?

A
  • trauma,
  • vasculitis (see below),
  • congenital defects (e.g., berry aneurysms typically in the circle of Willis; Chapter 28 ), and
  • infections (mycotic aneurysms).
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32
Q

Mycotic aneurysms can originate from what:

A
  • (1) from embolization of a septic embolus, usually as a complication of infective endocarditis;
  • (2) as an extension of an adjacent suppurative process; or
  • (3) by circulating organisms directly infecting the arterial wall.

Tertiary syphilis is now a rare cause of aorticaneurysms

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33
Q

Tertiary syphilis is now a rare cause of aorticaneurysms

T or F

A

True

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34
Q

How does Tertiary syphilis cause of aorticaneurysms

A

The obliterative
endarteritis
characteristic oflate-stage syphilisshows apredilection for small vessels, including
those of the vasa vasorum of the thoracic aorta.

This leads to ischemic injury of the aortic media and aneurysmal dilation, which sometimes involves the aortic valve annulus.

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35
Q

obliterative endarteritis characteristic of late-stage syphilis shows a predilection for what vessels?

A

for small vessels, including
those of the vasa vasorum of the thoracic aorta.

36
Q

Aneurysms associated with atherosclerosis occur most commonly where?

A

abdominal aorta.

37
Q

What is the pathophysiology of AAA?

A

Atherosclerotic plaque in the intima compresses the underlying media and compromises nutrient and waste diffusion from the vascular lumen into the arterial wall.

The media therefore
undergoes degeneration and necrosis that results in arterial wall weakness and consequent
thinning.

Nevertheless, as described above, the major influence that leads to aneurysm
formation is the production of MMP by inflammatory cell infiltrates.

38
Q

What is the major influence that leads to aneurysm
formation?

A

production of MMP by inflammatory cell infiltrates.

39
Q

AAA occur more frequently in what gender?

A

Abdominal aortic aneurysms occur more frequently in men and in smokers, and rarely develop
before age 50.

Atherosclerosis is a major cause of AAAs, but other factors clearly contribute since the incidence is less than 5% in men older than 60 years of age, despite almost universal abdominal aortic atherosclerosis in that population.

40
Q

Where does AAA usually positioned?

A

Usually positioned below the renal arteries and above the bifurcation of the
aorta
,

41
Q

What is the morphology of AAAs?

A

AAAs can be saccular or fusiform, up to 15 cm in diameter, and up to 25 cm in length (
Fig. 11-19 ).

Typically the intimal surface of the aneurysm shows severe complicated atherosclerosis with destruction and thinning of the underlying aortic media; the aneurysm frequently contains a bland, laminated, poorly organized mural thrombus that may fill some or all of the dilated segment.

42
Q

Occasionally the AAA can affect the renal and superior or inferior mesenteric arteries by producing what?

A

Occasionally the aneurysm can affect the renal and superior or inferior mesenteric arteries, either by producing direct pressure or by narrowing or occluding
vessel ostia with mural thrombi.

Not infrequently, AAAs are accompanied by smaller
aneurysms of the iliac arteries.

43
Q

Not infrequently, AAAs are accompanied by smaller
aneurysms of the iliac arteries.

T or F

A

True

44
Q

Two AAA variants merit special mention

A
  • Inflammatory AAAs
  • Mycotic AAAs
45
Q

What areInflammatory AAAs ?

A

are characterized by dense periaortic fibrosis containing

  • *abundant lymphoplasmacytic inflammation** with many macrophages and often giant
  • *cells.**

Their cause is uncertain.

46
Q

What are Mycotic AAAs ?

A

are lesions that have become infected by the lodging of circulating microorganisms in the wall, particularly in bacteremia from a primary Salmonella
gastroenteritis

. In such cases suppuration further destroys the media, potentiating rapid dilation and rupture.

47
Q
A

FIGURE 11-19 Abdominal aortic aneurysm.

A, External view, gross photograph of a large
aortic aneurysm that ruptured; the rupture site is indicated by the arrow.

