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carotid artery dissection, and stenotic disease away from the
carotid bifurcation and carotid pseudoaneurysms.
3 Cerebral Protection Devices
Procedural embolisation can happen at various stages dur-
ing carotid artery stenting procedure and may be caused by
thrombus and plaque fragments which are released into the
cerebral circulation and may lead to ischaemic symptoms,
or as silent ischaemia and diffusion-weigthed (DW) MRI
detectable lesions. To guard against cerebral embolisation
cerebral protection devices have been developed to try and
prevent emboli from reaching the cerebral circulation.
Currently the most commonly used methods are distal filter-
type protection devices. All available protection systems
have been shown to be capable of capturing emboli and
early results were promising for filter type devices (Yadav
et al. 2004; Mas et al. 2006). More recent evidence suggests
that some filter devices may in fact increase the number of
embolic events, as shown by surrogate endpoints of DW-
MRI and transcranial Doppler (Barbato et al. 2008; Mac-
Donald et al. 2010), although the fate and significance of
these lesions remains to be clarified. Rapp et al. 2009
showed that filter-type devices may create a pressure wave
effect which funnels some microemboli around the device
rather that catching them. Embolic episodes may also occur
when crossing the carotid plaque with a wire and delivery
system, which is larger than a simple guidewire. The
deployment of the filter in the distal carotid artery may
result in embolic events either because it causes endothelial
damage or because the distal internal carotid artery contains
atheromatous disease. However these findings, using mainly
surrogate markers of neuroischaemic events, are in conflict
with the clinical findings of benefit from the use of filter
protection devices.
Whatever the significance of these findings, the efficacy
of protection methods used to eliminate debris is important
for the wider treatment indications of CAS and improved
risk profile for treatment of symptomatic patients. Other
protection devices that use different methods to protect
against embolisation have been developed and the most
promising of these are the proximal protection devices.
These devices are becoming increasingly used and the
technique of flow reversal first introduced by Juan Parodi,
(Parodi et al. 2000) has grown in popularity. Using these
methods it is possible to stop and/or reverse the blood flow
in the internal carotid artery before inserting the guidewire
through a stenotic lesion and subsequent stenting. Both
stasis and reverse flow methods decrease the amount of
blood flow to the brain. When a reverse flow device is used
correctly blood is diverted away from the cerebral circula-
tion via an arterio venous shunt. The benefit of this type of
protection device is that the lesion does not need to be
disturbed prior to establishment of protection. In addition,
during the procedure, the emboli are continuously directed
away fromthe cerebralcirculation. The disadvantages arethat
patients are sometimes intolerant of these devices, due to the
associated reduction in brain perfusion, and they are also
relatively difficult to use adding complexity to the procedure.
In published clinical studies flow reversal not only controls
macroembolisation but also decreases the procedural rate of
microembolisation with good clinical effect (Criado et al.
2007; Adami et al. 2002; Parodi 2005). A recent large obser-
vationalstudy(Ansel 2010) hasfurther shown thebenefits and
decreased 30-day risks using proximal protection devices.
4 Technical Aspects
Preoperative imaging is essential for the endovascular
treatment of patients with carotid artery stenosis. All
patients should have had preoperative duplex, and for en-
dovascular treatment patients also need preoperative Mag-
netic Resonance Angiography (MRA) or CT angiography
(CTA) to assess for the degree of stenosis and also the
anatomy from the aortic arch to Circle of Willis, to assess
feasibility for stenting. Patients should be treated with
aspirin and clopidogrel for at least three days prior to the
procedure or have a loading dose regime. An overview of
the outline procedural steps are as follows for CAS using a
distal protection device:
1. Retrograde femoral access (although the brachial can
be used) and insertion of a sheath.
2. Heparin is administered after arterial access is gained
and prior to manipulation of catheters in the aortic arch
and brachiocephalic vessels.
3. Following selective catheterisation of the ipsilateral
common carotid artery (CCA) a selective angiogram is
performed (Fig. 1).
4. A longer (90 cm) sheath or guide catheter is then
advanced into the CCA.
5. Once the sheath is in place, the guidewire and dilator
are removed. Roadmapping can be used and is helpful
in crossing the lesion with an embolic protection device
or guidewire.
6. The devices are prepared (with special care to remove
all air from the system); Glycopyrrolate should be
given as prophylaxis against bradycardia and hypoten-
sion during balloon inflation in the carotid bulb.
