Transcript ECFのASSO

ACC/AHA 2005 Practice Guidelines
for the Management of
Pts With Peripheral Arterial Disease
(Lower Extremity)
peripheral arterial disease
• Encompasses a large series of disorders
affecting arterial beds exclusive of the
coronary arteries
LOWER EXTREMITY PAD-Risk Factors
Cigarette smoking
• 2 to 3 times more likely to cause lower
extremity PAD than CAD
• Increases the risk of lower extremity PAD by 2to 6-fold and the risk of intermittent
claudication by 3- to 10-fold
• More than 80% of patients with lower
extremity PAD are current or former smokers
Diabetes mellitus
• increases the risk of lower extremity PAD by 2to 4-fold
• present in 12% to 20% of persons with lower
extremity PAD
classic IC
• pain, ache, tightening, cramping, or sense of
fatigue in one or more of the lower extremity
muscle groups
• triggered by ambulation & relieved by rest
• have sufficient blood flow so that limb ischemic
symptoms are absent at rest.
• site of claudication is distal to the diseased
arterial segment
• buttock, hip, and thigh claudication are seen with
aortoiliac disease and calf claudication with
femoral-popliteal disease
critical limb ischemia
• rest pain, cold, or numbness of the feet, with or
without tissue loss (nonhealing ulcers or gangrene).
• Rest pain usually occurs at night (because of the
horizontal position, which deprives the patient of the
effect of gravity on blood flow through the tight
lesions)
• improves when the legs are in the dependent position.
• superimposed edema of the affected leg(s)
occasionally may be seen in those who tend to dangle
their legs overnight.
Foot Physical Examination and
Differential Diagnosis of Neuropathic
and Neuroischemic Ulcers
Clinical Presentation of Peripheral Arterial Disease
Most cases are asymptomatic.
•In symptomatic patients: Most have atypical exertional leg pain.
•Only 10% to 30% present with classic intermittent claudication.
•Minority progress to rest pain or ischemic ulcers (critical limb ischemia).
Risk of Cardiovascular Events
• 20% to 60% increased risk for MI
• 2- to 6-fold increased risk of death due to CAD
• Risk of stroke is increased by approximately
40%
• Men with LL-PAD -4 to 5 times more likely to
have a stroke / TIA
Ankle-Brachial Index Testing
overt clinical PAD presenting with claudication or more severe limb ischemic symptom
Age ≥ 70 years or older
Age = 50-69 years with history of diabetes or smoking
Age < 49 years with diabetes and one additional risk factor (smoking, hypertension, or
elevated cholesterol levels)
Abnormal lower extremity pulse examination
Known atherosclerotic disease elsewhere (coronary, carotid, or renal arteries)
Ankle-Brachial Index and Severity of
Peripheral Arterial Disease
Ankle-Brachial Index
Severity
>1.30
Noncompressible (calcific vessel; diabetes,
chronic renal insufficiency, and older age)
0.91-1.30
Normal
0.71-0.90
Mild
0.41-0.70
Moderate
0-0.40
Severe
Acute limb ischemia
• rapid or sudden decrease in limb perfusion
• threatens tissue viability
• form of CLI, may be 1stmanifestation of arterial
disease in asymptomatic pt
• form of CLI, may occur as an acute event causing
symptomatic deterioration in a pt with
antecedent LL-PAD and IC
• Progression of PAD from IC to CLI – gradual
(may also reflect cumulative effect of multiple
acute local thrombotic events that progressively
increase the intensity of ischemia)
Paresthesia and paralysis imply irreversible ischemia,
and muscle rigidity is a sign of a nonsalvageable limb.
