1. Aneurysms and Dissections
Aneurysm:
 A localized abnormal dilation of a blood vessel
or wall of heart.
 When aneurysm is bounded by arterial wall
components or attenuated wall of heart called
true aneurysm.
 Atherosclerotic, syphilitic, and congenital vascular
aneurysms and left ventricular aneurysm that can
follow a myocardial infarction are true aneuryms.

2.  False aneurysm (also called pseudoaneurysm) is
a breach in vascular wall leading to extravascular
hematoma that freely communicates with
intravascular space (pulsating hematoma ).
 The most common false aneurysms are:
 Post-myocardial infarction rupture.
 Leak at junction (anastomosis) of vascular graft
with natural artery.

3. Dissection:
 Arises when blood enters the wall of artery as
a hematoma and dissecting between its layers .
 Dissections may, but do not always, arise in
aneurysmal arteries.
 Both true and false aneurysms, also dissections,
can rupture.
Causes of Aneurysm:
 The two most important causes of
aortic aneurysms are:
o Atherosclerosis.
o Cystic medial degeneration of arterial media.

4.  Other causes include:
o Trauma: traumatic aneurysms or arteriovenous
aneurysms.
o Congenital defects such as berry aneurysms:
small spherical dilatations most frequently
occur in brain.
o Infections (mycotic aneurysms).
o Syphilis.
o Systemic diseases: in some vasculitides.

5.  Aneurysms can be classified by shape and size :-
o Saccular aneurysms: spherical and vary in size
from 5 to 20 cm , often partially or completely
filled by thrombus.
o Fusiform aneurysms: involving a long segment,
many involve the entire ascending and transverse
portions of aortic arch.
o These shapes and sizes are not specific for any
disease or clinical manifestations.

7. ABDOMINAL AORTIC ANEURYSMS ( AAA ):
Atherosclerosis is the most frequent etiology.
Morphology:
o Usually positioned below renal arteries and above
bifurcation of aorta.
o Saccular or fusiform.
o Prime sites for formation of athero emboli.

8. Arteriograph showing abdominal aortic aneurysm

9. Gross appearance of abdominal aortic aneurysm

10. Pathogenesis:
 AAAs rarely develop before age 50 and
are more common in men.
 There is a genetic susceptibility to AAA beyond
the genetic predisposition to atherosclerosis.
 As in Marfan syndrome: genetic defects in
connective tissue component which is
responsible for strength of aorta .

11.  An altered balance of collagen degradation
and synthesis mediated by local inflammatory
infiltrates and destructive proteolytic enzymes
they produce and regulate.
 In this regard, matrix metalloproteinases (MMPs)
in macrophages implicated in development of
aortic aneurysms through increased proteolysis
of extracellular matrix proteins.

12.  These enzymes have capacity to degrade all
components of EC matrix in arterial wall (collagens,
elastin, proteoglycans, laminin, fibronectin).
 Decreased level of tissue inhibitor of
metalloproteinases (TIMP) also reported in
aortic aneurysms.

13. Clinical Course:
 Rupture into peritoneal cavity or retroperitoneal
tissues with massive fatal hemorrhage.
 Obstruction of vessel (iliac, renal, or mesenteric)
leading to ischemic tissue injury.
 Embolism from atheroma or mural thrombus.
 Impingement on adjacent structures such as
compression of ureter, or erosion of vertebrae.
 Presentation as an abdominal mass (often pulsating)
that simulates a tumor.

14. SYPHILITIC (LUETIC) ANEURYSMS :
 Obliterative endarteritis, characteristic of
tertiary stage of syphilis (lues), shows
predilection for small vessels.
 Syphilitic involvement of vasa vasorum of
thoracic aorta can lead to aneurysmal dilation.
 Thoracic aortic aneurysms can give rise to signs
and symptoms:
1. Respiratory difficulties: due to encroachment on
lungs and airways.

15. 2. Difficulty in swallowing: due to compression
of esophagus.
3. Persistent cough: due to irritation of or pressure
on recurrent laryngeal nerves.
4. Pain: caused by erosion of bone (ribs and vertebral
bodies).
5. Cardiac disease: aortic valve dilation with valvular
insufficiency, or narrowing of coronary ostia
causing myocardial ischemia.
6. Rupture.