7. The distal protection device (0.014
00
) is advanced across
the lesion and deployed into the distal internal carotid
artery (ICA), above the stenosis (Fig. 2a).
8. The lesion is then predilated with an appropriately sized
angioplasty balloon (commonly 3 mm diameter)
(Fig. 2b).
114 S. D. Goode and T. J. Cleveland
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9. The stent (appropriately sized) is then deployed after
confirmation of a correct position, the deployed stent
usually covers the ECA origin unless a high ICA lesion
is being treated. The stent should be oversized by about
10% (compared with the largest diameter vessel—
usually the CCA) to ensure good apposition to the
vessel wall (Fig. 2c).
10. The lesion is then postdilated, to match the native ICA
(Fig. 2d).
11. Vasospasm can sometimes be encountered (and can
mimic dissection) and vasodilators should be adminis-
tered through the sheath (glyceryl trinitrate is com-
monly used).
12. A completion angiogram is then performed (Figs. 2e
and 3).
13. Access site haemostasis is achieved either with manual
pressure or a closure device.
5 Post-procedure Care
Following the procedure, the patient is monitored in the
recovery area followed by transfer to a monitored ward.
Some patients can suffer prolonged hypotension from car-
otid sinus stimulation; it is uncommon for this to be
symptomatic, but if so this should be managed with fluid
administration, pharmacological treatment of bradycardia,
and occasionally with intravenous vasopressors. A duplex
ultrasound scan is performed at 6 weeks and patients should
be maintained on dual antiplatelets for at least 1 month, and
a single antiplatelet for life (preferably Clopidogrel as per
NICE Guidance).
6 Complications Following CAS
Embolic stroke is the most common serious complication
reported for CAS; its incidence may be affected by the use
of cerebral protection devices although as mentioned above
the correct protection device to use is still unclear.
Advanced age and the presence of long or multiple lesions
have been implicated as independent predictors of proce-
dural stroke. Other complications have also been cited,
including prolonged bradycardia and hypotension, as well
as in-stent thrombosis. Cerebral hyperperfusion with asso-
ciated seizures and intracranial haemorrhage have also been
reported. Longer term in-stent restenosis may occur.
7 Limitations of and Contraindications
to CAS
Some limitations and contraindications to CAS are listed
below:
• Unfavourable aortic arch anatomy
• Severe tortuosity of the common or internal carotid
arteries
• Severely calcified/undilatable stenoses
• Lesions containing fresh thrombus
• Contrast-related issues:
• Renal impairment
• Previous contrast reaction
• Although both of these can potentially be overcome by
the use of either limited doses or gadolinium-contain-
ing contrast agents caution should be excercised if
contemplating the use of gadolinium-based contrast
agents in patients with significant renal failure.
Fig. 1 Carotid angiogram showing tight narrowing of the internal
carotid artery
Carotid and Vertebral Artery Intervention 115
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8 Vertebral Artery Intervention
Each vertebral artery (VA) begins in the root of the neck as
a branch of the first part of the subclavian artery. The
anatomic course is divided into four segments, V1–V4. The
V1 segment originates from the subclavian artery and runs
until it enters the transverse foramina of C5/C6. Here it
becomes the V2 which is a completely intraosseous seg-
ment running from C5/C6 to C2 level. Here segment V3
starts and runs to the level of the foramen magnum where is
pierces the dura and becomes the V4 segment. The latter is
entirely intracranial and extends to the formation of the
basilar artery. The V4 segment has several branches
including the posterior-inferior cerebellar artery and the
anterior spinal artery. The VAs feed the brain stem, cere-
bellum, and thalamus. In most people they also feed the
posterior temporal and occipital lobes as well 10 of the 12
cranial nerves. The course of the VA results in several
technical challenges which affect the treatment; in particular
Fig. 2 Diagrammatic representation of the carotid stenting procedure, a distal protection device placed, b predilation of the narrowing, c stent
deployment, d postdilation of the stent, e expanded stent with protection device removed
116 S. D. Goode and T. J. Cleveland
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the anatomical position of the V1 and V4 sections almost
precludes surgical treatment.
