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Angioplasty/Stenting of Mesenteric Arteries 161
a
b
c
d
f
g
e
Fig. 3 (a) Selective
angiography of the celiac
trunk through a cobra catheter
showing a sufficient supply of
splenic, liver, and
pancreatico-duodenal
branches without any large
collateral vessels visible to
the SMA. (b, c) High-grade
ostial stenosis of the IMA,
which is responsible for the
entire bowel supply. (d, e)The
stenosis has been crossed
with an 0.014-inch wire,
guided by a Sidewinder
catheter. The lesion is
predilated with a 5-mm
balloon. (f, g)After
predilation, a 7×19 mm is
stent positioned and
deployed. Completion
angiography shows a good
result
162 S. Müller-Hülsbeck
a
b
Fig. 4 (a, b) A severely stenosed aortomesenteric venous bypass graft. The images show the dis-
tal anastomosis before and after PTA using a 5 and 7×20-mm balloon in a 35-year-old young
lady (heavy smoker and Takayasu arteritis). There is a residual mild stenosis. N.B. A 0.014-inch
buddy wire was placed distal to the stenosis in the proximal part of the SMA. If there is recurrent
restenosis, cutting balloon angioplasty using a 6×20-mm balloon might be an appropriate treat-
ment method. Insertion of a stent is also an option, although should be avoided if possible in young
patients
a technical success rate close to 100%, a peri-procedural major and minor
complication rate of less than 10%, and mortality of below 4%.
• Percutaneous intervention for CMI is safe with durable early and mid-term
clinical success. However, repeated intervention may be required for improved
primary assisted patency, particularly if PTA rather than stenting was originally
performed.
• The symptom-free rates are around 95, 90, 72, and 54% at 0, 1, 24, and 30
months, respectively.
• Complication rates are very low.
Alternative Therapies
• The main alternative treatment is surgery. Surgical procedures include endarterec-
tomy and surgical bypass (e.g., aortoceliac and aortomesenteric bypass).
• Surgery may still be preferred in patients with long occlusions and a low operative
risk.
• Retrograde mesenteric stenting during laparotomy for acute occlusive mesenteric
ischemia is a potential hybrid endovascular and surgical option.
Angioplasty/Stenting of Mesenteric Arteries 163
a
b
Fig. 5 (a, b) Color duplex sonography during follow-up after previous stenting of a celiac trunk
stenosis indicates increased peak velocities within the stent. Repeat PTA is the treatment of choice
Complications
How to Treat
• Stent dislodgement:
b
If the stent is displaced behind the lesion and is still in the target vessel, the
stent should be deployed in the vessel. A second stent should be subsequently
advanced across the lesion and deployed in the correct location.
164 S. Müller-Hülsbeck
b
If the stent is partially in the aorta and is still partially mounted on the balloon,
the balloon and stent combination can be withdrawn into the iliac artery and
fully deployed in this location. A new stent can be deployed in the correct
location.
b
If the stent has become detached from the balloon, it will be necessary to snare
the stent using a snare introduced from the ipsilateral femoral artery.
This is best achieved by passing the snare catheter through the same sheath
as the stent.
It is essential to maintain the guidewire in place so that the stent does not
become detached from the guidewire.
If the sheath is too small for the snare catheter and the guidewire, the sheath
should be exchanged for a larger sheath.
The snare should be passed through the sheath with the loop over the
guidewire until the snare loop is at the level of the stent.
The lower end of the stent is snared by closing t he loop and is withdrawn
in a collapsed state through the sheath.
• Malposition of the stent: The stent should be deployed completely followed by
insertion of a second stent to cover the entire lesion.
• Vessel perforation: This is a rare complication. If it occurs, the first maneuver to
try is a prolonged low-pressure balloon inflation (for 3 min or longer). If this fails
to prevent contrast extravasation, a covered stent should be implanted. If this is
not possible or a covered stent is not available, the balloon should be kept inflated
across the lesion and a surgeon should be called.
How to Avoid
• Stent dislodgement: If it is not possible to pass the stent across the lesion, the
device should be removed carefully. After removal of the device, the lesion should
be predilated using a 4×20 mm balloon.
• Stent malpositioning:
a. This is avoided by performing repeat angiography until the stent is in the
correct position. When the correct position is achieved, the shaft of the bal-
loon catheter should be supported by hand pressure at the exit point from the
sheath, and a second operator can be asked to inflate the balloon to deploy
the stent.
b. The stent should be centered on the middle of the target lesion. If you are
not sure about the correct stent length that may be required, a longer stent
should be selected than one that might be too short.