B, Opened view, with the location of the rupture tract indicated by a probe. The wall of the aneurysm is
exceedingly thin, and the lumen is filled by a large quantity of layered but largely
unorganized thrombus

48
Q

The clinical consequences of AAA include

A
  • Rupture into the peritoneal cavity or retroperitoneal tissues with massive, potentially fatal hemorrhage
  • Obstruction of a branch vessel resulting in ischemic injury of downstream tissues, for example, iliac (leg), renal (kidney), mesenteric (gastrointestinal tract), or vertebral (spinal cord) arteries
  • Embolism from atheroma or mural thrombus
    • Impingement on an adjacent structure, e.g., compression of a ureter or erosion of
    vertebrae
  • Presentation as an abdominal mass (often palpably pulsating) that simulates a tumor
49
Q

What is the risk of rupture of AAA?

A

The risk of rupture is directly related to the size of the aneurysm, [60] varying from:

  • nil for AAAs of 4 cm or less in diameter,
  • to 1% per year for AAAs between 4 and 5 cm,
  • to 11% per year for AAAs between 5 and 6 cm,
  • and 25% per year for aneurysms greater than 6 cm in diameter.

Most aneurysms expand at a rate of 0.2 to 0.3 cm/yr, but 20% expand more rapidly. In general,
aneurysms of 5 cm and larger are managed aggressively, usually by surgical bypass involving
prosthetic grafts.

50
Q

THORACIC AORTIC ANEURYSMS
Thoracic aortic aneurysms are most commonly associated with_______

A

hypertension,

51
Q

What are the other
causes of THORACIC AORTIC ANEURYSMS

A

Marfan and Loeys-Dietz syndromes are increasingly recognized

52
Q

Regardless of etiology of THORACIC AORTIC ANEURYSMS, these give rise to signs and symptoms referable to

A
  • (1) encroachment on mediastinal structures,
  • (2) respiratory difficulties due to encroachment on the lungs and airways,
  • (3) difficulty in swallowing due to compression of the esophagus,
  • (4) persistent cough due to irritation of or pressure on the recurrent laryngeal nerves,
  • (5) pain caused by erosion of bone (i.e., ribs and vertebral bodies),
  • (6) cardiac disease as the aortic aneurysm leads to aortic valve dilation with valvular insufficiency or narrowing of the coronary ostia causing myocardial ischemia, and
  • (7) rupture.
  • Most patients with syphilitic aneurysms die of heart failure induced by
  • aortic valvular incompetence
53
Q

What is aortic dissection and how does it occur?

A

Aortic dissection occurs when blood splays apart the laminar planes of the media to form a

blood-filled channel within the aortic wall

  • this can be catastrophic if the dissection

then ruptures through the adventitia and hemorrhages into adjacent spaces.

54
Q

What is the difference of aortic dissection with atherosclerotic and syphilitic aneurysms?

A

In contrast to
atherosclerotic and syphilitic aneurysms, aortic dissection may or may not be associated with
aortic dilation
.

Consequently, the older term “dissecting aneurysm” should be avoided.

55
Q
A

FIGURE 11-20 Aortic dissection.

A, An opened aorta with proximal dissection originating
from a small, oblique intimal tear (identified by the probe) , allowing blood to enter the media
and creating an intramural hematoma (narrow arrows) . Note that the intimal tear has
occurred in a region largely free of atherosclerotic plaque and that propagation of the intramural hematoma is arrested at a site more distally where atherosclerosis begins (broad
arrow).

B, Histologic view of the dissection demonstrating an aortic intramural hematoma
(asterisk). Aortic elastic layers are black and blood is red in this section, stained with the
Movat stain.

56
Q

In general,
aneurysms of measurement are managed aggressively, usually by surgical bypass involving
prosthetic grafts.