9 Pathology
The pathology affecting the VA’s includes atherosclerosis,
dissection, Takayasu arteritis, giant cell arteritis, fibromus-
cular dysplasia, compressive mechanisms, and blunt or
penetrating trauma. Vertebrobasilar ischaemia (VBI) is
caused by embolic and haemodynamic mechanisms
including atherosclerotic stenosis, dissection, external
compression, and trauma. Embolization may present as a
transient ischaemic attack (TIA) or infarct in the basilar
artery territory with sources including the heart, aortic arch,
proximal subclavian and vertebral arteries. Haemodynamic
VBI is more common and is usually a result of athero-
sclerosis, patients having ischaemia due to stenosis or
occlusion of the VA and inadequate compensation from the
contralateral VA. The signs and symptoms of posterior
ischaemia are variable and include dizziness or vertigo,
posterior headache, syncopal episodes, diplopia, and gait
ataxia. Clinical signs on examination may include nystag-
mus, vertical gaze, past pointing, bilateral limb weakness,
or cranial nerve palsy. The most frequent sites of infarction
are in the cerebellum and occipital lobes. Dissection of the
extracranial cervical arteries (vertebral and carotid) is a
major cause of non-atherosclerotic cerebral infarction in
younger (30 to 50 years) adults.
10 Indications for Vertebral Artery
Intervention
Atherosclerotic stenosis (C50% lumen loss) at the origin of
the vertebral artery (V1) or in its intracranial course (V4) is
present in about one-third of the patients presenting with
posterior circulatory events (Flossman and Rothwell 2003;
Savitz and Caplan 2005). Out of these two areas of stenosis
the V1 section close to the subclavian artery is by far the
most common. Stenosis in this region predisposes to pos-
terior circulation stroke due to embolism or impaired hae-
modynamics (Caplan et al. 2004; Wityk et al. 1998).
Symptomatic vertebrobasilar disease refractory to medical
treatment is associated with 5–11% risk of stroke or death at
one year (Chimowitz et al. 1995). Surgical treatment of
these lesions is associated with good long-term outcomes.
However these procedures are associated with a high rate of
morbidity and mortality (3–13.6%) including recurrent
laryngeal nerve palsy, Horner’s syndrome (10%), and
chylo/pneumothorax due to the anatomical difficulties of the
procedure (Imparato 1985; Coward et al. 2005; Deriu et al.
1991). Percutaneous transluminal angioplasty (PTA) and
stenting is therefore an attractive alternative to open surgery
and it has been used since the 1980s to treat symptomatic
severe ([50%) VA stenosis (Caplan et al. 2004; Akins et al.
2008; Dabus et al. 2006). In contrast to carotid stenosis
there is relatively little research into the prognosis and the
prevention of recurrent vascular events in patients with
VAS. However, the currently reported periprocedural out-
comes are satisfactory. One of the main drawbacks for VAS
has been the reported relatively high incidence of instent
restenosis (ISR) of 10–67% (Dabus et al. 2006; Hatano
et al. 2005; Albuerquerque et al. 2003; Lin et al. 2006). In
more recent publications workers have started to examine
the use of drug-eluting stents to try and improve on this with
very encouraging early results and decreased rates of ISR
(Edgell et al. 2010; Park et al. 2010).
Fig. 3 Post-procedure carotid angiogram showing stent across the
carotid bifurcation
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11 Technical Aspects
Like CAS, VAS planning requires preprocedural imaging
usually utilising MRA or CTA. Care should taken with the
interpretation of these techniques, as the pulsation artefact
may be close to the VA origins, resulting in a significant
risk of artefactual ‘‘stenotic’’ disease. All patients, like those
with CAS, should be pretreated with dual antiplatelet
medication. The orientation of the VA origins is usually
such that approaching these from a brachial or radial access
point is technically difficult, and the majority of VASs are
done from a more traditional femoral approach. An over-
view of the outline procedural steps are as follows for VAS:
1. Arterial access is performed, and heparin is administered.
2. The left subclavian or the brachiocephalic artery is
selectively catheterised, and a suitably sized long sheath
or guiding catheter is placed with the tip in a stable
position as close to the VA origin as possible. This
allows for imaging and treatment (Fig. 4).
3. The VA stenosis is crossed, usually with either an 0.014
00
or an 0.018
00
steerable guidewire (depending on the bal-
loons and stents selected), under roadmapcontrol(Fig. 5).
4. If the lesion is particularly narrow predilatation with a
2- or 3-mm balloon is performed.
5. A suitably sized stent is selected. The VA origin is
usually markedly angulated and a short stent is usually
the most appropriate, matched to the diameter of the
normal vertebral artery. As accuracy of placement and
short length are used, balloon-mounted stents are the
most commonly utilised. As the VA origin is not usually
subjected to outside pressures, this is a reasonable choice
(unlike CAS).
