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Aortic Anatomy andthePathophysiology ofAcute Aortic Syndromes
https://t.me/med1917
histologic ndings to MFS, including elastic ber fragmentation and proteoglycan accumulation, are present in LDS patients [44]. Phenotypic manifestations
include cardiovascular, craniofacial, cognitive and skeletal abnormalities [43].
LDS is marked by arterial tortuosity with accompanying predisposition to dissection and rupture. Cases of thoracic aortic dissection have been reported in infancy
[45]. The rarity of this condition limits thorough epidemiologic studies, however
the burden of aortic dilatation among this population is signicant with cases of
dissection and fatality due to aortic or vascular disease accounting for premature
death. Guidelines for management of thoracic aortic disease reect the aggressiveness of this heritable aortopathy: recommendations include early and frequent
screening, beginning at 6months of age, and a lower threshold for consideration
of aortic repair [46].
35
Familial Thoracic Aortic Aneurysm andDissection (FTAAD)
Familial Thoracic Aortic Aneurysm and Dissection (FTAAD) denes a subset of
patients with isolated aortic disease characterized by more rapid aortic growth and
earlier presentation. Analysis of over 100 patients with a familial pattern of TAA but
without MFS revealed a predominantly autosomal dominant inheritance with a
male predilection [47]. Mutations in TGFB2, which encodes TGF-β2 may represent
the genetic driving factor for a subset of these patients [48]. This etiology underscores the importance of considering family medical history in the prognostication
of all patients with thoracic aortic disease.
Turner Syndrome
Turner syndrome (TS) is characterized by complete or partial absence of one of the
sex chromosomes in females, resulting in short stature and premature ovarian failure. TS also harbors a 100-fold increased risk of aortic dissection compared to the
general population [49]. Associated ndings of hypertension, BAV, aortic coarctation, and treatment with growth hormone all contribute to the increased risk.
Approximately 25% of patients with Turner syndrome have BAV.In the absence of
the aforementioned risk factors, TS is independently associated with aortic dilatation in the aortic root and ascending aorta [50]. Aortic dissection presents at median
age of 35years and most commonly involves the ascending aorta [51]. The mechanism of aortic degeneration in TS is unknown however histologic analyses have
described both cystic medial necrosis and an altered ratio of collagen subtypes [51].
The range of aortic anomalies in the presence of the monosomy of TS suggests a
genetic origin, though no specic defect has been identied.
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L. V. Huckaby and T. G. Gleason
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L. V. Huckaby and T. G. Gleason
Histopathology ofAcute Aortic Syndromes
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DavidRanney andRyanP.Plichta
Normal Anatomy andHistology
The aorta is the largest arterial vessel in the human body, providing a conduit for
blood ow from the heart to the iliac artery bifurcation. The wall of the aorta is
composed of three distinct layers: the intima, media, and adventitia [1] (Fig.1).
The innermost layer, the intima, is in direct contact with the circulating blood
volume via a layer of squamous epithelial cells known as the endothelium [2]. The
endothelium participates in hemostasis, coagulation, and is semi-permeable to the
blood and blood components. Beneath the endothelium is a layer of subendothelial
tissue comprised of collagen, elastic bers, and smooth muscle cells. The middle
layer of the aorta, the media, consists mostly of smooth muscle and elastic bers. As
the thickest layer of the aortic wall, it provides both the tensile strength necessary to
withstand repetitive impulses from cardiac ejection as well as the elastic recoil
required to maintain diastolic pressure and continuous blood ow [3]. Elastic bers
are more prevalent in the proximal aorta compared to the distal aorta, and thus offer
more compliance to accommodate undampened left ventricular ejection. The outermost layer of the aortic wall, the adventitia, is a layer of collagenous connective
tissue that contains lymphatics, nerve bers, and in the thoracic aorta, the vaso
vasorum, a small arterial network that provides blood ow to the outer portion of the
aortic wall. The inner portion is nourished by diffusion from the aortic lumen [1].