A

5 cm and larger

57
Q

Currently, aneurysm treatment is evolving toward ______________

A

endoluminal approaches using stent grafts (expandable wire frames covered by a cloth sleeve) in selected patients. [61]

58
Q

Timely surgery is critical; operative mortality for unruptured aneurysms is approximately 5%,

A
59
Q

What is the mortality rate of emergency surgery after rupture.

A

carries a mortality rate of more than 50%.

60
Q

It is worth
reiterating that because atherosclerosis is a systemic disease, a person with AAA is also very
likely to have atherosclerosis in other vascular beds and is at a significantly increased risk of
IHD and stroke.

T or F

A

True

61
Q

Aortic dissection occurs principally in two groups:

A
  • (1) men aged 40 to 60, with antecedent
  • hypertension (more than 90% of cases of dissection); and (2) younger patients with systemic or
  • localized abnormalities of connective tissue affecting the aorta (e.g., Marfan syndrome).
62
Q

When can Dissections be iatrogenic?

A

Dissections can also be iatrogenic (e.g., complicating arterial cannulations during diagnostic
catheterization or cardiopulmonary bypass).

63
Q

Rarely, for unknown reasons, dissection of the
aorta or other branches
, including thecoronary arteries, occurs during or after pregnancy.

T or F

A
64
Q

Why is dissection unusual in the presence of substantial atherosclerosisor other cause of medial
scarring such as syphilis?

A

presumably because the medial fibrosis inhibits propagation of the dissecting hematoma.

65
Q

What is the major risk factor in aortic dissection?

A

Hypertension

66
Q

Explain how does Hypertension contribute as the major risk factor in aortic dissection

A

Aortas of hypertensive patients have
medial hypertrophy of the vasa vasorum associated with degenerative changes in the aortic
media and variable loss of medial smooth muscle cells, suggesting that pressure-related
mechanical injury and/or ischemic injury (due to diminished flow through the vasa vasorum) is
contributory.

67
Q

A considerably smaller number of dissections are related to inherited or acquired connective tissue disorders causing abnormal vascular ECM.

Give examples.

A
  • Marfan syndrome,
  • Ehlers- Danlos syndrome,
  • vitamin C deficiency,
  • copper metabolic defects
68
Q

medial damage seems to be either a prerequisite for dissection or a guarantee that
dissection is imminent.

T or F

A

False

However, recognizable

  • *medial damage seems to be neither a prerequisite for dissection nor a guarantee that**
  • *dissection is imminent.**

Regardless of the underlying etiology causing medial weakness, the trigger for the intimal tear and initial intramural aortic hemorrhage is not known in most cases.

Nevertheless, once the tear has occurred, blood flow under systemic pressure dissects through
the media,
fostering progression of the medial hematoma.

69
Q

What therapy may be effective in limiting an evolving dissection?

A

Accordingly, aggressive pressurereducing
therapy may be effective in limiting an evolving dissection.

In some cases disruption of
penetrating vessels of the vasa vasorum can give rise to an intramural hematoma without an
intimal tear

70
Q

In some cases disruption of
penetrating vessels of the vasa vasorum can give rise to an intramural hematoma without an
intimal tear

T or F

A

True

71
Q

What is the most frequent preexisting histologically detectable lesion in aortic dissection?

A

In most cases, no specific underlying causal pathology is identified in the aortic wall.

The most frequent preexisting histologically detectable lesion is cystic medial
degeneration (see Fig. 11-18 ); inflammation is characteristically absent.

However,
dissections can occur in the setting of rather trivial medial degeneration, and the relationship
of the structural changes to the pathogenesis of dissection is uncertain.

72
Q

How is

In the vast majority of spontaneous
dissections, the tear is found in the ascending aorta, usually within 10 cm of the aortic valve
( Fig. 11-20A ). Such tears are typically transverse or oblique and 1 to 5 cm in length, with
sharp, jagged edges. The dissection can extend along the aorta retrograde toward the heart
as well as distally, sometimes into the iliac and femoral arteries. The dissecting hematoma
spreads characteristically along the laminar planes of the aorta, usually between the middle
and outer thirds ( Fig. 11-20B ). It often ruptures out through the adventitia causing massive
hemorrhage (e.g., in the thoracic or abdominal cavities) or cardiac tamponade (hemorrhage
into the pericardial sac). [62] In some (lucky) instances, the dissecting hematoma reenters
the lumen of the aorta through a second distal intimal tear, creating a new vascular channel
and forming a “double-barreled aorta” with a false channel. [62] This averts a fatal extraaortic
hemorrhage. In the course of time, false channels may be endothelialized and become
chronic dissections.