• Vessel perforation: This is very rare.
b
This can be avoided by using stents and balloons that are not too l arge for the
vessel.
Angioplasty/Stenting of Mesenteric Arteries 165
b
The use of a manometer during inflation of the balloon avoids excessive
inflation pressures and may prevent vessel rupture.
b
If the patient experiences pain during balloon inflation, the PTA should be
stopped and a larger balloon should definitely not be used.
Key Points
• Careful case selection is mandatory. Avoid treating patients with stenoses
of single vessels.
• Use the transbrachial approach if catheterization from the femoral route is
problematic.
• Use predilatation in severe stenoses to avoid plaque embolization and stent
dislodgement.
• Perform PTA and stent deployment under manometer control in order to
avoid overdilation and vessel perforation.
• Use balloon-expandable stents for ostial lesions.
• Perform repeat check angiograms in the appropriate projection (usually lat-
eral or close to lateral) to visualize the origin of the vessel to confirm that
the stent is in the correct location before deployment.
Suggested Reading
1. AbuRahma AF, Stone PA, Bates MC, Welch CA. Angioplasty/stenting of the superior mesen-
teric artery and celiac trunk: early and late outcomes. J Endovasc Ther 2003; 10:1046–1053.
2. Brandt LJ, Boley SJ. AGA technical review on intestinal ischemia. American Gastrointestinal
Association. Gastroenterology 2000; 118:954–968.
3. Cognet F, Ben Salem D, Dranssart M, et al. Chronic mesenteric ischemia: imaging and
percutaneous treatment. Radiographics 2002; 22:863–879.
4. Dunphy JF. Abdominal pain of vascular origin. Am J Med Sci 1936; 192:109–112.
5. Goodman GH. Angina abdominis. Am J Med Sci 1918; 155:524–528.
6. Landis MS, Rajan DK, Simons ME, Hayeems EB, Kachura JR, Sniderman KW. Percutaneous
management of chronic mesenteric ischemia: outcomes after intervention. J Vasc Interv
Radiol 2005 Oct; 16(10):1319–1325.
7. McShane MD, Proctor A, Spencer P, Cumberland DC, Welsh CL. Mesenteric angioplasty for
chronic intestinal ischaemia. Eur J Vasc Surg 1992; 6:333–336.
8. Nyman U, Ivancev K, Lindh M, Uher P. Endovascular treatment of chronic mesenteric
ischemia: report of five cases. Cardiovasc Intervent Radiol 1998 Jul–Aug; 21(4):305–313.
9. Resch T, Lindh M, Dias N, Sonesson B, Uher P, Malina M, Ivancev K. Endovascular recanal-
isation in occlusive mesenteric ischemia–feasibility and early results. Eur J Vasc Endovasc
Surg 2005 Feb; 29(2):199–203.
10. Schaefer PJ, Schaefer FK, Hinrichsen H, Jahnke T, Charalambous N, Heller M, Mueller-
Huelsbeck S. Stent placement with the monorail technique for treatment of mesenteric artery
stenosis. J Vasc Interv Radiol 2006 Apr; 17(4):637–643.
166 S. Müller-Hülsbeck
11. Schuler A, Dirks K, Claussnitzer R, Blank W, Braun B. Ligamentum arcuatum syndrome:
color doppler ultrasound diagnosis in abdominal pain of unknown origin in young patients.
Ultraschall Med 1998 Aug; 19(4):157–163.
12. Wyers MC, Powell RJ, Nolan BW, Cronenwett JL. Retrograde mesenteric stenting during
laparotomy for acute occlusive mesenteric ischemia. J Vasc Surg 2007 Feb; 45(2):269–275.
Carotid Stenting and Angioplasty
Gerald Wyse and Kieran J. Murphy
Introduction
• Ischemic stroke is a leading cause of death and disability in the developed
world. The costs in term of healthcare and lost productivity are enormous but
do not adequately reflect the human cost of such significant disability. Ischemic
strokes are commonly caused by cardiac emboli, small vessel arterial disease, and
atherosclerotic plaque at the carotid bifurcation. Carotid artery stenting (CAS)
is a minimally invasive endovascular procedure for the prevention of ischemic
stroke in patients with underlying carotid atherosclerosis.
• The development of new techniques and technology has made CAS an attractive
alternative to Carotid Endarterectomy (CEA). As a minimally invasive procedure
it has clear advantages in terms of the lack of a surgical incision, shorter pro-
cedure time, and shorter hospital stay. The procedure can be performed under
conscious sedation avoiding general anesthesia with clear advantages for those
with underlying medical co-morbidities. In addition, the temporary proximal
carotid occlusion of a CEA is avoided.