Signs and Symptoms of Acute Limb Ischemia
Pain
Pallor
Pulselessness
Poikilothermia
Paralysis
Paresthesia
Society for Vascular
Surgery/International Society for Cardiac Vascular Surgery
(SVS/ISCVS)
Magnetic Resonance Angiography
• RECOMMENDATIONS
Class I
• 1. MRA of LL -diagnose anatomic location and degree of stenosis
of PAD ( A)
• 2. MRA of LL should be performed with gadolinium enhancement
( B)
• 3. MRA of LL -useful in selecting pts with LL-PAD as candidates for
endovascular intervn ( A)
Class IIb
• 1. MRA of LL -may be considered to select pts with LL-PAD as
candidates for surgical bypass and to select the sites of surgical
anastomosis. (B)
• 2. MRA of LL -may be considered for postrevascularization
surveillance in pts with LL-PAD. (B)
MRA limitations
• Tends to overestimate degree of stenosis because
of turbulence
• May overestimate occlusions owing to loss of
signal from retrograde collateral flow
• Metal clips can cause artifacts that mimic vessel
occlusions
• Some metal stents will obscure vascular flow
• Pts with PPI and ICD and some cerebral aneurysm
clips cannot be scanned safely
• MRA performed with gadolinium has on rare
occasions been associated with renal toxicity in
patients with elevated creatinine levels
Computed Tomographic Angiography
• RECOMMENDATIONS
Class IIb
• 1. CTA of LL may be considered -anatomic
location and presence of signi stenosis in pts
with LL-PAD (B)
• 2. CTA of LL may be considered as a
substitute for MRA for pts with CI to MRA(B)
CTA has potential advantages over MRA
• Pts with PPI or ICD may be imaged safely with CTA
• Metal clips, stents, and prostheses usually do not cause
significant CTA artifacts
• Has higher resolution
• Can provide images of calcification in the vessel wall
• Scan times are significantly faster with CTA than with
MRA
• Claustrophobia not a problem
CTA also has potential disadvantages compared with MRA
• Requires iodinated contrast, which may be nephrotoxic
• Requires ionizing radiation
PAG-RECOMMENDATIONS
Class I
• 1. Recommended for evaluation of patients with LLPAD when revascularization is contemplated. (B)
• 2. Signi of an obstructive lesion is ambiguous → transstenotic P-gradients & supplementary angulated views
to be obtained. (B)
• 3. Pts with baseline renal insufficiency should receive
prior hydration. (B)
• 4. Follow-up clinical evaluation (physical Ex & RFT)recommended ≤2 weeks after contrast angio to detect
presence of delayed adverse effects, such as
atheroembolism, ↓ in RFT, or access site injury (C)
Class IIa
• 1. Noninvasive imaging modalities, including
MRA, CTA, and color flow duplex imaging, may
be used in advance of invasive imaging to
develop an individualized diagnostic strategic
plan, including
– assistance in selection of access sites,
– identification of significant lesions, and
– determination of the need for invasive evaluation
• 2. Treatment with n-acetylcysteine in advance of
contrast angiography is suggested for pts with
baseline renal insufficiency (Cr>2.0 mg/Dl)
CILOSTAZOL-RECOMMENDATIONS
Class I
• 1. Cilostazol (100 mg BD) is indicated to
improve symptoms & ↑walking distance in pts
with LL-PAD & IC (in the absence of CCF). (A)
• 2. A therapeutic trial of cilostazol should be
considered in all patients with lifestyle-limiting
claudication (in the absence of CCF). (A)
PENTOXIFYLLINE-RECOMMENDATIONS
Class IIb
• 1. Pentoxifylline (400 mg TID) 2-line
alternative therapy to cilostazol to improve
walking distance in patients with IC (A)
• 2. The clinical effectiveness of pentoxifylline as
therapy for IC is marginal & not well
established.(C)
Lipid-Lowering Drugs-RECOMMENDATIONS
Class I
• Statins indicated for all pts with PAD to achieve
a target LDL < 100 mg/Dl
Class IIa
• 1. Statins to achieve a target LDL <70 mg/dL is
reasonable for pts with LL-PAD at very high risk
of ischemic events
• 2. Fibrates can be useful for pts with PAD and
low HDL , normal LDL, & elevated TGL
Antiplatelet and Antithrombotic Drugs
RECOMMENDATIONS
Class I
• 1. Antiplatelets indicated to ↓ risk of MI, stroke,