16. Morphology:
 Inflammatory involvement begins in aortic adventitia,
particularly involving vasa vasorum.
 Inducing obliterative endarteritis rimmed by
an infiltrate of lymphocytes and plasma cells
(syphilitic aortitis).
 The narrowing of lumina of vasa causes ischemic
injury of aortic media, with patchy loss of medial
elastic fibers and muscle cells, followed by
inflammation and scarring.

17.  With destruction of media, the aorta loses its
elastic recoil and become dilated.
 Luetic aortitis may also cause aortic valve ring
dilation resulting in valvular insufficiency,
 Through stretching of valve cusps, widening of
commissures, and thickening and rolling of free
margins.
 Owing to aortic insufficiency, left ventricular wall
can undergo volume overload hypertrophy,
sometimes to 1000 gm (three times normal weight),
referred to (cow's heart).

18. Figure 1: A large swelling on left side
of anterior chest wall.
Figure 2: Chest roentgenogram showing
widening of mediastinum with
a radiopaque mass extending into superior
mediastinum occupying left upper and
mid-zone with right tracheal shift.

19. Figure 3: Three-dimensional
reconstructive image of
cardiac angiogram showing
aneurysm of arch of aorta
and ascending aorta
indicated by arrows.
Figure 4: Elastic Van-Gieson stain showing
wall of aneurysm composed of fibrohyaline
tissue with fragmented elastic fibers .

20. AORTIC DISSECTION (DISSECTING HEMATOMA) :
 Dissection of blood between and along laminar
planes of media, with formation of blood-filled
channel within aortic wall which often ruptures
outward causing massive hemorrhage.
 Aortic dissection may or may not be associated
with marked dilatation of aorta.
 For this reason the older term "dissecting aneurysm"
is discouraged.

21.  Aortic dissection occurs principally in
two groups of patients:
o More than 90% occur in men between ages
of 40 and 60 with antecedent hypertension.
o The second major group of patients,
usually younger, has a systemic or localized
abnormality of connective tissue that affects
aorta (Marfan syndrome).

22.  Dissection can also be iatrogenic,
as a complication of arterial cannulation
(during diagnostic catheterization or
cardiopulmonary bypass).
 Rarely, for unknown reasons, dissection of aorta
or its branches including coronary arteries
occurs during or following pregnancy

23. Morphology:
 Detectable aortic wall pathology is not always
present in dissection.
 The most frequent histologically detectable lesion
is medial degeneration (cystic medial degeneration).
 Characterized by elastic tissue fragmentation and
separation of elastic and fibro muscular elements
of tunica media by small cleft like spaces.
 These are not truly "cysts“.

24.  Thus, the term "cystic medial necrosis" is inaccurate
because neither necrosis nor cysts are present.
 Inflammation is absent.
This aortic dissection occurred just above
the aortic root in a patient with Marfan's
syndrome.

25. Microscopically, the tear (arrow) in this aorta extends through the media,
blood also dissects along the media (asterisk).

26. Pathogenesis:
 Hypertension is the major risk factor , but its
contribution to aortic medial damage is uncertain.
 Some dissections are related to inherited connective
tissue disorders (Marfan syndrome) an autosomal
dominant disease of connective tissue fibrillin
characterized by skeletal, cardiovascular, and
ocular manifestations.
 The cause of spontaneous dissections not associated
with hypertension or genetic disorders is unknown.

27. Clinical Course:
 Depend strongly on level of aorta affected.
 Classified into two types :
o More common (more serious ) proximal lesions:
involving either ascending portion only, or both
ascending and descending aorta (type A).
o Distal lesions: not involving ascending part and
usually occur distal to subclavian artery (type B).

28.  The classic clinical symptom is sudden onset of
excruciating pain, beginning in anterior chest,
radiating to back, and moving downward as
dissection progresses.
 This intense pain can be confused with that of
acute myocardial infarction.
 The most common cause of death is rupture of
dissection outward into any of three body cavities
(pericardial, pleural, or peritoneal).

29.  Retrograde dissection into aortic root can cause
disruption of aortic valvular apparatus.
 Extension of dissection into great arteries of neck ;
or into coronary, renal, mesenteric, or iliac arteries,
causing critical vascular obstruction.
 Compression of spinal arteries may cause
transverse myelitis.
 Aortic dissection was usually fatal.