The document provides an overview of aortic diseases and pericarditis, detailing the anatomy and function of the aorta, various imaging techniques for diagnosis, and specific conditions like aortic dissection, intramural hematomas, and penetrating atherosclerotic ulcers. It discusses the importance of timely imaging, such as echocardiography, CT, and MRI, in evaluating and managing acute aortic syndromes and highlights the associated risks and diagnostic challenges. Additionally, it covers pericarditis, including causes and imaging findings related to constrictive pericarditis.

1. Aortic diseases and pericarditis

2. • The aorta is the main artery delivering
oxygenated blood from the left ventricle to all
parts of the body., it has three histologically
distinct layers: an intima consisting of a thin
endothelial layer; a media containing an
elastic lamella, smooth muscle and connective
tissue; and a thin outer adventitia made of
connective and elastic tissues also containing
nerves, lymphatics and the vasa vasorum

3. • The aortic root 3 cm in diameter. A normal aorta passes
superiorly and slightly to the right for approximately 5
cm, then arches posteriorly over the root of the left
lung, descending within the thorax beside the vertebral
column, gradually achieving the median plane, and
becoming the abdominal aorta, after it passes through
the aortic hiatus in the diaphragm. The abdominal aorta
is approximately 2 cm in diameter;
• aortic root and most of the ascending aorta are
contained within the pericardium

4. Vaiation
• ascending aorta forms the right mediastinal border on a
posteroanterior (PA) chest radiograph. It becomes the
aortic arch at the origin of the innominate artery and also
gives rise to the left common carotid and left subclavian
arteries (LSAs). Approximately75% show this ‘normal’
branch pattern of the supra-aortic arteries, but in 20% the
innominate and left common carotid arteries have a
common origin and in 6% the left vertebral artery arises
directly from the aortic arch. The aortic arch ends and the
descending thoracic aorta begins immediately beyond the
origin of the LSA.

5. Chest X-Ray and Echocardiography
• CXR may identify only indirect signs of aortic
aneurysm or dissection such as a widening of
the upper mediastinum or an abnormal aortic
contour increase , additional imaging is almost
invariably required.
• Transoesophageal echocardiography (TOE) is
superior to TTE for thoracic aorta evaluation,
and it can be easily performed at the bedside

6. Angiography
• imaging technique for diagnosis and preoperative
evaluation of aortic diseases
• invasive, relatively costly and needed a well-
organised and experienced team.
• provided limited information about the aortic wall,
because angiography provides only ‘luminographic’
data. Thus it provided limited information about an
intramural haematoma (IMH) and could be
misleading in aortic dissection with a complete false
lumen thrombosis

7. Computed Tomography and Magnetic
Resonance Imaging
• CT and MRI combine noninvasiveness with high spatial and
temporal resolution and can provide information about the entire
length of the thoracic or thoracoabdominal aorta.
• MRI, though highly accurate for acute aortic disease evaluation, is
usually confined to cases of severe renal insufficiency or absolute
contraindications to iodinated contrast medium; it is useful for
subsequent follow-up studies
• The high diagnostic accuracy of MR in patients with acute aortic
syndrome is based on its high contrast resolution between the
lumen and the vessel wall provided by black-blood fast spin-echo
(BBFSE) and SSFP imaging, which allows differentiation of aortic
wall alterations (e.g. IMH) from atheromatous plaques or aortitis.

9. Acute Aortic Syndrome
• comprises all aortic diseases characterised by a sudden clinical
presentation that require acute hospitalisation (within 15 days
from symptom onset) and often need urgent surgical or
endovascular repair
• It includes
1) aortic dissection
2) IMH,
3) penetrating aortic ulcer,

10. Aortic Dissection
• most common nontraumatic acute aortic emergency,
• The aetiology is frequently unknown but is related to advancing age
and hypertension.
• Cystic medial degeneration in connective tissue disorders such as
Marfan syndrome and Ehlers–Danlos syndrome is a predisposing
factor, as are coarctation, bicuspid aortic valve, aortitis, pregnancy
and blunt chest trauma. Some authorities believe that dissection can
progress from a penetrating aortic ulcer and IMH
• Aortic dissection is initiated by an intimal tear, which allows blood to
penetrate into the medial layer, producing a cleavage plane (false
lumen) between the inner two-thirds and outer one-third of media.
The true lumen is separated from the false lumen by an intimomedial
flap.