or vascular death in pts with atherosclr LL-PAD
• 2. Aspirin ( 75 - 325 mg)- safe & effective
antiplatelet therapy
• 3. Clopidogrel (75 mg ) -effective alternative
antiplatelet therapy to aspirin
Class III
• Oral anticoagulation therapy with warfarin is
not indicated
Indications for Revascularization in IC
Before a pt with IC is offered any invasive therapy,the following
considerations must be taken into account:
• a predicted or observed lack of adequate
response to lifestyle therapy and
pharmacotherapies
• the presence of a severe disability
• absence of other disease that would limit
exercise even if IC improved
• the morphology of the lesion (appropriate
intervention would have ↓risk & a ↑ probability
of initial & long-term success)
Morphological Stratification of Iliac Lesions
TASC type A iliac lesions:
• 1. Single stenosis <3 cm of the CIA or EIA (unilateral/bilateral)
TASC type B iliac lesions:
• 2. Single stenosis 3 to 10 cm in length, not extending into the CFA
• 3. Total 2 stenoses <5 cm in CIA and/or EIA & not extending into CFA
• 4. U/L CIA occlusion
TASC type C iliac lesions:
• 5. B/L 5-10 cm-long stenosis of CIA and/or EIA, not extending into CFA
• 6. U/L EIA occlusion not extending into the CFA
• 7. U/L EIA stenosis extending into the CFA
• 8. B/L CIA occlusion
TASC type D iliac lesions:
• 9. Diffuse, multiple U/L stenoses of CIA, EIA, & CFA (usually >10 cm)
• 10. U/L occlusion involving both the CIA and EIA
• 11. B/L EIA occlusions
• 12. Diffuse disease involving Ao& both iliac arteries
• 13. Iliac stenoses with an abd Ao aneu/other lesion requiring Ao/iliac sx
Morphological Stratification of Femoropopliteal Lesions
TASC type A femoropopliteal lesions:
• 1. Single stenosis <3 cm SFA or popliteal A
TASC type B femoropopliteal lesions:
• 2. Single stenosis 3 - 10 cm, not involving distal popliteal A
• 3. Heavily calcified stenoses ≤3 cm in length
• 4. Multiple lesions, each <3 cm (stenoses or occlusions)
TASC type C femoropopliteal lesions:
• 6. Single stenosis or occlusion >5 cm
• 7. Multi stenoses or occlusions, each 3-5 cm, with or
without heavy calcification
TASC type D femoropopliteal lesions:
• 8. Complete CFA or SFA occlusions or complete popliteal
and proximal trifurcation occlusions
Endovascular Treatment for IC- RECOMMENDATIONS
Class I
• Preferred revascularization technique for TASC type A
iliac & femoropopliteal lesions
• Translesional P gradients (with and without
vasodilation) should be obtained to evaluate signi of
angiographic iliac stenoses of 50%-75% D before intervn
• Provisional stentng indicated for use in iliacs as salvage
therapy for a suboptimal/failed result from POBA
Class IIa
• Stents can be useful in femoral, popliteal, & tibial
arteries as salvage for a suboptimal or failed result from
POBA
Summary of preferred
options in
interventional
management of iliac
lesions
Summa
ry of
preferr
ed
options
for
interve
ntional
treatm
ent of
femoro
poplite
al
lesions
Thrombolysis for A/c & C/C LI -RECOMMENDATIONS
Class I
• Catheter-based thrombolysis is indicated for
pts with a/c limb ischemia of ≤14 days (A)
Class IIa
• Mechanical thrombectomy devices can be
used as adjunctive therapy for a/c LI due to
peripheral arterial occlusion
Thanks…
ACC/AHA 2005 Practice Guidelines
for the Management of
Pts With Peripheral Arterial Disease
(Renal artery)
Clinical clues to RAS
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Onset of HTN < 30 yrs (I)
Severe HTN >55 yrs (I)
Accelerated, resistant or malignant HTN (I)
New azotemia/wors RFT aft adm of ACEI/ARB (I)
Unexpl atrophic kidney/size discrep >1.5 cm (I)
Sudden unexpl Pulm Edema (I)
Unexpl ↓RFT, inc pts on RRT (IIa)
Multi-vessel CAD (IIb)
Unexplained CCF (IIb)
Refractory angina (IIb)
Prevalence in gen population (RA duplex)
• ≥65 yrs (834)
• →6.8% (Women-5.5% , Men-9.1%)
Screening RA angio at CAG
• RA disease →30%
• Significant RAS→11%-18%
• Significant RAS →22%-59% pts with PAD
ESRD in HD >20-years (683pts)
• 12% had documented RAS as a cause of ESRD.
