The document provides a comprehensive overview of ascending aortic aneurysms, detailing definitions, historical context, classifications, risk factors, and pathophysiology. It discusses specific genetic conditions associated with aneurysms, diagnostic methods, and management strategies, including both medical and surgical interventions. Additionally, the document addresses the implications of different surgical procedures and considerations for patient care.

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