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34 Interventional radiology and endovascular procedures
Conclusion
Endoleaks are common complications post endovascular aortic aneurysm repair,
and lifelong surveillance is required to avoid continued sac expansion and aneurysm rupture. Multimodality imaging may be required for correct characterization,
which inherently dictates subsequent management. In most cases, ELs are amenable
to endovascular treatment, with open surgical conversion rarely required
A final word from the expert
There are several types of endoleak after endovascular aneurysm repair. Types I and III
require urgent treatment, as there is evidence that these ELs are associated with late
aneurysm rupture and death. Whether type II ELs are a risk factor for late rupture is
controversial, and accordingly there is limited evidence to support intervention. There is
a general consensus, though not evidence based, that an enlarging aneurysm sac in the
presence of a type II EL should be treated.
Treatment of Type I and III ELs involves the insertion of additional endograft components or the
use of large-calibre balloon-expandable stents. Both these techniques require the use of largecalibre vascular sheaths, necessitating either a femoral arteriotomy or a large-vessel closure
device. As a result, these procedures are generally performed in operating theatres, usually by
vascular surgeons or by vascular surgeons in collaboration with interventional radiologists.
Interventional radiologists are key players in the treatment of type II ELs. The main options
involve either embolization of the culprit lumbar and/or inferior mesenteric arteries by the
transarterial route, or direct access into the endoleak cavity by direct percutaneous puncture
of the aneurysm sac. Both routes have their proponents, and there are insufficient data to
inform us as to which route is preferable, or if indeed embolization of type II ELs by either
route is effective in reducing sac growth.
Until conclusive evidence is available, our practice is first to perform type II EL embolization
via the transarterial route, reserving the direct sac puncture technique for failure to access
the endoleak by the transarterial route.
References
1. Harris PL, Vallabhaeneni RS, Desgranges P, et al. Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aor tic aneurysms: the
EUROSTAR experience. J Vasc Surg 2000; 32: 739–49.
2. Iezzi R, Controneo AR, Filippone A, et al. Multidetector CT in abdominal aor tic aneurysm treated with endovascular repair. are unenhanced and delayed phase enhanced
images effective for endoleak detection? Radiology 2006; 241: 915–21.
3. Stolzmann P, Frauenfelder T, Pfammatter T, et al. Endoleaks after endovascular abdominal aor tic aneurysm repair: detection with dual-energy dual-source CT. Radiology 2008;
249: 682–91.
4. Sommer WH, Becker CR, Haack M, et al. Time-resolved CT angiography for the detection
and classication of endoleaks. Radiology 2012; 263: 917–26.
5. Gorich J, Rilinger N, Sok iranski R, et al. Leakages after endovascular repair of aortic aneurysms: classication based on ndings at CT, angiography, and radiography.
Radiology 1999; 213: 767–72.
6. Pitton MB, Schweitzer H, Herber S, et al. MRI versus helical CT for endoleak detection
after endovascular aneurysm repair. AJR Am J Roentgenol 20 05; 185: 1275–81.
7. Lockstein RA, Goldman J, Pukin L, et al. Time-resolved magnetic resonance angiography
as a noninvasive method to characterize endoleaks: initial results compared with conventional angiography. J Vasc Surg 2004; 39: 27–33.
8. Shah A, Stavropoulos SW. Imaging Surveillance following endovascular aneurysm repair.
Semin Intervent Radiol 2009; 26(1): 10–16.
9. Faries PL, Cadot H, Agarwal G, et al. Management of endoleak after endovascular aneurysm repair: cuffs, coils, and conversion. J Vasc Surg 2003; 37: 1155–61.
10. Veith FJ, Baum RA, Ohki T, et al. Nature and signicance of endoleaks and endotension:
summary of opinions expressed at an international conference. J Vasc Surg 2002; 35:
1029 –35.