• Renal function in pts with athero RAS on
medical therapy (28/12 follow up)
• 46%→ ↑S.Cr
• 29%→ 25%-50% ↓GFR
• 37%→↓kidney size by > 10%
Median survival for
• ESRD with renovascular disease- 25/12
• ESRD due to malignant HTN- 55/12
• ESRD due to polycystic KD- 133/12
Clinical Clues to the Diagnosis of RAS –RECOMMENDATIONS
Performance of diagnostic studies
Class I
• 1. Onset of HTN <30 yrs
• 2. Onset of severe HTN >55 yrs
• 3. Characteristics:
– (a) acc HTN
(sudden & persistent worsening of prev controlled HTN)
– (b) resistant HTN
– (c)malign HTN
(A/C decomp CCF, A/C visual/neuro disturb &/ adv retinopathy)
• 4. New azotemia /Worsening RFT aft an ACEI or an ARB
• 5. Unexp atrophic kidney/Discrepancy in size of >1.5 cm
• 6. Sudden, unexp pulm edema (esp azotemic pts)
Class IIa
• 1.Unexp RF, including pts starting RRT
• Class IIb
• 1. The performance of arteriography to
identify signi RAS - reasonable in pts with
multivessel CAD & none of the clinical clues
or PAD at the time of arteriography.(B)
• 2. Diagnostic studies -reasonable in pts with
unexpl CCF or refractory angina(C)
Atherosclerosis
• 90% of all renovascular stenotic lesions
• Most often affects the aorto-ostial segment,
including the proximal 1 cm of main RA
Fibromuscular Dysplasia
• nonatherosclerotic, noninflammatory disease
• HTN in a young woman (can occur in both genders
at any age)
• Middle & distal ⅔ of main RA
• May involve RA branches (25%- segmental arteries)
• Tends to occur in 25 - 50 yr old women
• Often involves both RA (B/L in 60% )
• Characteristic - “string of beads” appearance
• Medial fibroplasia ≈ 80% of FMD
• Intimal fibroplasia - relatively rare (thin, discrete
web)
• Also affects other arteries, inclu Carotid &
Vertebral, & less commonly, Iliac & Mesenteric
• Appears to be an asso betw Carotid &
Vertebral FMD and intracranial aneurysmal
disease
• MRA of head should be performed in all
patients with cervicocranial FMD
Classification of Fibromuscular
Dysplasia
Classification
Frequency
Pathology
Angiographic
Appearance
1.Medial
fibroplasia
80%
Alternating thin
media & thick
ridges
“String of beads”
"beading“> D
2.Perimedial
fibroplasia
10% to 15%
Ext collagen depots
in outer media
“Beading”
“beads”<D
3.Medial
hyperplasia
1% to 2%
True SM hyperplasia ,No fibrosis
Concentric smooth
stenosis
Intimal fibroplasia
< 10%
Deposition of
collagen in intima
Concentric focal
band
Adventitial
(periarterial)
fibroplasia
< 1%
Dense collagen
replaces fibrous
tissue of adventitia
So rare, classic
angiographic
findings -not known
Medial dysplasia
• Renovascular HTN may also be caused by
renal artery aneurysms
• Aneurysm rupture is of greatest concern with
noncalcified aneurysms >2 cm D, particularly
in premenopausal women
Other causes of renovascular disease
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Takayasu’s arteritis
Atheroemboli
Thromboemboli
William’s syndrome
Neurofibromatosis
Spontaneous renal artery dissection
Arteriovenous malformations or fistulas
Trauma (e.g.,lithotripsy, direct injury, or surgery)
Prior abdominal radiation therapy
Retroperitoneal fibrosis
Diagnostic Methods
RECOMMENDATIONS
Class I
• 1. Duplex USG recommended screening test to establish
∆ of RAS (sens 84%-98% and speci 62%-99%). (B)
• 2. CTA (pts with N-RFT ) recommended screening test to
establish ∆ of RAS. (B) (sens 59%-96% and speci 82%-99%)
• 3. MRA recommended screening test to establish ∆ of
RAS. (B) (sensi 90%-100% and speci 76%-94%)
• 4. Clinical index of suspicion high &
Results of noninvasive tests inconclusive
Angiography recommended as a diagnostic test (B)
Duplex Ultrasound
• Excellent- to monitor RA patency aft
endovascular/surgical revascularization
