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44 PART | I Overview
https://t.me/med1917
insufficient to meet the metabolic needs of the thick aortic wall [10]. Vasa vasorum are also present in the outer part
of the tunica media of the thoracic aorta but absent from the abdominal aortic media [15]. The adventitia assumes
great importance for surgeons who consider this the “strength layer” of the aorta, essential for secure suturing of
aortic tissues [2].
HISTOLOGY OF AORTIC ANEURYSM AND DISSECTION
Aortic wall degeneration underlies aneurysm formation and dissection occurrence. The histopathologic changes observed
in both instances primarily affect the aortic media, specifically the lamellar unit, which is the basic structural and functional
unit of the aortic wall [13]. These changes include cystic medial necrosis, elastin fragmentation, fibrosis, and medionecrosis
[18–23]. The grading system for each of these features was described by Schlatmann and Becker [24]:
l Cystic Medial Necrosis: This term is used interchangeably with the term cystic medial degeneration. It refers to the deposition of
amorphous and acellular basophilic ground substance in the tunica media [25,26]. Pooling of this material disrupts the lamellar
architecture of the aortic media, forming cyst-like (these are not true cysts with a distinct lining) spaces within it (Fig. 3.4) [24,26].
Contrary to the popular nomenclature, necrosis is usually not an accompanying feature.
l Grade 1: Minute cysts present within a single lamellar unit [24].
l Grade 2: Increased number and size of the cysts, covering the width of one whole lamellar unit [24].
l Grade 3: Large cysts extending over more than one lamellar unit [24].
l Elastin Fragmentation: This refers to the loss and fragmentation of elastic fibers of the aortic media, disrupting their
regular layered pattern (Fig. 3.5).
l Grade 1: The presence of less than five foci of elastin fragmentation in one microscopic field (200× magnifica-
tion), with each focus consisting of two to four adjacent elastic lamellae. The orientation of smooth muscle cells
is preserved [24].
l Grade 2: The presence of five or more foci with elastin fragmentation in a solitary microscopic field (200× magnifi-
cation), with each focus consisting of two to four adjacent elastic lamellae. The orientation of smooth muscle cells is
preserved [24].
l Grade 3: The presence of foci with elastin fragmentation in five or more adjacent elastic lamellae, regardless of the
number of foci in each microscopic field. The orientation of the smooth muscle cells is disturbed [24].
l Fibrosis: This refers to increased collagen deposition within the aortic media, which may replace the smooth muscle
cells and disrupt the parallel arrangement of lamellar units (Fig. 3.6).
l Grade 1: An increase in the quantity of collagen in an area less than one-third of the total width of the media [24].
l Grade 2: An increase in the quantity of collagen in an area between one-thirds and two-thirds of the total width of the
media [24].
l Grade 3: An increase in the quantity of collagen in an area greater than two-thirds of the total width of the media [24].
l Medionecrosis: This is defined as the focal loss of smooth muscle cell nuclei in the tunica media. This term is somewhat
a misnomer because necrosis is not demonstrable and the visualized loss of nuclei may be a consequence of smooth
muscle cells being replaced by collagen fibers (Fig. 3.7) [24].
l Grade 1: Focal loss of smooth muscle cell nuclei in an area less than one-third the total width of the media [24].
l Grade 2: Focal loss of smooth muscle cell nuclei in an area between one-third and two-thirds of the total width of the
media [24].
l Grade 3: Focal loss of smooth muscle cell nuclei in an area greater than two-thirds of the total width of the media
[24].
Although these features are also present in disease-free aging aortas, quantitatively higher grades of these degenerative
changes are observed in diseased aortas [18,27].
The histopathological changes afflicting the tunica intima include intimal hyperplasia and varying degrees of atheromatous plaque formation [28]. The tunica adventitia may develop inflammation, fibrosis, and vasa vasorum fibrosis [28]
(Figs. 3.8 and 3.9).
