עדי ר. בכר כלי דם שערי - צדק. Aneurysms are focal dilatations of a 50% larger...

ABDOMINAL AORTIC DISEASE

. בכר ר עדידם כלי

צדק- שערי

BACKGROUND

Aneurysms are focal dilatations of a 50% larger than the expected normal arterial diameter.

Normal aortic diameter is 1-2 cm. Typically diagnosed if aortic diameter

is ≥ 3.0 cm Nearly all AAAs involve the infrarenal

aorta, 25% of AAAs also involve the iliac arteries.

PREVALENCE OF AAA

In the US, AAA causes almost 14 000 deaths each year and accounts for 63 000 hospital discharges

Abdominal aortic aneurysm (AAA) is diagnosed in 5%–10% of men above the age of 65.

There is mounting evidence that the population aged above 80 years will significantly increase over the next 20 years.

Age (per 7-year intervaD:^Female se<;

Black race (compared with white)Other race (compared with white)

Height (per 7-cm intervai)*Weight (per 16-kg interval)-tWaist circumference (per 11 -cm tnterval)1Family history of abdominal aortic aneurysmHistory of smoking§

HypertensionHigh cholesterol levelsCoronary artery diseaseClaudicationCerebral vascular diseaseDeep venous thrombosisDiabetes mellitusChronic obstructive pulmonary diseaseCancer at site other than skinAbdominal imaging in past 5 years

1.52(1.45-1,60)0,62(0,41-0.94)0.72( 0.59-0.87)0,85(0,67-1.09)1.20(1.14-1.26)

0 97(0,89-1,06)1 06(0,98-1,14)

1.96(1,68-2,28)2 .72(2,37-3,11)

1.25(1,14-1,37)1,33(1,20-1,48)1.42(1,30-1,55)1.39(1 20-1,62)1-22(1,09-1,37)

0 90(0 76-1,06)0.68(0,60-0 77)1.04(0,92-1 16)0.90(0,80-1,03)1.06(0,96-1,18)

Aortic Diameter 3,0-3,9 cmCompared vi/ith < 3.0 cm

1.65(1,53-1.78)0.22(0,07-0,68)

0 49(0,35-0,69)0 91( 0,63-1,33)

1,21( 1,12-1 30)1.08(0,95 1 23)1.15(1,03-1,29)1.95(1 56-2 43)5.57(4,24-7,31)1,16(1,01-1,32)1,54(1,31-1.80)1-62(1,41-1.84)0,96(0,74-1,25)

1 19(0,99-1.42)0,67(0.50-0.8810,54(0,44-0.65)1-28(1,09-1,50)0,90(0,74-1,09)0,80(0,67-0,94)

Aortic Diameter -- 4,0 cmCompared with < 3 0 cm

Multivariabie Models of Factors Associated with Abdominal Aortic Aneurysm as Defined by Infrarenal AorticDiameter

Numbers of cases (controls) were 2217 (66 638) for aortic diameter 3 to 3. 9 cm, 985 (65 638) for aortic diameter 4. 0 or greater

March 1997 • Annals of Intenud Medicine • Volume 126 • Number 6

Prevalence

of AAA

Patients Who

Smoked

Prevalence

of AAA

Patients Who

Never Smoked

Age

% n % n y

0.30.91.51.92.52.9

435958191119

1412913008

5669

00

0.20.20.50.8

115214812965419846792544

50-5455-5960-6565-6970-7475-79

15 March 1997 • Annals of Internal Medicine • Volume I2. Number 6

Prevalence of Abdominal Aortic Aneurysm 4.0 cm or Larger Detected by Screening in Men

ETIOLOGY AND PATHOGENESIS OF AAA

Destruction of the structural and cellular components of the aortic wall

Proteolitic degradation of the elstin lead to weakening dilatation.

Progressive irreversible degeneration of the elastic media

Degradation in the aneurysm wall is contributed by the matrix metalloproteinase family (MMP)

Several studies suggested an imbalance between MMP and TIMPs (tissue inhibitorof metalloproteinase)

PATHOGENESIS OF AAA

Circulation Journal Vol.77, December 2013

MEDICAL TREATMENTS FOR AAA

A promising potential molecular target of pharmacological treatment for AAA is MMPs

Other potential medical treatments include anti-hypertensives, statins, and antibiotics.

(some of which might work as MMP inhibitors)

BETA-BLOCKERS

Hypothesis: Propranolol might affect the growth of an aneurysm by lowering blood pressure and its biochemical effects on matrix proteins.

Several animal studies have indicated that propranolol reduces the growth of an aneurysm and rupture risk.

Propranolol for small abdominal aortic aneurysms: results of a randomized trial.(JVS 2002 Jan;35(1):72-9)Patients with AAAs do not tolerate propranolol well, and the drug did not significantly affect the growth rate of small AAAs

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE INHIBITORS)AND ANGIOTENSIN RECEPTOR BLOCKERS (ARB)

ACE inhibitors have found to both stimulate and inhibit MMPs depending on cell types and animal models

Transforming growth factor-β (TGF-β) plays an important role in the pathogenesis of Marfan syndrome- Losartan, an ARB and also TGF-β antagonism suppressed the progressive matrix degradation in the mouse model of Marfan syndrome.

Results are inconsistent yet

STATIN

It has pleiotropic effects such as anti-inflammatory activities and has the ability to stabilize plaque as well as to control serum lipid levels.