6. Once the stent has been deployed successfully, the wire
and catheters are removed following completion of
angiogram (Figs. 6).
7. The access site is closed using manual pressure or a
closure device.
12 Post-procedural Care
There is limited data to guide aftercare for VAS. Most
operators would recommend a similar antiplatelet regime
for CAS, by extrapolation, as above. With the data indi-
cating the potential benefit of drug-eluting stents and their
use increasing, dual antiplatelet therapy should be pro-
longed for one year, as suggested by the data for coronary
drug-eluting stents. Unlike CAS, the stented segment in
VAS is usually not amenable to routine follow up by
Duplex, therefore routine imaging is not usually recom-
mended. However if there is a recurrence of symptoms the
stents can be imaged using CTA or catheter angiography.
In-Stent Restenosis can be retreated by balloon and/or an
additional stent.
Fig. 4 Preprocedure angiogram showing stenosis of the right verte-
bral artery and also a right subclavian artery stenosis
Fig. 5 Right vertebral artery accessed from the right brachial artery
approach with steerable guidewire
118 S. D. Goode and T. J. Cleveland
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13 Complications
VAS is subject to complications relating to arterial access
and the use of iodinated contrast, as described above for
CAS. Problems specific to VAS may occur due to embolic
events at the time of placement or subsequently, stent
thrombosis, arterial dissection, and hyperperfusion
bleeding.
14 Conclusion
The evidence in relation to the use of CAS is at times
conflicting. There are clearly advantages to its use when
compared to CEA, in particular in relation to effective
elimination of the risks of cranial nerve injury and wound
haematoma. However, some trials have shown a signifi-
cantly greater risk of stroke, although these are generally in
the minor stroke category. Currently CAS can be recom-
mended for patients with symptomatic carotid artery ste-
nosis who are unfit for CEA, have ‘‘hostile‘‘ necks and
unfavourable anatomy.
There is demonstrable clinical benefit with the use of
cerebral protection devices during CAS procedures.
Although a number of device types are available there
appears to be some potential problems with filter devices
when compared to those involving flow stasis or flow
reversal. The best device to use remains unclear.
Surgical treatment forvertebral artery stenoses isgenerally
effective but very challening due to the anatomy and conse-
quently associated with relatively high complication rates.
As aresult vertebralartery stentingis a very attractiveoption.
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Management of Renal and Visceral
Arterial Stenoses
M. G. Cowling
Contents
1 Introduction.......................................................................... 121
2 Renal Artery Stenosis.......................................................... 121
3 Investigation of RAS ........................................................... 123
4 Technique of Renal Revascularisation.............................. 123
4.1 Renal Angioplasty ................................................................. 123
4.2 Renal Stenting ....................................................................... 124
4.3 Intervention in Renal Transplants......................................... 125
5 Results ................................................................................... 125
5.1 Fibromuscular Dysplasia ....................................................... 125
5.2 Atheromatous Renal Artery Stenosis.................................... 126
6 Complications....................................................................... 127
7 Management of Visceral Artery Stenoses ........................ 127
8 Indications for Treatment .................................................. 128
9 Technique.............................................................................. 128
10 Results ................................................................................... 129
11 Complications ....................................................................... 129
12 Conclusion ............................................................................ 129
References...................................................................................... 130
Abstract
The two most common causes for renal artery stenosis
are fibromuscular dysplasia (FMD) and atheromatous
renal artery stenosis (ARAS). FMD may cause uncon-
trolled hypertension, usually in younger patients, and is
amenable to treatment with balloon angioplasty. ARAS
is a more complex disorder and does not always require
treatment. However, where therapy is required it is
generally best treated by the insertion of a balloon
expandable stent. Visceral arterial stenoses causing
symptomatic gut ischaemia are relatively uncommon,
but can be successfully treated with angioplasty or stent
insertion.
1 Introduction
The two main aetiologies for renal artery stenosis (RAS) are
fibromuscular dysplasia (FMD), a cause of secondary
hypertension in younger patients, and atheroma. Other
aetiologies such as neurofibromatosis and middle aortic
syndrome are much rarer. With increased longevity and
improved survival after events such as myocardial infarc-
tion and stroke, atheromatous renal artery stenosis (ARAS)
is becoming a more prevalent disorder. The availability of
non-invasive imaging techniques also means that it is being
diagnosed more frequently. Visceral artery stenoses causing
symptomatic gut ischaemia are fairly uncommon, but en-
dovascular therapy can play an important role in their
management.