HISTOLOGY OF THE TRANSITION FROM ACUTE TO CHRONIC DISSECTION
The vast majority of patients presenting with acute Stanford type A dissections are treated surgically upon initial presentation [29], and, therefore, the natural transition to a chronic state is seldom observed in these cases. On the other hand, medical management is the initial treatment of choice for most uncomplicated acute Stanford type B dissections [29], permitting
Histology of Aortic Disease and Progression of Aortic Dissection From Acute to Chronic Chapter | 3 45
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FIGURE 3.4 Grade 1, Grade 2, and Grade 3 cystic medial necrosis in the aortic media. Hematoxylin and eosin stain: the number of cyst-like spaces
increase in size and number from Grade 1 to Grade 3.
46 PART | I Overview
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FIGURE 3.5 Grade 1, Grade 2, and Grade 3 elastin fragmentation in the aortic media. EVG (Elastin–Verhoef–van Greson) stain: elastic fibers
color black and are seen to lose structure from Grade 1 to Grade 3.
Histology of Aortic Disease and Progression of Aortic Dissection From Acute to Chronic Chapter | 3 47
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FIGURE 3.6 Grade 1, Grade 2, and Grade 3 fibrosis in the aortic media. (Gomori) Trichrome stain. Increased collagen (fibrosis = blue) relative to
smooth muscle (pink/red) as the grade progresses from 1 to 3.
48 PART | I Overview
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FIGURE 3.7 Grade 1, Grade 2, and Grade 3 medionecrosis in the aortic media. Hematoxylin and eosin stain with progressive loss of blue nuclei
and thinning of the structure observed from Grade 1 to Grade 3.
Histology of Aortic Disease and Progression of Aortic Dissection From Acute to Chronic Chapter | 3 49
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(A) (B)
FIGURE 3.8 (A) Intimal atheroma (red star) and (B) intimal hyperplasia (red star).
the observation of the natural transition to the chronic state (without surgical or endovascular intervention during acute and
subacute phases).
Recent investigations by our group have shed light on the natural history of the histopathological changes occurring over
time during the transition of a dissection from the acute phase (up to 2 weeks after the onset of symptoms) to the subacute
phase (between 2 weeks and 3 months after the onset of symptoms) and finally into the chronic state (greater than 3 months
after the onset of symptoms) [8,28]:
l Stanford Type B Dissections: Histological changes in the tunica intima (atheroma formation and intimal hyperplasia)
and adventitia (fibrosis, inflammation, and vasa vasorum fibrosis), and medial atrophy, are all seen in each of the
acute, subacute, and chronic phases of type B dissections [28]. However, their presence does not change significantly
over time during the transition from acute to chronic states and they may simply represent an underlying atheroscle-
rotic state [28].
FIGURE 3.9 Vasa vasorum fibrosis and inflammation.
50 PART | I Overview
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FIGURE 3.10 Histopathology changes in Type B dissection over time. (A) Cystic medial necrosis; (B) elastin fragmentation; (C) fibrosis; (D) medionecrosis. Note: The initial grade of pathological remodeling was high. Histopathological grading of elastin fragmentation (B) and fibrosis (C) significantly
increases over time. For example, Grade III elastin fragmentation and fibrosis represented 64% and 50% of cases, respectively, in the acute state after
dissection. As time progressed, Grade III elastin fragmentation and fibrosis both represented >90% in the chronic state. Reproduced with permission from:
Peterss S, Mansour AM, Ross JA, et al. Changing pathology of the thoracic aorta from acute to chronic dissection: literature review and insights. J Am
Coll Cardiol 2016;68:1054–65.
The aortic media is markedly abnormal during all three phases, especially so in the chronic state. Our study demonstrated that a high percentage of aortas bore Grade 3 cystic medial necrosis, elastin fragmentation, fibrosis, and medionecrosis in all three states, especially in the subacute and chronic phases [28] (Fig. 3.10).