11. , type A dissection leads to death in most cases, whereas type B dissection can be
successfully managed with medical therapy

12. Imaging
• Aortography -was
traditionally the ‘gold
standard’ in suspected
aortic dissection but CT,
MRI and TOE have rapidly
substituted invasive
angiography
• TOE performed at the
bedside in unstable pts
• haemodynamic
information about flow in
the true and false lumen,
• valuable information
about the functional
status of the aortic valve

13. In BBFSE sequences it appears linear inside the black vessel lumen
(Fig. 17.3). The false lumen can be differentiated from the true
lumen by its higher signal intensity due to the slower flow
Magnetic resonance imaging.
MRI is one of the most accurate tools for
aortic dissection evaluation

14. • Intravascular ultrasound (IVUS) at 12.5 MHz
provides intraluminal cross-sectional images of
vessels and is able to demonstrate the entry tear
and extent of dissection but is particularly useful
in differentiating the true and false lumen and
demonstration of dynamic obstruction.
However, since the transducers are single use
only and expensive, its role is almost exclusively
confined to interventional applications.

15. • Computed
tomography-modern
MDCT provides high
image quality with
much shorter
acquisition times
• Injection of contrast
medium via the left
upper limb should be
avoided because the
very high attenuation
from contrast
medium within the
left brachiocephalic
vein can produce
streak artefact across
the aortic arch,
potentially causing
diagnostic
difficulties.

16. The differentiation of the false lumen from the true lumen is essential; a number of imaging
findings can be helpful, such as the cobweb sign, described before. In most cases the true lumen
is smaller and more medially located. On most contrast-enhanced CT images it may be identified
by its continuity with the undissected portion of the aorta (Fig. 17.9)

17. • An unusual type of
aortic dissection is the
intimointimal
intussusception
produced by
circumferential
dissection of the
intimal layer, which
subsequently
invaginates like a
wind sock; CT shows
one lumen wrapped
around the other one,
with the inner lumen
invariably being the
true one (Fig. 17.10).

18. Intramural Haematoma
• IMH is a lesion confined to the aortic wall and invasive angiography is
not able to detect it. It is considered the consequence of a
hypertensive rupture of the vasa vasorum within the medial layer and
eventually results in a circumferentially oriented blood collection.
• occur spontaneously but may also arise from a penetrating aortic ulcer
in a severely atheromatic aortic wall. It has also been described
following trauma.
• aortic wall thickening, symmetric or asymmetric, variable in thickness
from 3 mm to more than 1 cm, and it must be differentiated from
mural thrombus or plaque. Intimal displacement of calcification canaid
in distinguishing these entities, because the IMH is a subintimal lesion,
with calcifications displaced on top of the lesion facing the lumen

19. Acute IMH is hyperdense on unenhanced CT. Another difference is the shape
of the aortic wall thickening: in IMH the borders are generally smooth, while a
thrombus or a plaque is typically characterised by irregular margins (Fig.
17.13).

20. e acute phase the haematoma appears as a crescent-like aortic wall thickening typically
hyperdense on unenhanced CT with respect to the aortic lumen, whereas after
enhancement the density of wall and lumen are reversed, with the IMH remaining
unenhanced, unlike the false lumen in aortic dissection

21. T1 weighted images reveal a typical crescent-shaped area of abnormal signal intensity within the
aortic wall.
MRI is also the only imaging technique able to assess the age of the haematoma, exploiting the
influence on MRI signal intensity of the different degradation products of haemoglobin: in the
acute phase (0 to 7 days after the onset of symptoms) on T1 weighted spin-echo images,
oxyhaemoglobin shows intermediate signal intensity, whereas in the subacute phase (>8 days),
methaemoglobin shows high signal intensity.
However, when the signal intensity is medium to low, it can be difficult to distinguish IMH from
mural thrombus. T2 weighted spin-echo sequences may help in differentiating the two entities:
signal intensity is high in recent haemorrhage but low in chronic thrombosis (Fig. 17.14).
Fig. 17.14 Magnetic Resonance Black-Blood Fast Spin-Echo Images of an Intramural
Haematoma (IMH) 8 Days After Symptoms Onset. In a
T2 weighted fat-saturated axial image (A) the signal is high, excluding
a chronic disease definitely. Left serosal pleural effusion is associated.