2 Renal Artery Stenosis
The two main aetiologies of RAS are quite distinct in
their clinical manifestations and tend to present at dif-
ferent times of life. FMD is rare, but its importance lies
in the fact that with suitable treatment it represents a
M. G. Cowling (&)
University Hospital of North Staffordshire NHS Trust,
Newcastle Road, Stoke-on-Trent ST4 6QG, UK
e-mail: mark.cowling@uhns.nhs.uk
M. G. Cowling (ed.), Vascular Interventional Radiology, Medical Radiology. Diagnostic Imaging,
DOI: 10.1007/174_2011_516, Ó Springer-Verlag Berlin Heidelberg 2012
121
https://t.me/med1917
potentially curable cause of hypertension in young
patients. FMD causes web-like stenoses which narrow the
renal artery lumen (Fig. 1). The consequent reduction in
renal perfusion activates the renin-angiotensin system,
causing hypertension which may be very difficult to
control pharmacologically. Although it may progress, it
rarely causes renal artery occlusion or renal dysfunction.
The nature of the pathology makes it eminently suitable
for treatment by angioplasty, with good and sustained
long-term clinical results (Surowiec et al. 2003). How-
ever, a more recent meta-analysis has suggested that the
benefits of treatment are moderate, rather than good, with
considerable variation across the studies examined
(Trinquart et al. 2010). Atheromatous renal artery steno-
sisisrathermorecomplex.
ARAS occurs in an older patient group than FMD, and as
such its role in causing hypertension is much less clear cut.
Most of these patients will have essential hypertension,
which may even be a contributory cause of the atheroma
which has led to RAS. Despite this, however, it is clear that
there is a group of patients in whom there is a renovascular
component to their hypertension. This is usually apparent
where blood pressure has become impossible to control
adequately with drug therapy. Although cure of hyperten-
sion will not be possible, renal revascularisation may make
pharmacological control easier.
Renal impairment may also be associated with ARAS,
and in the author’s experience this is the most common
reason for consideration of renal revascularisation. How-
ever, the number of patients being treated for ARAS in our
unit has reduced noticeably since the publication of the
ASTRAL trial (The ASTRAL trial investigators 2009). The
most straightforward patient group are those who present
with a rise in serum creatinine after commencing an
Angiotensin Converting Enzyme Inhibitor (ACEI). If the
patient requires treatment with this class of drug, and most
with cardiovascular disease will benefit from such treat-
ment, there is a strong case to perform renal
revascularisation.
Impaired renal function alone is not necessarily an
indication for treatment. The trend in renal function is very
important in this setting. A patient with a stable serum
creatinine may well be best left untreated, as that situation
could persist for many years without progression to dial-
ysis. In that setting, the risk of renal revascularisation is
considered by most workers not to be justified, and this
position would be supported by the findings of the
ASTRAL trial (The ASTRAL trial investigators 2009).
However, in the case of deteriorating renal function, there
is a strong case for revascularisation, as without it the
likely outcome is end-stage renal failure and dialysis. This
is especially true in cases of bilateral renal artery stenosis,
or where there is a single kidney. It is probably not worth
treating where the serum creatinine has risen above
300–350 lmol/l. Similarly, patients who are already
receiving dialysis therapy are unlikely to benefit from renal
revascularisation. The exception in both of these cases is
where there has been a very rapid deterioration in renal
function. In this instance long-term renal damage may not
yet have occurred, and if revascularisation can be per-
formed within a few hours or days the results can be
striking.
Finally so-called ‘‘flash’’ pulmonary oedema represents
an infrequent but strong indication for intervention. The
pathophysiology of this condition is not well understood,
but it tends to occur in patients with coronary artery disease
and either bilateral ARAS or ARAS affecting a single
functioning kidney.
Fig. 1 a Selective right renal
arteriogram showing classical
features of FMD in a 32-year-old
patient with hypertension not
controlled by multiple agents;
b Flush aortography performed
via a long sheath. This image
demonstrates that appearances in
the treated artery have improved
considerably, but have not been
abolished completely.
Nonetheless there was an
excellent clinical response. Note
also a smaller upper pole artery
which is unaffected by FMD
122 M. G. Cowling
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3 Investigation of RAS
Having identified a patient who is clinically suspected of
having RAS and in whom treatment is thought likely to be
indicated, it then becomes necessary to investigate them.
