Aortic aneurysm basic, types and management

Nice presentation of aortic aneurysm.
It's classification, diagnosis and management.
Interventional + surgical management.

2. ASCENDING AORTIC
ANEURYSM
Dr. Rashid Aziz
Moderator
Dr. Zubair Brohi
Clinical Fellow
NICVD

3. INTRODUCTION
What is aortic aneurysm ?
Arbitrarily as a 50% enlargement of normal aorta

4. Annuloaortic ectasia: combination of dilation of
the ascending aorta and dilation of the aortic
annulus
 False aortic aneurysm: is a localized dilation
involving adventitia, some or all of the media,
and compressed periaortic tissue

6. HISTORY
Galen, who observed in gladiators injured during battle in
the second century.
1543 Andeas, Vesalius described a thoracic aortic
aneurysm.
1769 Morgagni seen postmortem findings of ruptured
thoracic aneurysms
1773 Alexander Monro described three coats of the arterial
wall, and the destruction in the formation of true and false
aneurysms

7. 1952 Cooley and DeBakey first report of a descending
aortic repair . Performed on a saccular aneurysm
without cardiopulmonary bypass (CPB).
1956, Cooley and DeBakey performed replacement of
the ascending aorta with a segment of homograft with
CPB
1963 Bentall and De Bono first composite aortic root
replacement.

8. 1964 Wheat et al, resected the ascending aorta and
entire aortic root except for the aortic tissue
surrounding the coronary arteries, then performed a
mechanical valve insertion
in 1981, Cabrol et al described the use of an 8 to 10
mm Dacron graft to attach to independently mobilized
coronary artery buttons

10. ANATOMY

12. CLASSIFICATION
LOCATION
Ascending aorta,
Aortic Arch
Descending aorta
Morphology
Fusiform
Saccular
Etiology
Medial degeneration
Infection
Inflammation
Chronic aortic dissection

13. Medial degeneration
Idiopathic degeneration
Heritable disorders of connective tissue

Marfan syndrome (MFS)

Ehlers-Danlos syndrome (EDS)

Loeys-Dietz syndrome

Familial thoracic aortic aneurysms and dissections (TAAD)

Bicuspid aortic valve (BAV)

Turner and Noonan syndromes
Infection
 Mycotic aneurysms
 Syphilitic aneurysms
Inflammatory
Takayasu arteritis
Behcet disease
Giant cell arteritis
Chronic aortic dissection

14. INCIDENCE
Estimated 5-10% per 100000 person/ year
60% involve aortic root/ ascending aorta
35% descending aorta
<10% aortic arch

15. RISK FACTORS?
Age
Atherosclerosis
Aortitis
BAV
Connective tissue disorders
Dissection
DM
Hypertension
Infections
Pregnancy
Smoking
Trauma

16. INDEPENDENT RISK FACTOR FOR RUPTURE
Age
Aortic diameter
Pain or symptoms of expansion
COPD
Smoking

17. PATHOPHYSIOLOGY
The media of the aorta is composed of smooth muscle
cells within a matrix of elastin & collagen.
Other structural proteins, including fibrillin, laminin,
proteoglycans, and fibronectin.
Collagen provides the necessary structural strength.
Elastin conveys the arterial recoil capabilities.
Defects in either protein can cause aortic pathology.

19. IDIOPATHIC MEDIAL
DEGENERATION
Triad of
1.Loss of non-inflammatory smooth muscle cells
2.Fragmentation of elastic fibers
3.Accumulation of basophilic ground substance in
depleted areas
First weakens the aortic wall, thereby increasing the
wall tension, which can induce aortic dilatation

20. MARFAN SYNDROME
Most prevalent inherited connective tissue disorder, 80%
develop Artic root aneurysm
Mutations in the fibrillin- 1 gene & recently identified
mutations in the (TGF-B) gene
Defective coding of fibrillin leading to elastin derangement &
excessive TGF-B activity negatively impact on smooth
muscle
Additional cardiovascular complications
Mitral valve prolapse and regurgitation
Left ventricular dilation,
Aortic root dilation is the most common cause of morbidity and
mortality

23. EHLERS-DANLOS
SYNDROME(EDS)
Rare autosomal dominant inherited disorder of
connective tissue
Site: carotid , descending and aortic arch
Defective type III collagen
Carries a substantial risk of rupture of the aorta.