11. van Marrewijk C, Buth J, Harris PL, et al. Signicance of endoleaks after endovascular
repair of abdominal aortic aneurysms: the EUROSTAR experience. J Vasc Su rg 2002; 35:
461–73.
12. Gelfand DV, White GH, Wilson SE. Clinical signicance of type II endoleak after endovascular repair of abdominal aortic aneurysm. Ann Vasc Surg 2006; 20: 69–74.
13. Jones JE, Atkins MD, Brewster DC, et al. Persistent type 2 endoleak after endovascular
repair of abdominal aortic aneurysm is associated with adverse late outcomes. J Vasc
Surg 2007; 46: 1–8.
14. Greenhalgh RM, The United Kingdom EVAR Trial Investigators. Endovascular versus
open repair of abdominal aortic aneurysm. N Engl J Med 2010; 362: 1863–71.
15. Hobo R, Buth J, EUROSTAR collaborators. Secondary interventions following endovascular abdominal aortic aneur ysm repair using current endografts: a EUROSTAR report. J
Vasc Su rg 2006; 43(5): 896–902.
16. Gilling Smith G, Brennan J, Harris PL, et al. Endotension after endovascular aneurysm
repair: denition, classication, and strategies for surveillance and intervention. J
Endovasc Surg 1999; 6: 305–7.
17. Naughton PA, Garcia-Toca M, Rodriguez HE, et al. Endovascular treatment of delayed
type 1 and 3 endoleaks. Cardiovasc Intervent Radiol 2011; 34: 751–7.
18. Sheehan MK, Barbato J, Compton CN, et al. Effectiveness of coiling in the treatment of
endoleaks after endovascular repair. J Vasc Surg 2004; 40: 430–4.
19. Henrikson O, Roos H, Falkenberg M. Ethylene vinyl alcohol copolymer (Onyx) to seal
type I endoleak: a new technique. Va scu lar 2011; 19(2): 77–81.
20. May J, White GH, Yu W, et al. Conversion from endoluminal to open repair of abdominal
aortic aneurysms: a hazardous procedure. Eur J Vasc Endovasc Surg 1997; 14:4–11.
21. Patatas K, Ling L, Dunning J, et al. Static sac size with a type II endoleak post-endovascular abdominal aortic aneurysm repair: surveillance or embolization? Interact
Cardiovasc Thorac Surg 2012; 15(3): 462–6.
22. Rial R, Serrano FJ, Vega M, et al. Treatment of type ii endoleaks after endovascular repair
of abdominal aor tic aneurysms: translumbar puncture and injection of thrombin into the
aneurysm sac. Eur J Vasc Endovasc Surg 2004; 27: 333–5.
23. Richardson WS, Sternbergh WC 3rd, Money SR. Laparoscopic inferior mesenteric artery
ligation: an alternative for the treatment of type II endoleaks. J Laparoendosc Adv Surg
Tech 2003; 13(6): 355–8.
24. Ryu RK, Palestrant S, Ryu J, et al. Sac hygroma after endovascular abdominal aortic
aneurysm repair: successful treatment with endograft relining. Cardiovasc Intervent
Radiol 2007; 30: 488–90.
25. van Marrewijk CJ, Fransen G, Laheij RJ, et al. Is a type II endoleak after EVAR a harbinger of risk? Causes and outcome of open conversion and aneurysm r upture during followup. Eur J Vasc Endovasc Surg 2004; 27: 128–37.
35Case 4 Management of endoleaks after abdominal EVAR
CASE
5
Carotid artery stenting: how to
treat restenosis
Alessandro Cannavale
Expert commentary Fabrizio Fanelli
Case history
A 63-year-old female with history of arterial hypertension, type II diabetes mellitus,
and smoking underwent carotid endarterectomy (CEA) of the left internal carotid
artery (ICA) because of a symptomatic (transitory dysphasia and right facial weakness resolved within an hour) 75% stenosis. A few years previously the patient
had had a right ischaemic stroke due to complete occlusion of the right ICA, which
resulted in left-side hemiparesis that was partially improved with rehabilitation. The
patient was under antiplatelet therapy with aspirin (100mg/day).