• Limitations
– absolute dependence on operator skill
– diminished ability to visualize accessory RA
– Difficulty to image obese/pts with intervening
bowel gas
Computed Tomographic Angiography
• Not ideal screening for pts with renal
insufficiency
• Metal stents may be imaged & in-stent restenosis
detected
• Higher spatial resolution than MRA
Magnetic Resonance Angiography
Catheter Angiography
• Pts -clinical clues- definitive diagnostic
noninvasive images cannot be obtained
• Pts -prespecified clinical indications & in
whom concomitant angiographic access has
been obtained for PAG/CAG
Clinical clues to RAS
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Onset of HTN < 30 yrs (I)
Severe HTN >55 yrs (I)
Accelerated, resistant or malignant HTN (I)
New azotemia/wors RFT aft adm of ACEI/ARB (I)
Unexpl atrophic kidney/size discrep >1.5 cm (I)
Sudden unexpl Pulm Edema (I)
Unexpl ↓RFT, inc pts on RRT (IIa)
Multi-vessel CAD (IIb)
Unexplained CCF (IIb)
Refractory angina (IIb)
Hemodynamically signi Asympto(incidental)RAS
Defined as RAS in the absence of
• end organ dysfunction (e.g., idiopathic pulmonary
edema, stroke,visual loss, hypertension, or
refractory angina)
But in the presence of
• (a) ≥50%-70% D stenosis by visual estimation +
peak trans-lesional gradient ≥ 20 mm Hg/mean
gradient ≥10 mm Hg OR
• (b) any stenosis ≥ 70% D stenosis OR
• (c) ≥ 70% D stenosis by IVUS
Asymptomatic Stenosis
RECOMMENDATIONS
Class IIb
• 1. PTA may be considered – B/L or solitary
viable kidney with a hemodynamically signi
RAS (C)
• 2. PTA in U/L hemodynamically signi RAS in a
viable kidney- Not well established, Clinically
unproven (C)
Hypertension
RECOMMENDATIONS
Class IIa
PTA- reasonable if hemodyn signi RAS &
• Acc HTN, resis HTN , malign HTN,
• HTN with unexpl unilateral small kidney
• HTN with intolerance to medication (B)
Preservation of Renal Function
RECOMMENDATIONS
Class IIa
• PTA- reasonable – RAS & progressive CKD
with B/L RAS or a RAS to a solitary
functioning kidney (B)
sudden-onset/“flash” pulm edema
Pts with hemodyn sign B/L or solitary RAS
• Volume-overload state- lack N renal function
to respond to P natriuresis
• ↑LV afterload secondary to angiotensinmediated vasoconstriction
• Contribute to unstable coronary syndromessudden ↑ in myocardial O2 demand in CAD
pts secondary to peripheral vasoconstriction
CCF and UA
RECOMMENDATIONS
Class I
• PTA indicated in hemodyn signi RAS &
recurrent, unexpl CCF or sudden, unexpl
pulm edema(B)
Class IIa
• PTA reasonable in hemodyn signi RAS &
UA(B)
Potential physiological benefits
Reperfusion of ischemic kidney(s)
• ↓stimulus to renin production,
• ↓angiotensin & aldosterone production,
• ↓peripheral arterial vasoconstriction
• ↓tendency to ↑ECF Volume
Improvement in renal perfusion
• ↑glomerular filtration
• ↑natriuresis
Finally, in patients with a solitary kidney or bilateral RAS,
ability of pt to tolerate long-term adm of angiotensin
antagonist medications may be facilitated by relief of a
hemodynamic renal artery obstruction.
INTERVENTION
• Class I
• 1. Renal stent placement for ostial
atherosclerotic RAS lesions meeting the
clinical criteria for intervention (B)
• 2. Balloon angioplasty with bailout stent
placement for FMD lesions (B)
Surgery for RAS
Class I
• 1. Fibromuscular dysplastic RAS with clinical
indications for interventions (same as for PTA)
– complex disease that extends into segmental arteries
– macroaneurysms
• 2. Atherosclerotic RAS & clinical indications for
intervention
– multiple small renal arteries
– early primary branching of main RA
– in combination with pararenal aortic reconstructions
Indications for renal revascularization.