Several imaging techniques are available including con-
ventional angiography, CT angiography (CTA), MR angi-
ography (MRA) and finally captopril renal scintigraphy.
Conventional catheter angiography is regarded by many
as the ‘‘gold standard’’ technique. It has the disadvantages
of being invasive, with the attendant complications, as well
as requiring iodinated contrast media and ionising radiation.
However, in the case of FMD, in the author’s view, it
remains the only one of the techniques named above that
has the spatial resolution sufficient to confidently exclude
the diagnosis (v.i.).
CTA also has the disadvantages of using ionising radiation
and requiring iodinated contrast. The latter is a particular
disadvantage in patients with diabetes and/or renal impair-
ment, who are at a higher risk of contrast-induced nephrop-
athy. For this reason CTA has become our second line for the
non-invasive investigation of RAS. Nonetheless, particularly
with the advent of multislice technology, CTA is capable of
producing very high quality renal arteriograms. It provides a
useful second line where MRA is not possible, for example in
patients with cardiac pacemakers. CTA has a high sensitivity
and specificity (90–98%), and being a cross-sectional tech-
nique provides information about the best projection angles to
use when planning renal artery intervention (Fleischmann
2003). CTA is also of value in the assessment of restenosis
within renal artery stents (Raza et al. 2004).
MRA is noninvasive and does not involve the use of
iodinated contrast media. Non-contrast-enhanced renal
MRA using time-of-flight or phase contrast techniques has
significant limitations. These are largely overcome by using
Gadolinium-enhanced renal MRA. Many series are avail-
able, and the sensitivity and specificity of Gadolinium-
enhanced MRA in the detection of renal artery stenosis have
been reported as 88–100% and 70–100%, respectively
(Zhang and Prince 2004). Like CTA, MRA also allows the
renal artery anatomy to be examined prior to intervention to
facilitate planning which obliques should be used. This not
only shortens the procedure, but also reduces the amount of
iodinated contrast required during intervention. It has more
recently been claimed that MRA can be used for the
detection of FMD (Rountas et al. 2007) although this was
based on only four patients who actually had stenosis.
Furthermore, the total number of renal arteries examined
was only 132, meaning that it remains doubtful as to whe-
ther this technique can exclude the diagnosis.
Unfortunately, it has also become apparent that Gado-
linium contrast agents are associated with nephrogenic
systemic fibrosis (NSF) when administered to patients with
significant renal impairment (Marckmann et al. 2006). The
mechanism is still not understood but the risks of NSF
restrict the use of gadolinium in patients with renal
impairment.
Captopril renal scintigraphy relies on the principle that
administration of the ACE inhibitor produces a significant
reduction in renal blood flow in a kidney affected by RAS.
The technique is rather cumbersome and expensive, and has
largely fallen out of use.
Once the decision has been made to investigate a patient
for RAS, it is now possible to noninvasively establish the
diagnosis. Our first line investigation, in common with
many, if not most, other centres, is renal MRA in patients
who do not have renal impairment. If there is renal
impairment, CTA with good preprocedure hydration will be
considered. If a significant stenosis is revealed, and it is
considered suitable for intervention, the patient will then
undergo renal revascularisation. In our practice there are
two main exceptions to this where we would elect to pro-
ceed directly to catheter angiography. The first is in the
presence of accelerated hypertension in a young patient, in
whom FMD is suspected, as in our view this is the only way
to totally exclude the diagnosis. The second is in patients
presenting with rapidly deteriorating renal function with or
without pulmonary oedema, in whom renal artery stenosis is
strongly suspected. In this setting we would proceed
directly to intervention if a stenosis is found.
4 Technique of Renal Revascularisation
Before commencing the procedure, fully informed consent
is vital. The patients must understand the reasons why the
procedure is being undertaken, be it for uncontrolled
hypertension, renal impairment or flash pulmonary oedema.
In the case of hypertension it should be clear that the only
realistic aim is improved control rather than cure. With
regard to renal impairment, they should understand that the
aim is to halt a decline in renal function rather than to
reverse it. Similarly, renal function may be worsened in a
significant proportion of patients. The risk of losing a kid-
ney altogether is probably around 1%. Patients with a single
kidney must be aware that in this event they would require
dialysis which would most likely be life long, as trans-
plantation is unlikely.
4.1 Renal Angioplasty
The procedure is most commonly performed through a fem-
oral artery approach, and this will described in detail. How-
ever, if required by the patient’s anatomy, for example the
Management of Renal and Visceral Arterial Stenoses 123
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