Ultrasound colour Doppler (USCD) conrmed occlusion of the right ICA and the
presence of an irregular hypo-echoic plaque at the level of the left carotid bifurcation
with 75% severe stenosis and a peak systolic velocity (PSV) of 250cm/s. The ndings
were also conrmed with computed tomography angiography (CTA) which revealed
the presence of a soft ulcerated plaque. There was no sign of ischaemia at the level of
the ipsilateral cerebral parenchyma. There was a lacunar area at the level of the right
parietal lobe. CEA was performed and the aspirin dose was increased to 325mg/day
post-operatively.
A year later, the patient reported right hand shaking and transitory right arm
weakness which resolved within 30 minutes. The episode was highly suspicious
of a transient ischaemic attack (TIA), and a USCD was performed which revealed
restenosis at the level of the previous CEA (80%). This time the patient underwent
endovascular treatment with a balloon expandable stent which was deployed at the
level of the recurrent stenosis. A few days later the patient was discharged in good
clinical condition with the following antiplatelet therapy: clopidogrel 75mg/day for
the rst month, followed by aspirin 325mg/day indenitely.
Seven months later, during clinical and imaging follow-up (Table 5.1), USCD
revealed an increase in PSV at the proximal end of the stent (PSV of 325cm/s); the
Table 5.1 Suggested imaging protocol before and after CEA and/or CAS
Pre-procedure Post-procedure
24 h 1 month 3 months 6 months 9 months 12 months
Clinical evaluation
Neurological
examination
USCD
CTA
DSA To be performed in case of abnormal findings or for stent and/or CEA revision
Diagnostic DSA should be avoided in the pre-treatment evaluation because diagnostic angiography of the carotid
arteries is correlated with 0.5% stroke and 2.5% procedure-related complications.
✓ ✓ ✓ ✓ ✓ ✓ ✓
✓ ✓
✓ ✓ ✓ ✓ ✓
✓
In cases of doubt
38 Interventional radiology and endovascular procedures
Clinical tip Imaging
assessment in patients with
carotid restenosis.
Imaging assessment is generally
based on USCD and CTA; however,
if there is still doubt on the exact
grade of restenosis due to beam
hardening artefacts (extensive
calcified plaque, presence of stent)
after USCD and CTA, DSA may be
performed as reference standard
diagnostic to determine whether
any kind of operative treatment is
necessary. Moreover, diagnostic
DSA may be the test of choice in
patients with renal dysfunction
to limit the amount of contrast
material required [2].
end diastolic velocity (EDV) was 110cm/s. These values suggested type I restenosis
according to the classication by Lal et al. [1]. Moreover, the stent appeared collapsed in the same area. A complete neurological examination showed a National
Institutes of Health Stroke Scale (NIHSS) score of 8, a Barthel index of 8, and a
Rankin scale of 3 (moderate disability).
Expert comment Carotid DSA technique
From a conventional common femoral artery approach a 4Fr pigtail catheter is advanced into the
ascending aorta. Images are acquired in the lateral anterior oblique (LAO) projection of 40° in order
to have a better view of the aortic arch and the origin of the supra-aortic vessels. Non-ionic contrast
media (30cm3) is injected via an injector at a flow rate of 20cm3/s and images are acquired at a
frame rate of 3 frames/s. Then a selective injection of the common carotid artery (CCA) is suggested,
preferably with a vertebral catheter.
Evidence base
Leading international guidelines [2–5] advise a close clinical imaging follow-up of patients who have
undergone carotid revascularization. In particular, USCD is considered the first-line imaging tool after the
intervention, and should be performed within at least one month, at six months, and annually thereafter.