A

An aortic dissection usually initiates with an intimal tear.

73
Q

In the vast majority of spontaneous
dissections, the tear is found in the _________
( Fig. 11-20A )

A

ascending aorta, usually within 10 cm of the aortic valve

. Such tears are typically transverse or oblique and 1 to 5 cm in length, with sharp, jagged edges.

74
Q

The dissection can extend along the aorta retrograde toward the heart as well as distally, sometimes into the iliac and femoral arteries.

T or F

A

True

75
Q

The dissecting hematoma
spreads characteristically along the________ ( Fig. 11-20B ).

A

laminar planes of the aorta, usually between the middle
and outer thirds

76
Q

Aortic dissection often ruptures out through where?

A

It often ruptures out through the adventitia causing massive hemorrhage (e.g., in the thoracic or abdominal cavities) or cardiac tamponade (hemorrhage into the pericardial sac). [62]

77
Q

What is a “double-barreled aorta” ?

A
In some (lucky) instances, the dissecting hematoma reenters the lumen of the aorta through a second distal intimal tear, creating a new vascular channel
and forming a “double-barreled aorta” with a false channel. [62]

This averts a fatal extraaortic
hemorrhage. In the course of time, false channels may be endothelialized and become
chronic dissections.

78
Q

The risk and nature of complications of aorta dissection depend strongly on the region(s)
affected; the most serious complications occur with dissections that involve the____________

A

aorta from the
aortic valve to the arch.

79
Q

aortic dissections are generally classified into two types ( Fig. 11-
21 ). They are named after Dr. Michael DeBakey, a pioneer in vascular surgery

A
  • • More common (and dangerous) proximal lesions (called type A dissections ), involving either both the ascending and descending aorta or just the ascending aorta (types I and II of the DeBakey classification)
  • • Distal lesions not involving the ascending part and usually beginning distal to the subclavian artery (called type B dissections or DeBakey type III)
80
Q
A

FIGURE 11-21 Classification of dissections. Type A (proximal) involves the ascending aorta,
either as part of a more extensive dissection (DeBakey I) or in isolation (DeBakey II). Type B
(distal or DeBakey III) dissections arise beyond the takeoff of the great vessels. The serious
complications predominantly occur in type A dissections.

81
Q

What are the classic clinical symptoms of aortic dissection?

A

The classic clinical symptoms of aortic dissection are the sudden onset of excruciating pain,
usually beginning in the anterior chest, radiating to the back between the scapulae, and moving
downward as the dissection progresses; the pain can be confused with that of myocardial
infarction.

82
Q

What is the most common cause of death in aortic dissection?

A

The most common cause of death is rupture of the dissection outward into the pericardial,
pleural, or peritoneal cavities.

83
Q

What is the reason why in Retrogade dissection the common clinical manifestations include :

  • cardiac tamponade,
  • aortic insufficiency, and myocardial infarction or extension of the dissection into the greatarteries of the neck or into the coronary, renal, mesenteric, or iliac arteries, causing critical vascular obstruction and associated ischemic consequences; compression of spinal arteries may cause transverse myelitis ?
A

Retrograde dissection into the aortic root can cause disruption of the aortic valvular apparatus.

84
Q

In the past aortic dissection was typically fatal, but the prognosis has markedly improved.

Rapid diagnosis and institution of intensive antihypertensive therapy, coupled with surgical procedures involving plication of the aortic wall, permit 65% to 75% of stricken individuals to be saved.

A
85
Q
A