Additionally, as the dissection process evolves over time into the chronic state, increasingly higher grades (Grade 3) of cystic
medial necrosis, elastin fragmentation, fibrosis, and medionecrosis are observed [28]. This increase is especially pronounced during the transition from the acute to subacute phase (except in the case of medionecrosis) and for the features of elastin fragmentation and fibrosis [28]. Our study showed that 64% and 50% of aortas bore Grade 3 elastin fragmentation and fibrosis, respectively,
during the acute state; in the chronic state, 91% of aortas were seen to have Grade 3 elastin fragmentation and fibrosis [28]
(Fig. 3.10). These findings correlate with the thickening and stiffening of the dissection flap over time and a lack of longitudinal
progression of the dissection during its evolution into the chronic state, as detailed subsequently in this chapter.
l Stanford Type A Dissections: A meaningful histopathological analysis of the natural transition to the chronic phase of a
type A dissection is difficult due to early surgical intervention. Similar to type B dissections, histological changes in the
tunica intima (atheroma formation and intimal hyperplasia) and adventitia (fibrosis, inflammation, and vasa vasorum
fibrosis), and medial atrophy are seen in the acute and subacute phases but their presence does not change significantly
during the transition [28].
Pathological remodeling is present in the aortic media in both the acute and subacute phases [28]. Our study showed
that either Grade 2 or Grade 3 cystic medial necrosis, elastin fragmentation, fibrosis, and medionecrosis were present in the
majority of aortas in both the acute and subacute phases [28] (Fig. 3.11).
Histology of Aortic Disease and Progression of Aortic Dissection From Acute to Chronic Chapter | 3 51
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FIGURE 3.11 Histopathology changes in type A dissection over time. (A) Cystic medial necrosis; (B) elastin fragmentation; (C) fibrosis; (D)
medionecrosis. Note: No significant differences were seen in grading of cystic medial necrosis, medionecrosis, elastin fragmentation, or fibrosis between
acute, subacute, and chronic type A dissections, with the restriction of the admittedly (and expectedly) low numbers of late operated type A dissection
patients. Despite the lack of statistical significance, a gradually increasing trend is grossly discernible in elastin fragmentation and medionecrosis over
time. Reproduced with permission from: Peterss S, Mansour AM, Ross JA, et al. Changing pathology of the thoracic aorta from acute to chronic dissec-
tion: literature review and insights. J Am Coll Cardiol 2016;68:1054–65.
As the type A dissection transitions from the acute to subacute phase, a modest increase in Grade 3 cystic medial
necrosis, elastin fragmentation, and medionecrosis occurs [28] (Fig. 3.11).
MACROSCOPIC CHANGES OF THE TRANSITION FROM ACUTE TO CHRONIC
DISSECTION
Stanford Type B Dissections
Expansion of the Dissected Aorta
A significant majority of patients experience descending aortic enlargement, primarily in the proximal portion [30,31],
after an uncomplicated acute type B dissection despite medical therapy [31–37]. Different rates of aortic growth have
been reported in various investigations during the transition of a type B dissection from the acute to chronic state
and are tabulated in Table 3.2, along with various factors influencing aortic enlargement. These differences may be
in part due to evaluation of different segments of the aorta, diversity of the study populations, and varying lengths of
the follow-up.
52 PART | I Overview
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+ Initial diameter
Completely
Thrombosed FL, n% Other Factors
<4.0 cm
− Female sex
− Asian race
− Presence of an intra-
mural hematoma
− Use of calcium
channel blockers
+ Male gender
+ Age < 60 years
− Circular configura-
tion of the true lumen
2%−GR = −2.4 ± 6.1 mm/
year
− False lumen
location on outer
curvature
− Increasing age
− Increased number of
intimal tears
− Increasing age at
8.3%, GR = 1.51 ± 5.65 + Male gender
presentation
+ Location of entry
site in arch
11.3%−GR = −0.2 ± 0.6
Partially
Thrombosed FL, n%
34.9% 17.1% + White race
Patent False Lumen
(FL), n%
48%. There was
a trend toward
increased aortic
Aortic Enlargement
During Follow-Up
(F/U)
aortic enlargement
during F/U.
Mean Aortic Growth
Rate (GR), mm/year
growth in this subset
of patients but it was
nonsignificant.
48%+++ Saccular Partially
thrombosed FL
Nonsaccular
GR = 3.0 ± 5.0
Saccular
GR = 7.8 ± 13.6
50% (based on 248
dissected aortic seg-
ments analyzed)
GR = 2.5 ± 4.5
segments analyzed)
85.1% showed
enlargement, 14.9%
showed no change or
decrease in size.