22. DD-THROBOSED FALSE LUMEN
• IMH maintains a constant circumferential
relationship to the wall (subintimal lesion),
whereas the thrombosed false lumen tends to
longitudinally spiral around the aorta.
• Secondly, IMH does not reduce the lumen,
which maintains its regular shape, whereas
the false lumen can variably compress the true
lumen .

23. Penetrating Atherosclerotic Ulcer
• generated by erosion of an atheromatous plaque
disrupting the internal elastic lamina, exposing the
media to pulsatile arterial flow and subsequent
haematoma formation. This is distinguished from an
atheromatous plaque by the presence of a focal,
contrast medium–filled outpouching surrounded by
an IMH. An atheromatous plaque does not extend
beyond the intima, is frequently calcified and lacks
an IMH

24. • The extension of the ulceration to the medial layer can also evolve in localised
dissection or even break through into the adventitia, creating an aortic
pseudoaneurysm.
• If the adventitia ruptures, only the mediastinal tissue can contain the haematoma;
otherwise, the rupture is complete.
• Penetrating atherosclerotic ulcers (PAUs) are mainly located in the descending aorta
but may be also seen in the aortic arch.
• Ulcers can be multiple and are frequently associated with a severe atherosclerotic
aortic wall.
• The imaging diagnosis of PAUs is based on the visualisation of a crater-like, contrast-
filled outpouching with jagged edges, of variable extension, which may result in a
large pseudoaneurysm
• Unenhanced CT has the advantage of visualising intimal calcification displacement.

26. Coarctation of the Aorta
• Aortic coarctation most commonly affects the aortic
isthmus
• M>F. In females, coarctation is associated with Turner
syndrome.
• infantile type of coarctation is usually proximal to the
ductus arteriosus, consequent increased strain on the
heart leads to heart failure because no collateral pathways
DEVELOP in utero.
• adult type of coarctation is usually located just distal to the
ductus arteriosus and the LSA, and therefore collaterals
develop in utero

27. Chest X-Ray
• Rib notching usually takes several years to develop. It is caused by
pressure erosion of the inferior aspects of the upper adjacent ribs by
enlarged and tortuous intercostal arteries.
• usually bilateral but asymmetric and most often spares the first two
ribs where intercostal arteries arise from the costocervical trunk
proximal to the usual site of coarctation and therefore do not form
part of the collateral circulation
• Other radiographic features include -cardiomegaly, particularly in
older adults, a prominent ascending aorta (especially with a bicuspid
aortic valve) and various aortic knuckle abnormalities. There may be
a ‘3’ sign due to enlargement of the LSA arising proximally of the
coarctation, the narrowed segment itself and subsequently a
localised segment with poststenotic dilatation of the aorta.

29. Magnetic Resonance Imaging
• MRI is the imaging technique of choice in both infantile
and adult coarctation
• T1 weighted spin-echo sequences will show the whole of
the aorta, the major branches and the larger collaterals
• Cine phase-contrast imaging can be used to visualise the
turbulence through the stenosis, whereas phase-
contrast imaging allows the quantification of the
pressure gradient across the coarctation and the
collateral circulation as percentage increment of flow
from isthmic to diaphragmatic aorta.

31. Computed Tomography CT
• The prevalent role of CT
versus MR is still
controversial. Advocates of
MR argue that MRI eventually
is able to recognise all major
complications like aortic
dissection and identify
stenosis by functional indirect
signs (pressure gradient),
while CT’s major limitation is
related to the radiation dose
in the usually young
population.

32. Pericarditis
• Inflammation of the pericardium (pericarditis) may occur in
response to a variety of insults. Viral infection is the most
common cause.
• most common imaging manifestation of acute pericarditis is a
pericardial effusion, the nature of the fluid varying with the
underlying cause.
• Thickened, inflamed pericardium can appear as moderate-to-
high signal intensity on spin-echo MRI, and pericardial
enhancement may be seen on either MRI or CT performed after
IV contrast medium administration. Delayed images on contrast
media-enhanced CT are useful for demonstrating pericardial
enhancement

34. Constrictive Pericarditis
• Constrictive pericarditis is the condition in
which a thickened, fibrotic and often calcified
pericardium restricts diastolic filling of the
heart.
• most common causes of constrictive
pericarditis are cardiac surgery and radiation
therapy. Other causes include infection (viral,
tuberculous), connective tissue disease,
uraemia, neoplasm or idiopathic

37. •Thank you