עדי ר. בכר כלי דם שערי - צדק. aneurysms are focal dilatations of a 50% larger...
TRANSCRIPT
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
רבה תודה
לשכוח לפעמים שעוזר דמיון לי יש
אותך תוביל לוגית חשיבההדימיון, Bלנקודה Aמנקודה
". מקום לכל אותך יוביל