Clinical Features
Carotid Atherosclerosis
• The underlying mechanism of ischemic stroke from carotid disease is plaque rup-
ture with ulceration. The exposed vascular wall leads to clot formation within
the lumen of the vessel. Embolization of clot leads to distal vessel occlusion
and resultant ischemia. Although uncommon in the carotid artery, plaque rup-
ture may result in thrombosis and occlusion at the site of rupture. The majority
of atherosclerotic disease in the carotids occurs at the carotid bifurcation and
extends into the proximal internal carotid artery. The flow dynamics at the carotid
bifurcation result in reduced flow velocity and sheer stress at the lateral aspect of
the flow divider leading to plaque formation (Fig. 1).
167
R.A. Morgan, E. Walser (eds.), Handbook of Angioplasty and Stenting Procedures,
Techniques in Interventional Radiology, DOI 10.1007/978-1-84800-399-6_14,
C
Springer-Verlag London Limited 2010
168 G. Wyse and K.J. Murphy
• Atherosclerotic formation is associated with the usual vascular risk factors:
b
Hypertension
b
Hyperlipidemia
b
Smoking
b
Diabetes
• The underlying pathological progression is similar to that of coronary artery dis-
ease. The initial lesion is the intimal xanthoma, the so-called fatty streak. This
progresses to intimal thickening and an overlying fibrous cap, which can cause
luminal narrowing. Further progression leads to a high-risk plaque with a thin
fibrous cap. Thinning and weakening of the fibrous cap leads to fissures and
eventually plaque rupture.
a
c
e
b
d
f
Fig. 1 (a, b) AP and lateral angiograms reveal a tight atherosclerotic stenosis in the proximal
internal carotid artery. (c) A lateral radiograph demonstrating angioplasty of this atherosclerotic
lesion. (d) A lateral radiograph post stent deployment. (e, f) AP and lateral digital subtraction
angiograms post angioplasty and stenting of this symptomatic carotid atherosclerotic lesion
Carotid Stenting and Angioplasty 169
Fig. 2 A lateral radiograph
demonstrating primary
angioplasty of the internal
carotid artery with a distal
embolic filter
Angioplasty and Stenting
• Large surgical trials have shown a clear benefit in terms of risk reduction from
stroke with CEA in the setting of significant atherosclerotic narrowing.
• CAS is a minimally invasive alternative to CEA for the prevention of ischemic
stroke:
b
Angioplasty expands the lumen of the vessel increasing antegrade flow. The
stent prevents recoil and plaque from projecting into the lumen.
b
Stenting effectively covers the underlying plaque, sealing the diseased vessel
surface and resulting in a neo-intima and endothelialization of the stent.
b
Angioplasty without stenting was commonly performed in the past. Retenosis
rates are high with this technique, in the 20–30% range in the coronary
arteries.
b
Stents avoid these problems but issues do exist with acute stent thrombosis
and delayed endothelialization which can take about 3–4 months to heal.
170 G. Wyse and K.J. Murphy
Medical Management
• Since the large surgical endarterectomy trials, there have been considerable
advances in the medical management of carotid atherosclerotic disease:
b
Aspirin
b
New lipid-lower agents (statins)
b
Newer antiplatelet agents (Clopidogrel)
b
Aggressive management of blood pressure and blood glucose
Diagnostic Evaluation
Clinical
• Symptoms of hemispheric cerebral ischemia
b
Transient ischemic attacks (TIAs)
• Amaurosis Fugax (monocular temporary blindness or visual defects)
• Reversible ischemic neurologic deficits (RINDs)
• Ischemic stroke events lasting >24 h and resulting in non-disabling cerebral
infarct:
b
Severe, disabling strokes not considered for CAS/CEA
• Sex/age − octogenarians may do worse with CAS versus CEA possibly due to
small and/or tortuous aortas and carotid arteries
• Cardiac disease − High risk for CEA:
b
Left ventricular ejection fraction (LVEF) <30%
b
Congestive heart failure (CHF) Class III/IV
b
Unstable angina, recent myocardial infarction (MI)
b
Multi-vessel coronary artery disease (CAD)
• Pulmonary disease − High risk for CEA:
b
Forced expiratory volume and 1 sec (FEV1) <50% predicted
b
Severe obstructive pulmonary disease or emphysema
• Systemic diseases − High risk for CEA:
b
Dialysis-dependent renal failure
b
Liver failure
b
Uncontrolled diabetes
• Past medical/surgical history − High risk for CEA:
b
Prior neck irradiation/surgery:
Significant risk of nerve injury during CEA