25. LOEYS-DIETZ SYNDROME(LDS)
Aortic aneurysm syndrome that has widespread systemic
involvement.
Mutations in TGFBR1 and TGFBR2
Loss of elastin conten in the aortic media.
The phenotype overlaps with that of MFS (aortic aneurysm,
arachnodactyly, dural ectasia) ,
Its distinctive features such as hypertelorism, bifid uvula and
generalized arterial tortuosity
Average age at a first cardiovascularevent much lower than that for
patients with untreated MFS or vascular EDS

27. FAMILIAL THORACIC AORTIC
ANEURYSMS AND DISSECTIONS(TAAD )
Patients without genetic syndromes also manifest familial
clustering of thoracic aortic aneurysms and dissections
20% of aneurysm probands have a first-order relative with an
aortic aneurysm.
TAAD 1 locus mapped to the long arm of chromosome 5, with
approximately half of the identified families.
Early tendency to rupture in <5cm
Therefore, TAAD is now a recognized heritable disorder of
connective tissue.

28. TURNER AND NOONAN
SYNDROMES
Chromosome constitution is 45-XO; it has an
incidence of 1 in 5000 live births
Cardiovascular problems include
BAV (present in one-third of subjects)
Coarctation of the aorta
Hypertension
Aortic root dilation in 40 %

29. BICUSPID AORTIC VALVE DISEASE
Prevalence of 1 to 2 % with male predominance
First -degree relative with BAV is 9%
AS in three-quarters of patients & AR in 15%
Independent risk factor for progressive aortic dilation
Cause of this initially was attributed to "poststenotic dilation
Aortic valvular cusps and ascending arterial media both a rise from
common neuralcrest cells.
Increased elastic fragmentation & smooth muscle cell apoptosis
within the aortic media

31. CHRONIC AORTIC DISSECTION
Chronic aortic dissections tend to dilate over time
Debakey and colleagues found that aneurysms developed
46% with uncontrolled hypertension
17% with controlled hypertension
Griepp and coworkers found that after repair of acute
type A dissections, the growth of the distal aorta
 0.85 mm a year for the aortic arch
1.24 mm a year for the descending thoracic aorta.

32. MYCOTIC ANEURYSMS
Rare but can be fatal if they are not diagnosed early.
Staphylococcus aureus and salmonella predominant organisms
Site: femoral , abdominal & visceral artery( coronary artery)
Hematogenous spread to the intima or the vasa vasorum,
lymphatic spread, or direct extension from an adjacent infected
focus.
Endothelial intimal lining of the aorta is generally highly
resistant to infection, but disruption of this barrier by
atherosclerosis reduces resistance

33. SYPHILITIC ANEURYSMS
Once perhaps the most common cause of ascending aortic
aneurysms (Treponema pallidum)
Females 20 - 30 years
Stie: Arch of aorta
Type: Saccular
Inflamation of adventetia & vasavasorum endarteritis
reduce blood flow that weakens aortic wall
Aneurysm develop 10 to 20 years after onset of disease

35. INFLAMMATORY ANEURYSMS
Walker and colleagues were the first to defined the term
inflammatory aneurysm
Takayasu arteritis
Pulmonary artery, the subclavian artery, and abdominal aorta
Behcet disease
Cardiovascular involvement only 7 to 29 percent
Arterial lesion develops in the aorta and the pulmonary artery
Giant cell arteritis
17.3 times more likely to develop a thoracic aortic aneurysm
than is the general population

36. NATURAL HISTORY
TAA growth rate of 0.2 - 0.4cm/year and marked
individual variability
5year survival of about 40%
Mean rate of Rupture or Dissection
2%/ year for < 5 cm
5%/ year for 5 - 5.9 cm
10%/ year for > 6 cm

37. CLINICAL PRESENTATION ?
Mostly clinically silent in many cases
Anatomic location and the space-occupying nature
Hoarseness
Stridor
Dysphagia
Dyspnea
Plethora and edema
Signs and symptoms of AR.
Chest or back pain may indicate acute expansion or leakage
of the aneurysm

38. SIGNS
Often normal in a patient without rupture aneurysm
Large aneurysm can be palpated in the suprasternal notch
Venous distention due to SVCl or innominate vein
obstruction
Signs of AR
Abdominal aortic aneurysms are present in 10 - 20 %
EDS, LDS & Marfanoid features

39. DIAGNOSTIC INVESTIGATIONS
BLOOD TESTS
XRAY
ECHO
CT SCAN
MRI
ANGIOGRAPHY

40. XRAY

41. ECHO
Can visualize the aortic root and ascending aorta
accurately
Less ideal for full extent of the aortic arch and origins of
neck vessels.
Assessment AR, LV function, and hemopericardium
TEE is the modality of choice for the diagnosis and
exclusion of aortic dissection in a n unstable patient