D. Ranney · R. P. Plichta (*)
Duke University, Durham, NC, USA
e-mail: ryan.plichta@duke.edu
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_3
39© Springer Nature Switzerland AG 2021
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Fig. 1 Cross section of the
aorta demonstrating the (a)
intima, (b) media, and (c)
adventitia. Duke University
School of Medicine
Fig. 2 Aortic media
stained for elastin. Duke
University School of
Medicine
Predisposing Histopathology
D. Ranney and R. P. Plichta
The aorta is a dynamic organ that is vulnerable to several processes known to precede clinical disease. With increasing age, the native aorta experiences degeneration
and fragmentation of elastic bers, which reduces the compliance of the vessel and
hence its ability to withstand repetitive impulses [4, 5] (Fig.2).
Additional histologic changes take place with aging that contribute to elongation
of the aorta and eventual tortuosity [3]. Aging also leads to increasing aortic diameters, particularly in the ascending aorta, though this is not considered to be aneurysmal until its diameter exceeds dilation by at least 50% of normal. Rates of
increase in diameter vary according to the segment of the aorta, with a rate of change
of 0.07 to 0.2cm/year for the ascending aorta and arch [6]. The effects of aging on
the aorta are exacerbated by hypertension and atherosclerosis, which are frequent
comorbidities in the same patient population. Smoking and COPD are additional
risk factors that accelerate these degenerative processes.
Atherosclerosis is a distinct process that is commonly observed in settings such
as coronary, carotid, and peripheral vascular disease. This same process also contributes to the development of aortic disease. The endothelial damage incurred by
circulating lipoproteins, inammation, and deposition of debris and smooth muscle
cells leads to degradation of the aortic wall that can be seen on a histologic level.
This atherosclerotic weakening then follows a similar mechanism by which either
aneurysmal development occurs, or intimal injury followed by AAS.Atherosclerotic
changes tend to predominate in the descending thoracic and abdominal aorta, as
compared to the ascending aorta, where degradation of elastic tissue is more frequently encountered [3].
Histopathology ofAcute Aortic Syndromes
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41
A separate common pathway for aortic disease is characterized histologically by
both elastic fragmentation and loss of smooth muscle cells in the aortic media.
These components are replaced by ground substance forming cyst-like structures, a
process referred to as cystic medial degeneration (CMD) (previously cystic medial
necrosis). CMD is observed in the aging aorta as well as conditions such as Marfan’s
syndrome and Ehlers-Danlos syndrome [4, 7]. It is frequently seen in the setting of
aortic aneurysm and dissection, thus it is recognized as a predisposing factor
for AAS.
Acute Aortic Syndromes
Aortic Dissection
Aortic dissection is a highly morbid and lethal condition with an incidence of 2000
patients per year in the U.S. alone [3]. This disease process is characterized by a tear
in the aortic intima that communicates with a channel forming within the aortic
media (Fig.3).
This channel, referred to as the “false lumen” has the tendency to propagate in
either the antegrade or retrograde direction, as it is pressurized by the blood ow
within the aorta. The torn intima produces a ap that compresses the “true lumen”
and, along with an expanding false lumen, can lead to various malperfusion syndromes or aortic valve insufciency depending on the location and extent of the
injury. Some of these malperfusion syndromes have lethal consequences, such as
bowel or cerebral ischemia, and high rates of morbidity with carotid or spinal cord
ischemia. Furthermore, the false lumen is bounded only by adventitia and a thin,
outer remnant of aortic media. As a result, sustained pressurization can lead to rupture, or subsequent aneurysmal degeneration if not repaired during the acute phase,
as is often the case with uncomplicated aortic dissections of the descending and
abdominal aorta [4, 8].
Fig. 3 Aortic dissection, as characterized by separation of layers within the media, and associated
intimal ap. Intima (Int), media (Med), adventitia (Adv), true lumen (TL), false lumen (FL).
University of Michigan Medical School
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D. Ranney and R. P. Plichta
While it is commonly accepted that an intimal tear is an inciting event for aortic
dissection, there are several conditions which facilitate its occurrence. With regard
to the quality of the aortic tissue, connective tissue disorders (CTD), CMD, and
atherosclerosis are all risk factors for dissection. With regard to hemodynamics;
hypertension, states of hypervolemia, and catecholamine release are risk factors for
AAS.Intimal damage, trauma, and iatrogenic injury are also prerequisites for dissection [3].