USCD is considered to be the leading imaging tool to detect restenosis after CAS/CEA. However,
USCD in-stent restenosis (ISR) criteria are not definitely established because of the reduced
compliance of the stented vessel wall which may increase peak systolic velocity. Recent studies
[1,6–10] suggest several morphological and velocity criteria (PSV, EDV, ICA/CCA ratio) to define ISR,
and we may consider the following thresholds:
●
stenosis <30%: PSV<100cm/s; EDV <40 cm/s
●
stenosis 30–50%: PSV = 100–170cm/s; EDV = 80cm/s
●
stenosis 50%–70%: PSV = 171–299cm/s; EDV = 90cm/s
●
stenosis > 70%: PSV >300cm/s; EDV >120cm/s.
In general a value of PSV above a threshold of 300cm/s is now considered diagnostic for significant
ISR (>70%) [8,9].
Lal et al. [1] described morphological classification of ISR as follows.
●
Type I: focal end stent
●
Type II: focal intra-stent
●
Type III: diffuse intra-stent
●
Type IV: diffuse proliferative
●
Type V: total occlusion.
Clinical tip Clinical and neurological assessment
Clinical assessment includes complete neurological evaluation with the National Institute of Health
Stroke Scale (NIHSS), the Barthel index, and the modified Rankin scale.
The NIHSS is a 15-item neurological examination scale used to evaluate the effect of acute cerebral attack
on the levels of consciousness, language, neglect, visual field loss, extra-ocular movement, motor strength,
ataxia, dysarthria, and sensory loss. A trained observer rates the patient’s ability to answer questions and
perform activities. Ratings for each item are scored with 3–5 grades with 0 as normal, and there is an
allowance for untestable items. Assessment of a single patient requires less than 10 minutes to complete.
The Barthel index and the modified Rankin scale should also be used to evaluate the degree of disability or
dependence in the daily activities, especially in patients with history of previous neurological symptoms.
The components of the Barthel index include feeding, moving from wheelchair to bed and returning,
grooming, transferring to and from a toilet, bathing, walking on a level surface, going up and down
(continued)
stairs, dressing, and bowel and bladder continence. Each item is assessed by a score (1–2–3 or
5–10–15), reaching a potential maximum total of 20 or 100 scores depending on the institution.
The Rankin scale runs from perfect health without symptoms (0) to death (6).
0 No symptoms.
1 No significant disability: able to carry out all usual activities, despite some symptoms.
2 Slight disability: able to look aftertheir own affairs without assistance, but unable to carry out all
previous activities
3 Moderate disability: requires some help, but able to walk unassisted.
4 Moderately severe disability: unable to attend to own bodily needs without assistance, and unable to
walk unassisted.
5 Severe disability: requires constant nursing care and attention, bedridden, incontinent.
6 Dead.
CTA revealed deformation of the stent at the level of its proximal part (Figure 5.1).
Cerebral CT was also included in the pre-treatment protocol to assess recent/previous
cerebral damages; no recent signs of cerebral ischaemia/haemorrhage were detected.
The lacunar area in the right cerebral parenchyma was conrmed. To assess any
eventual cerebral injury MRI was also performed using diffusion-weighted imaging
(DWI) sequences, which did not show any acute ischaemic cerebral lesion (Figure 5.2).
39Case 5 Carotid artery stenting: how to treat restenosis
(a) (b) (c)
Figure 5.1 CT angiography: (a, b) Multiple intensity projections (MIPs) and axial reconstructions of the left
carotid artery show deformation of the proximal end of the stent (white arrow) with a severe restenosis (70%) of
the internal carotid artery. Note also hypoplasia of the right vertebral artery (red arrow). (c) MIP reconstruction
shows complete occlusion of the right internal carotid artery; the external carotid artery appears patent.
Figure 5.2 Pre-operative brain MRI: DWI
sequences confirmed the lacunar area within the
right parietal lobe. There is no evidence of recent
ischaemic lesions.