42. CT-SCAN
Currently the most common diagnostic imaging for the aorta
Provides rapid and precise evaluation of the ascending aorta
in regards to size, extent, and location
Excellent visualization of the aorta and its branch vessels
Advantage of demonstrating aortic wall thickening,
calcification, and luminal thrombus
Entire thoracic and abdominal aorta for evidence of
concomitant aneurysm disease in the arterial tree.
64-bit scanners also are capable of imaging coronary arteries

44. MRI
Emerging as the premier imaging method for the
diagnosis of diseases of the thoracic aorta in stable
patients
( CE-MRA) is the most widely used MRA method
Assessment of the vessel wall and AR in the presence of
disease of the ascending aorta

45. MEDICAL MANAGEMENT
The main aim of medical therapy is to reduce the shear
stress on the diseased segment of aorta by reducing BP
& cardiac contractility.
Smoking cessation.
Competitive sports should be avoided in pts with
enlarged aorta.
In chronic conditions BP should be controlled below
140/90 mm Hg, with lifestyle changes &
antihypertensives.

46. Prophylactic use of B-B, ACE, ARBs reduce
either progression/ occurrence of
complications.

47. OPERATIVE INDICATIONS ?
1.Aortic diameter 5 - 5.5 cm.
2.LDS > 4cm
3.MFS 4 - 4.5 cm
4.BAV 4.5 - 5 cm
5.EDS or TAAD > 5cm
6.< 5.0 cm
1.Rapid growth (more than 1 cm/year),
2.Family history of premature aortic dissection
3.Presence of moderate or severe AR
4.Symptoms suggest impending to rupture

48. INDEXING AORTIC SIZE
Sevensson et all reported that if aorta were
replaced when cross section area to the height
r(cm) / height(m) >10
95% of dissection in their retrospective would
have been avoided

49. ESC GUIDELINES

51. CHOICE OF OPERATIONS
Underlying pathology and quality of the aortic wall
Skill of the operating surgeon
Status of the aortic valve
Age and expected survival
General well-being of the patient
Risk of anticoagulation

52. SURGICAL OPTIONS ?
1.Reduction Aortoplasty
2.Supporting Aortoplasty
3.Interposition Graft
4.Wolfe procedure
5.Interposition Graft + AVR
6.Valve Sparing Aortic Root
7.Modified Bental
8.Cabrol
9.Homograft
10.Ross

59. ANESTHESIA CONSIDERATIONS
Induction reduces sympathetically mediated vasoconstriction
and tachycardia due to acute thoracic aortic disruption
Femoral cannulation under local anesthesia with simultaneous
institution of GA and CPB in the setting of aneurysmal rupture
Left and right radial artery pressures
Pulmonary artery catheter.
Intraoperative TEE
Thermistor probe in bladder and in tympanic

60. CARDIOPULMONARY BYPASS
Arterial cannulation
Distal ascending aorta
Axillary artery or innominate arteries
Femoral cannulation
Venous cannulation
Bicaval venous cannulation

61. CEREBRAL PROTECTION
Permanent and Transient neurologic dysfunction (TND)
TND was observed commonly with ischemic periods longer than
40 to 60 min
Hypothermia
Cerebral monitoring
Ante grade and retrograde perfusion
Metabolic monitoring
Pharmacologic

62. DHCA
This technique allows the open distal anastomosis in
better visualization
Disadvantages: coagulopathy, increased CPB time, renal
& neurologic dysfunction
As low as 18°C the safe arrest time is 30 to 40 min
Precise temperature of the brain, monitoring sites
esophageal, rectal, bladder, nasopharyngeal, tympanic &
pulmonary arterial

63. CEREBRAL MONITORING
EEG- isoelectric between 20°C - 18°C,
BIS
SjVo2 >95%
Core temprature
DHCA time and the age of the patients are the
most important risk factors for mortality and
postoperative neurologic deficit

64. ANTIGRADE CEREBRAL PERFUSION
Using the axillary artery or selective carotid cannulation
Cerebral auto regulation is significantly better preserved
Flow rate 10ml/kg/m( 700-900l/m)
Perfusion pressure 30-70mmhg
Recent trend away from low temperatures toward
moderate hypothermia up to 25°c with selective cold
( 15°C)

