An aneurysm is an abnormal dilation of a blood vessel or heart wall. True aneurysms involve all layers of the vessel wall, while false aneurysms involve only some layers. The most common causes of aneurysms are atherosclerosis and cystic medial degeneration. Abdominal aortic aneurysms usually occur below the renal arteries and are more common in men over 50. Aortic dissections involve blood entering the vessel wall and dissecting between layers, sometimes rupturing outward and causing hemorrhage. Hypertension is a major risk factor.

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.