Expert comment
Evaluating the indications for
re-intervention: this patient was
asymptomatic but with significant
restenosis (ISR >50%) and with
deformation of the stent. Even
though the guidelines are not
completely clear for such cases
[2–5], this is a high-risk patient,
and new endovascular treatment is
considered as the most appropriate
approach in the case of restenosis
after stenting/CEA.
40 Interventional radiology and endovascular procedures
Treatment with placement of a new carotid stent was decided after a multidisciplinary meeting. The patient was prepared in standard sterile condition. Aspirin
(325mg/day) was maintained prior to the procedure, and 75mg clopidogrel was
administered 24 hours before the procedure.
The procedure was performed without sedation to allow continuous monitoring of the patient’s neurological conditions. The right common femoral artery
was punctured in a retrograde fashion under local anaesthesia (mepivacaine 2%;
Industria Farmaceutica Galenica Senese, Siena, Italy). A 7Fr introducer sheath
(25cm) was placed through the common femoral artery and a bolus of 75IU/
kg of heparin was administered. Left CCA catheterization was performed using
a ‘direct approach’ technique with a 7Fr guiding catheter (Mach 1–40°; Boston
Scientic, Natick, MA, USA). The guiding catheter was managed in combination
with a standard 0.035 inch (180cm) angled-tip hydrophilic guidewire (Terumo
Co, Tokyo, Japan) to enter the CCA. The activated clotting time (ACT) was kept
between 275 and 300 seconds. To avoid thrombus formation, the guiding catheter
was connected to a pressurized heparinized saline bag in order to ush its inner
lumen continuously.
Angiography conrmed signicant restenosis at the third proximal of the stent
with deformation of the stent mesh (Figure 5.3a). AP and lateral angiography of the
cerebral vascularity was then performed. Subsequently a lter device (Angioguard
6mm; Cordis Europe, Waterloo, Belgium) was advanced, crossing the stenosis into
the third distal of the extra-cranial part of the ICA (Figure 5.3b). A 7mm × 3cm
stent (Precise Rx; Cordis Europe, Waterloo, Belgium) was placed at the level of
the lesion with its proximal end at the CCA level (Figure 5.3c). Post-dilation of
the stent was performed using a low-prole rapid-exchange balloon (5.5mm in
diameter) in accordance with the stent diameter (Figure 5.3d). Immediately before
stent dilation, 1mg of atropine was injected intravenously to prevent sinus reex.
Temporary dysphasia, which resolved within 2 minutes, occurred immediately
after stent dilation. After stent deployment and before lter removal, angiography
was performed to ‘clean’ any possible plaque debris from the inner lumen of the
stent (Figure 5.3e). After lter removal, nal angiography showed no evidence
of arterial spasms and good ow within the stent, with restoration of the normal vessel calibre. Finally an angiogram of the intracranial circle in two projections showed good ow within the arteries (Figure 5.3f). A vascular closure device
(Angioseal 8Fr; St Jude Medical, St Paul, MN, USA) was used to seal the right
common femoral access.
To assess any eventual cerebral injury DWI MRI was performed, which did not
show any acute ischaemic cerebral lesion. Post-procedural care involved monitoring vital parameters for 24 hours (controlling blood pressure and heart rate) and
performing a complete clinical–neurological examination. Neurological examination and NIHSS score (8 as before the procedure) did not reveal any changes
compared with the neurological status of the patient before the procedure. The
patient was discharged after 2 days in a stable clinical condition with antiplatelet
therapy: aspirin 325mg/day indenitely and clopidogrel 75mg/day for 4 weeks.
She was followed up by regular clinical and imaging examinations. She remained
asymptomatic and follow-up USCD over two years did not show any further ISR
(Figu re 5.4).