Although statins are expected to be one of the promising drugs for the medical treatment of AAA, further studies are still needed to establish the evidence of their beneficial effects

MACROLIDES

Several studies have reported that Chlamydia pneumoniae (C. pneumoniae) has been associated with the atherosclerotic lesions of arteries.Few discrepant studies that do not clarify the pharmacological mechanism in respect to the development of AAA, and no clear beneficial effecton AAA expansion

TETRACYCLINE (DOXYCYCLINE)

There are numerous reports with respect to the suppressive effects on MMP by tetracycline.There is some limited evidence that Doxycylin may have a slight protective effect in retarding the expansion rates of small AAAs.Further investigation is required.

Weak low Statin

Weak low Doxycycline

Weak low Roxithromysin

Weak low ACE inhibitors

Weak low Angiotensin receptor blockers

SVS Guideline Recommendation in the MedicalManagement of AAA During the Surveillance Period

Quality ofEvidence

Level ofRecommendatio

n

GROWTH RATE OF AAA

Initial size (cm)

Mean growth rate (cm/yr) 95% CI

3.0- 3.9 0.39 0.20-0.57

4.0-4.9 0.36 0.21-0.50

5.0-5.9 0.43 0.27-0.60

6.0-6.9 0.64 0.16-1.10

AAA: RISK OF RUPTURE Risk of rupture for untreated aneurysm within 5

years (%)

010

7060

4050

3020

80

25%35%

75%

Aneurysm size5-

5.9cm6-

6.9cm≥7cm

RUPTURE OUTCOMES

Mortality rate can be as high as 80%More than one third of rupture cases die outside the hospital

Ruptured AAA

ACC/AHA GUIDELINES AAA REPAIR

Infrarenal AAA ≥ 5.5 cm should undergo repairInfrarenal AAA size 4.0-5.4 cm, ultrasound/CT scans every 6-12 mo

AAA <4.0cm, ultrasound every 1-2 years is reasonable

Intervention not recommended asymptomatic infrarenal/ juxtarenal AAAs <5.0 cm (men) or <4.5 cm (women)

OTHER CONSIDERATIONS

Female gender Rapid expansion- aneurysm growth

of >5 mm in six months or 10 mm per year

Coexistent aneurysm or PAD Symptomatic patient

SYMPTOMATIC AAA

Abdominal/back/flank pain — Patients presenting with abdominal/back/flank pain in association with AAA should be admitted for further evaluation and monitoring

Thromboembolism Aortic infection Inflammatory aneurysm

TREATMENT OPTIONS•Open surgery Endovascular stent

grafting

Open surgery

AORTIC ANEURYSM

Aneurysm content

OPEN REPAIR: ADVANTAGES

Established procedure more than 40 years of clinical experience

Excludes aneurysm and prevents sac growth

Proven, long-term results

• Significant incision in the abdomen• 30–90 minute cross-clamp• Up to 4-hour procedure• 1–2 days intensive care

7–14 days hospitalization4–6 weeks recovery time

OPEN REPAIR: DISADVANTAGES

Prolonged

convalescen

ce

Complication

s

Patients Don’t Want a Big Operation

Endovascular aneurysm repair (EVAR)

• Benefits• minimally

invasive• reduced risk of

perioperative death

• faster recovery

Arterial Puncture

Arteriotom

y

devise insertion

Flexible tip

Sheath marker

Distal radio-opaques markers

FreeFlo

Fluoroscopy of Talent Stent graft Inside delivery system catheter

CONTRALATERAL LIMB IMPLANT

39

•Complete lining of the arterial

wall, exclusion of the aneurysm sac

with no residual blood flow (endoleak)

Final Angiogram

AAA Repair:Closure of Incisions

ANATOMIC SUITABILITY

Aortic neck diameter

Aortic neck length

Aortic neck angulation

Iliac artery and access vessel morphology

LONG TERM COMLICATION

Postprocedural Renal Impairment

observed a 10% decrease in creatinine clearance over the first year

Life table analysis suggests that between 25% and 36% of EVAR patients have developed renal impairment by 3 years after the procedure,which compares to a 19% rate of renal impairment at 3 years following open repair.

EVAR produces a steady deterioration in renalfunction over time

LONG TERM COMLICATION- ENDOLEAK

ENDOLEAK TYPE 1

ENDOLEAK TYPE 2

Device migration after endovascular aneurysm repair

Trial Endpoint EVAR OPEN P

EVAR [1]

N=1082 ≥ 5.5 cm

Mortality 1.7 % 4.7 % 0.009

Secondary interventions

9.8 % 5.8 % 0.02

DREAM [2] N=345

≥ 5.0 cm

Mortality 1.2 % 4.6 % 0.1

Mortality & severe complications

4.7 % 9.8 % 0.1

EVAR VS OSR 30-DAY OUTCOMES

Endpoint EVAR OPEN P

Survival 89.7% 89.6% 0.86

Survival free of moderate-severe complications 65.6% 65.9% 0.88

Aneurysm-related death 2.1% 5.7% 0.05

EVAR VS OSR 2-YEAR OUTCOMESDREAM

SUMMERY

An aneurysm is an increase in the diameter of the aorta to more than 3 cm

Prevalence of AAA is 5%–10% of men above the age of 65.

The risk of rupture depends on the axial diameter of the aneurysm

The current available treatments of AAA is either open surgical repair or endovascular aneurysm repair.

Since first described by Parodi in 1991, endovascular aortic repair (EVAR) has progressively and dramatically changed the approach to treating abdominal aortic aneurysm (AAA) disease

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