Intramural Hematoma
Intramural hematoma (IMH) is a variant of aortic dissection, and, like dissection, is
characterized by hemorrhage/thrombus formation within the aortic media with variable distances of propagation. Unlike dissection, however, the overlying intima
remains intact. IMH is hypothesized to occur as a result of rupture of the vaso vasorum [3, 4]. Untreated, pressure necrosis or injury of the overlying intima can occur,
leading to communication with the aortic lumen, a condition indistinguishable from
aortic dissection. As such, IMH is managed as an AAS (Fig.4).
Penetrating Atherosclerotic Ulcer (PAU)
In the setting of atherosclerotic disease, intimal damage can result in a small tear
with contained extravasation into the aortic media. Known as a penetrating atherosclerotic ulcer (PAU), these lesions are at risk for propagation and thus evolving into
an IMH or dissection. PAUs arise in different locations and geometries, and management is determined accordingly.
Fig. 4 Intramural
hematoma. Intima (Int),
media (Med), adventitia
(Adv), true lumen (TL),
false lumen (FL). Duke
University School of
Medicine
Histopathology ofAcute Aortic Syndromes
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43
Special Populations
Connective Tissue Disorders
CTDs exist in many forms and subtypes and are a signicant risk factor for aneurysm and dissection. Marfan Syndrome (MFS) is an autosomal dominant CTD,
though sporadic forms are also encountered. This disorder is characterized by
derangements in the gene encoding brillin-1, a structural protein found in the aortic wall that is necessary for functional elastic structure. As such, aneurysmal disease is present in up to 80% of MFS patients, necessitating surgical intervention in
the majority [3]. The aortic root is more typically involved in MFS compared to
other aneurysmal etiologies. As aortic diameter increases, so does the risk for rupture and dissection. Loeys-Deitz Syndrome (LDS) is another autosomal dominant
CTD characterized by a mutation in transforming growth factor beta (TGF-B), also
leading to medial elastic ber fragmentation and aortic root aneurysms. Compared
to MFS, patients with LDS tend to develop complications of aneurysm and dissection at younger ages, and typically at smaller aortic diameters [9]. Ehler-Danlos
syndrome is another CTD characterized by defective type III collagen production.
The result is a thin, friable aortic wall, particularly in the arch and descending thoracic aorta, predisposing to aneurysm and dissection. Ehler-Danlos also affects
large and small arteries throughout the body, leading to rupture at various locations.
Bicuspid Aortic Valve Syndrome
Approximately 1–2% of the general population have a bicuspid aortic valve [3].
Associated with this nding is dilation of the proximal aorta that predisposes to
aneurysm and dissection. While this syndrome is not fully understood, there are
both sporadic and familial patterns observed, as well as additional associations with
other conditions such as Turner’s syndrome and coarctation of the aorta. Abnormal
neural crest cell migration has also been suggested as a mechanism for BAV development, given its role in outow tract septation and semilunar valve modeling [10].
The BAVS phenotype appears to be an endpoint for several genetic, structural, and
hemodynamic mechanisms, or combinations thereof [11]. Histologically, the aortic
wall in BAVS is characterized by elastic fragmentation, loss of smooth muscle, and
increased levels of matrix metallic proteinases. These proteinases, though necessary
for normal extracellular matrix maintenance, can lead to elastic destruction when
overproduced, resulting in histologic ndings that precede aneurysm and dissection.
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D. Ranney and R. P. Plichta
Familial Thoracic Aortic Disease
It is estimated that 20% of patients with thoracic aortic aneurysms have a rst degree
relative with an aortic aneurysm, and similar associations among patients with aortic dissection has been observed [3]. This demonstrates the presence of underlying
genetic predispositions for aortic disease, beyond those that exist among patients
with CTD.Although patterns of inheritance are quite variable, there are certain gene
mutations that have been linked to aortic aneurysm and dissection, such as TGFBR1,
TGFBR2, MYH11, and SMAD3. The histologic manifestations of these mutations
result in similar phenotypes of disease, leading to often earlier surgical intervention
in an effort to prevent AAS.
Conclusion
Acute aortic syndromes remain a challenging clinical entity that carries signicant
morbidity and mortality. Improved understanding of the genetic, histologic, and
pathology mechanisms behind these syndromes will lead to better patient specic
management and novel clinical therapies.
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