41Case 5 Carotid artery stenting: how to treat restenosis
)(
(a)
(e) (f)
Figure 5.3 (a) Selective angiography of the left common carotid artery confirms the deformation of the
proximal end of the stent with the presence of severe in-stent stenosis. (b) A filter device is advanced
through the stent until the third distal of the extracranial part of the internal carotid artery. (c, d) A selfexpandable stent (7mm × 3cm; Precise Rx, Cordis) was released at the level of stenosis and then dilation
with low-profile undersized balloon was performed. (e) A final angiogram before removal of the filter
shows expansion of both stents with good flow along the entire internal carotid artery. (f) Arteriography
of the intracranial circle shows good flow in the contralateral cerebral vessels.
(b) (c
d)
Figure 5.4 After two years, USCD shows good flow within the stents with normal values of PSV
(83.4cm/s) and EDV (46.3cm/s). Note minimal parietal intimal hyperplasia alongside the stent wall.
42 Interventional radiology and endovascular procedures
Discussion
Recurrent stenosis after carotid artery stenting (CAS) is a relatively rare condition
with 3–15% incidence in ve years follow-up [1,2]. The majority of ISRs occur within
the rst year after intervention and they are mainly related to neo-intimal hyperplasia (early ISR) or recurrent atherosclerosis (late ISR). Restenosis rates appear to be
signicantly higher after CAS than after CEA; however, this is not always linked to
symptoms [9,11,12].
Landmark trial CREST trial: restenosis after carotid artery stenting and endarterectomy [9].
A prospective randomized multicentre trial was performed at 117 clinical centres in the USA and
Canada between 21 December 2000 and 18 July 2008 which included 2,191 patients (1,086 treated
with CAS; 1,105 underwent CEA). Prospective USCD was performed at baseline and at 1, 6, 12, 24,
and 48 months after revascularization. Sixteen Doppler waveform samples were obtained at every
examination: eight samples were taken from each side of the neck, six at 1–2cm intervals along the
common and internal carotid arteries, one from the external carotid artery, and one from the vertebral
artery. Waveform: 60° angulation—highest PSV to identify restenosis with a threshold of 300cm/s.
●
Secondary analysis of CREST trial, main endpoint: composite of restenosis (≥70% diameter reducing
stenosis) or complete occlusion at two years.
●
Two-year composite outcome (restenosis and occlusion): 120 patients (58 CAS; 62 CEA). Frequency
of restenosis (Kaplan–Meier estimation) was 6.0% for CAS and 6.3% for CEA (hazard ratio (HR) 0.90,
0.95% CI 0.63–1.29; p = 0.58).
●
Restenosis alone (113 patients): 56 CAS and 57 CEA Kaplan–Meier estimate of the two-year
frequency of restenosis was 5.8%.
●
Risk of neurological events: patients who had restenosis or occlusion within two years were at
greater risk for ipsilateral stroke after the peri-procedural period up to the end of follow-up than
those who did not have restenosis (HR 4.37, 95% CI 1.91–10.03; p=0.0005).
Recurrent stenosis after stenting may also be related to stent fracture or deformation, which may occur in 2–29% of patients treated with CAS [13]. Neo-intimal
proliferation has been related to peri-interventional inammation markers and may
be inuenced by stent size and geometry [12,14]. Open-cell stents and highly calcied plaques are considered independent predictors of stent deformation [13]. The
patient described here developed restenosis one year after CEA and seven months
after CAS. Both surgical and endovascular intervention represent a vessel injury
which may lead to an inammation process (increased values of plasma C-reactive
protein have been found by Wasser et al. [15]) and neo-intimal proliferation through
the stent mesh. Recent studies have highlighted potential clinical and technical risk
factors for ISR after CAS: advanced age [12,14]; previous treatment for a radiogenic
stenosis or a recurrent stenosis after CEA [12]; contralateral ICA occlusion [12]; signicant residual stenosis after CAS (PSV >120cm/s)[16]; presence of cardiovascular
risk factors such as tobacco use; diabetes mellitus; dyslipoproteinemia; and certain
procedure-related factors (a narrow or long stent, insufcient stent adaptability after
CAS or the use of multiple stents) [12]. In the case described here we found a history of contralateral ICA occlusion and previous stenting for restenosis after CEA, so
that the increased PSV of 325cm/s at level of the proximal end of the stent, which
appeared deformed, was highly suggestive for in-stent restenosis. This would reinforce the need for regular and closer clinical and imaging follow-up of such patients
who are sometimes referred to the emergency department because of the sudden
appearance of neurological symptoms.