3.15 ± 6.36 (248 dissected aortic
FL)
GR = 4.25 ± 10.18
44%, GR = 2.1 ± 5.56 47.6%, + (vs. patent
sected aortic segments
evaluated) Aortic
enlargement occurred
in 81.6% of segments
with patent FL, 78.4%
segments with partial
3.0 ± 8.1 (A total of 273 dis-
28.2% (of these,
15% were saccu-
60.6%+GR = 4.9 ± 4.5
FL thrombosis and
65.2% of segments
with complete throm-
bosis of the FL.
ments enlarged during
4.1 ± 4.5 72.4% (152/210) seg-
lar and 85% were
nonsaccular)
GR = 4.0 ± 4.3
Nonsaccular
GR = 2.6 ± 2.7
+ Saccular
F/U.
27.6% (58/210) seg-
ments showed no
change or decrease
in size.
GR = 12.7 ± 1.1
TABLE 3.2 Aortic Growth Rates in Medically Treated Acute Type B Dissections and Factors Affecting Aortic Dilation and Outcome
Authors
Jonker et al. [34] 3.1 59% of patients had
Tolenaar et al.
[35]
Trimarchi et al.
[36]
Sueyoshi et al.
[33]
+ Female
https://t.me/med1917
(3.3 ± 5.2 mm/
year) versus male
(1.2 ± 6.6 mm/year)
gender
+ chronic obstructive
28.8% (based on
177 aortic segments
analyzed)
– (vs. patent FL)
GR = −1.4 ± 8.6
Histology of Aortic Disease and Progression of Aortic Dissection From Acute to Chronic Chapter | 3 53
pulmonary disease
(COPD) present
(5.9 ± 7.0 mm/year)
versus COPD absent
(1.4 ± 5.8 mm/year)
diameter >22 mm
at the level of the
proximal descending
thoracic aorta
+ Increased aortic size
at the level of the mid-
descending thoracic
aorta
+ Marfan syndrome
proximally located
large entry tear and
initial maximum
descending aortic
diameter are all pre-
dictive of complica-
tions in the long term
in patients with type B
dissections with patent
false lumen.
tic diameter ≥ 40 mm
− + Initial maximal aor-
aneurysm: important
predictor of mortality
during F/U.
History of athero-
sclerosis: important
9.5% History of aortic
predictor of mortality
during F/U
Note: In this study,
the FL was classified
as either having blood
flow (patent) or no
blood flow (com-
pletely thrombosed).
Distinction was not
71.2% (based on
177 aortic segments
analyzed)+GR = 3.3 ± 4.2
83.9% of patients had
at least 1 aortic seg-
ment enlarge during
F/U.
GR of thoracic aortic
lesions: 4.1 ± 6.5
GR of abdominal aor-
tic lesions: 1.2 ± 5.9
made between a
patent or partially
thrombosed FL.
n/r n/r n/r + Initial false lumen
24.5% of patients
with acute type B dis-
section experienced
aneurysmal dilation
during follow up.
ing thoracic aorta:
3.05 ± 3.12
Mid-descending
thoracic aorta:
2.87 ± 2.53
Lower descending
thoracic aorta:
2.45 ± 1.61
Abdominal aorta:
1.28 ± 1.92
n/r n/r Marfan syndrome,
a patent false lumen
(postsurgically treated
type A and medically
treated type B dissec-
tion) included.
0.48 n/r Only patients with
Type B dissections
with a persistent pat-
ent false lumen are
at a significant risk of
complications in the
long term
as either patent or
closed (completely
thrombosed)
predictor of mortality
during F/U. 2.7 times
increased risk of death
compared to patients
with a completely
patent FL
Sueyoshi et al.
[32]
Song et al. [31] Upper descend-
Evangelista et al.
[47]
Marui et al. [37] n/r 42.6% + FL status classified
Tsai et al. [40] n/r n/r 56.7% 33.8%, independent
+ Denotes factors associated with increased aortic dilation; − denotes factors associated with decreased aortic dilation; n/r, not reported. All GR are in mm/year.
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