66. RETROGRADE CEREBRAL PERFUSION
Mills and Ochsner in 1980 as a treatment for massive air
embolism
Via a cannula placed in the SVC
Maintenance of cerebral hypothermia, washout of
embolic air or debris, cerebral perfusion, and metabolic
support
Flow rate 250-400ml/m and pressure 25-40mmhg
Compared with ASCP, less effective but still provides
some what more brain preservation than does DHCA

67. VALVE-SPARING AORTIC SURGICAL
REPAIR
Yacoub and subsequently david pioneered
Yacoub procedure is the remodeling technique
David procedure is the reimplantation technique
Aortic root aneurysms if the aortic valve is structurally
normal
If AR is present because of STJ dilation or cusp prolapse, can
be corrected
Operative mortality rate for either procedure is low

68. Need to return to the operating room for bleeding was six
fold higher after a Yacoub than after David
Yacoub group 22% of patients had moderate AR at follow-
up (median follow-up of 3 years)
Prevalence of late AR was lower in David's series, but 25%
of patients at 10 years
In David's series, it is remarkable that no patient required
reoperation, only 9 patients remained at risk at 8 years.
Yacoub's experience, in which 17% patients required
reoperation by 10 years

70. MODIFIED BENTAL PROCEDURE
After the aorta is cross clamped proximal to the origin of
the innominate artery
Antegrade and retro cardioplegia
Aorta is completely transected proximal to the aortic
clamp and just above the level of the main coronary
artery ostia
Aortic valve then is excised, and a CVG repair
commences

71. Mechanical valve, a dacron valved conduit is sutured
into the annulus with 2-0 pledgeted horizontal mattress
sutures.
Biological valve, a porcine root replacement is instituted
with interrupted 3-0 horizontal mattress sutures.
Left and right coronary artery orifices are excised from
the aorta, leaving a 4- to 5-mm rim of aortic wall.
1 to 2 cm of the coronary arteries are mobilized carefully
to avoid tension;

72. the left coronary button is anastomosed to the valved
conduit, using a running 5-0 polypropylene suture.
To avoid traction and subsequent distortion of the right
coronary artery, the distal graft anastomosis is completed
valve conduit is measured transected, and sutured end to
end to the distal aorta with a running 4-0 polypropylene
suture and allowed to fill retrograde,
followed by the right coronary button anastomosis
before the completion of this suture line, the heart is filled
with blood and standard de-airing maneuvers

75. REPLACEMENT WITH HOMOGRAFT OR
XENOGRAFT
In infective aneurysm is a good option
After radical debridement of all infected or devitalized tissue.
The proximal end of t he graft is sutured to the native aortic annulus
with interrupted or continuous 4-0 polypropylene sutures
Occasionally suture line is reinforced with a strip of pericardium to
ensure hemostasis
Homograft anterior mitral valve leaflet can be utilized to patch
erosions into the septum
Native left and r ight coronary artery ostia and the corresponding
coronary ostia of the aortic homograft

76. RE ESTABLISHING CORONARY FLOW
Large aneurysms the coronary ostia are laterally displaced from
the new aortic lumen
Cabrol and coworkers described connecting the two coronary
ostia end-to-end with a separate Dacron interposition graft t hat
then was anastomosed side-to-side to the aortic conduit
modified Cabrol technique involves resecting the entire aortic
wall and forming coronary ostial buttons, which are mobilized,
sutured end-to-end with a smaller Dacron tube graft, and
anastomosed side-to-side with the aortic conduit.
Kay-Zubiate technique' relies solely on autologous tissue;
saphenous vein as an interposition graft for the displaced
coronary ostia

78. COMPLICATIONS
Bleeding (2.4 – 11%)
Myocardial infarction (0.5 – 1%)
Temporary Heart block (3 – 6%)
Neurologic injury (1.9 – 5%)

80. OUTCOMES/PROGNOSIS
Operative mortality rates of 2 to 5%
Operative mortality varies with
Acuity of the operation,
Patient age,
LV function, and
Extent of operation.
The late survival rate after operation is
approximately
65% at 5 years
55% at 7 years

81. FOLLOW UP
Primarily on medical therapy
Surveillance should be perform after 6month then
yearly
Under going repair
First month to exclude early complication
Surveillance should be at 6,12month then yearly

82. TEVAR
Endovascular stent is a fabric tube supported by
metal wires stents
Reinforces the weak spot in the aorta by sealing the
area tightly above & below the aneurysm