CT angiography after USCD is considered the reference imaging examination for
the assessment of post-CAS/CEA restenosis and the depiction of the anatomy of
supra-aortic vessels in order to plan endovascular or surgical intervention. The role
of MR angiography in patients with carotid stents is still controversial: poor lumen
visibility is linked to carotid stainless steel stents, but the majority of (nitinol) stents
can be assessed with MRI [17]. Cerebral-MRI is now in widespread use for pre- and
post-procedure assessment of ischaemic neurological events.
Neurological assessment (general neurological examination, NIHSS scale, Barthel
index, and Rankin scale) should be performed before and after every procedure so
that improvement or lack of improvement can be noted. It is highly recommended
that, as well as neurological evaluation, medical therapy should be adjusted before
treating restenosis. In fact correct medical therapy is a leading method of preventing
restenosis and thus the development of adverse neurological events such as TIA or
ischaemic stroke.
Clinical tip
During clinical follow-up in these patients the physician should also consider specific issues.
●
After first successful recanalization the mean arterial pressure should be reduced to 10–20% less than
the baseline value.
●
Presence of carotid sinus dysfunction: prolonged bradycardia and/or hypotension requiring
intravenous vasopressors or ionotropic agents.
●
Fluctuation of blood pressure: use 24 hour monitoring of pressure because of increased baroflex
sensitivity in patients who have undergone CAS or CEA.
●
Recent/previous TIA or stroke: our patient had a prior stroke event and subsequently two episodes
of TIA related to the ‘native’ left ICA stenosis and then to restenosis of the CEA. However, the
NIHSS score remained stable because TIA episodes usually do not have a permanent influence
on neurological function. Some authors [18] have recently reported that in the case of unilateral
ICA occlusion, contralateral endovascular treatment resulted in delayed cerebral blood flow
haemodynamic improvement in both cerebral hemispheres.
43Case 5 Carotid artery stenting: how to treat restenosis
Learning point Antiplatelet and anticoagulant therapy to prevent ISR and secondary
neurological events.
Antiplatelet and anticoagulant therapy for secondary prevention of stroke has recently been addressed
in current guidelines [19].
●
Aspirin (50–325mg/day) monotherapy (Class I; Level of Evidence A); a combination of aspirin 25mg
and extended-release dipyridamole 200mg twice daily (Class I; Level of Evidence B); clopidogrel
75mg monotherapy (Class IIa; Level of Evidence B) are all acceptable options for initial therapy.
●
The addition of aspirin to clopidogrel increases risk of haemorrhage and is not recommended for
routine secondary prevention after ischaemic stroke or TIA (Class III; Level of Evidence A).
●
For patients who have an ischaemic stroke while taking aspirin, there is no evidence that increasing
the dose of aspirin provides additional benefit (Class IIb; Level of Evidence C).
Considering our case, initial antiplatelet therapy alone (aspirin 100mg) after a
previous right-sided stroke (occlusion of right ICA) was generally correct, obviously
accompanied by control of hypertension and diabetes, and encouraging cessation
of tobacco use. Moreover, she had a contralateral TIA treated with CEA; after that
aspirin dosage was increased to 325mg/day. However, a non-denitive control of
restenosis and neurological events was achieved, as stated in the guidelines.
After CEA restenosis was treated with stenting placement, antiplatelet therapy was
switched to clopidogrel 75mg/day for the rst month and then aspirin 325mg/day
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