ACC/AHA 2005 Practice Guidelines
for the Management of
Pts With Peripheral Arterial Disease
(Mesentry)
Acute intestinal ischemia (AIO)
• most frequently occlusive but also non-occlusive
(low flow states)
• Occlusive AIO without treatment is nearly always
fatal
• Exceptions -ischemic injury confined to mucosal
layer, gradual development of collateral
circulation
Chronic intestinal ischemia (CIO)
• always the result of arterial obstruction
Occlusive Acute Intestinal Ischemia
• ⅔ women, median age 70 yrs,most have h/o preexisting CAD
Diagnosis
RECOMMENDATIONS
Class I
• 1. A/C abd pain out of proportion to physical findings & h/o
CAD- Suspect AIO
• 2. A/C abd pain aft arterial interventions in which catheters
traverse visceral Ao or any prox arteries or who have
arrhythmias or recent MI - Suspect AIO
Class III
• In contrast to CIO, duplex sonography of abd- not an
appropriate diagnostic tool for suspected AIO
ARTERIOGRAPHY
• Diagnostic & can differentiate occlusive V/S nonocclusive
• Catheter-directed therapy - intra-arterial vasodilators,
thrombolysis, or mechanical thrombectomy
• Knowledge of extent & nature of intestinal A lesions, if
surgery reqd
Decision for arteriography - best individualized
• Very A/C presentation, High likelihood of arterial obstr,
Susp bowel infarction→ Immediate laparotomy -Best
approach
• More delayed presentation/ high likelihood of
nonocclusive ischemia→ Arteriography indicated
Endovascular Treatment
RECOMMENDATION
Class IIb
• Percutaneous interventions (including
transcatheter lytic therapy, balloon
angioplasty, and stenting) -appropriate in
selected patients with occlusive AIO. Patients
so treated may still require laparotomy
Chronic Intestinal Ischemia
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most often female (70%)
severe abd pain induced by eating
Majority –h/o CAD
30%-50%- previous operations for
atherosclerotic disease (mostly coronary &
lower extremity bypass)
Chronic Intestinal Ischemia
Diagnosis
RECOMMENDATIONS
Class I
• 1. Abdominal pain and weight loss without
explanation, esp with CAD- Suspect CIO
• 2. Duplex ultrasound, CTA, and MRA- useful
initial tests for CIO
• 3. Diagnostic angiography, including lateral
aortography, in pts suspected of having CIO for
whom noninvasive imaging is
unavailable/indeterminate
Arteriography
• Definitive diagnosis
• Lateral aortography- best suited for typical
origin lesions
• Presence of an enlarged “arc of Riolan” arteriographic sign of proximal mesenteric A
obstruction
Interventional Treatment
RECOMMENDATION
Class I
• Percutaneous endovascular treatment of
intestinal arterial stenosis is indicated in
patients with chronic intestinal ischemia (B)
Thanks…
ANEURYSMS OF THE ABDOMINAL
AORTA
• Generally, however, an AAA is
• considered to be present when the minimum
anteroposterior
• diameter of the aorta reaches 3.0 cm. The size of the aorta
• can be measured in any plane that is perpendicular to the
vessel
• axis, but in practice, the anteroposterior diameter is
measured
• most easily and reproducibly. Accordingly, most screening
• studies define AAA in this manner (
Symptomatic Aortic or Iliac Aneurysms
• RECOMMENDATIONS
• Class I
• 1. In patients with the clinical triad of abdominal
and/or
• back pain, a pulsatile abdominal mass, and
hypotension,
• immediate surgical evaluation is indicated.
• (Level of Evidence: B)
• 2. In patients with symptomatic aortic aneurysms,
• repair is indicated regardless of diameter. (Level of
• Evidence: C)
Endovascular Aortic Aneurysm Repair
• In an attempt to overcome the risk of distal
migration and
• proximal attachment failure, a growing
number of new
• devices now incorporate barbed hooks that
are sufficiently
• long to secure the metallic frame of the stent
graft to the visceral
• segment of the aorta above the renal arteries
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5.2.7.1.1. ANATOMIC LIMITATIONS. Even with suprarenal fixation
of its metallic exoskeleton, the fabric component of an
endograft obviously cannot be permitted to overlap the origins
of the renal arteries. Accordingly, at least 1 cm of proximal
aortic cuff (1.5 cm for commercially available grafts)
presently is optimal for elective endograft repair below the
renal arteries. For devices without a suprarenal fixation
device, the optimum infrarenal aortic diameter at the time of
this writing is 25 mm or less, and for devices with a
suprarenal fixation component, it is 28 mm or less. Because
of the inflexibility of externally supported grafts, this segment
of the aorta must not be severely angulated. This
requirement may impose a gender bias in patient selection,
because in addition to the fact that their small external iliac
arteries often present problems with respect to vascular
access, women also appear to have a higher prevalence of
short, angulated aneurysm necks than men (1138,1139
Management Overview
RECOMMENDATIONS
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Class I
1. Open repair of infrarenal AAAs and/or common iliac
aneurysms is indicated in patients who are good or
average surgical candidates. (Level of Evidence: B)
2. Periodic long-term surveillance imaging should be
performed to monitor for an endoleak, to document
shrinkage or stability of the excluded aneurysm sac,
and to determine the need for further intervention in
patients who have undergone endovascular repair of
infrarenal aortic and/or iliac aneurysms. (Level of
Evidence: B)
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Class IIa
Endovascular repair of infrarenal aortic and/or common
iliac aneurysms is reasonable in patients at high
risk of complications from open operations because of
cardiopulmonary or other associated diseases. (Level
of Evidence: B)
Class IIb
Endovascular repair of infrarenal aortic and/or common
iliac aneurysms may be considered in patients at
low or average surgical risk. (Level of Evidence: B)