• ~10-20% of ischemic strokes are caused by internal carotid artery (ICA) stenosis
    • the risk of stroke or vascular death in symptomatic ICA stenosis >70% is up to 26%/2 years, depending on symptomatology, gender, and severity of stenosis  [Rothwell, 2005]
    • for asymptomatic ICA stenosis >60%, the risk is ~11%/5 years
  • revascularisation procedures lead to a reduced risk of stroke,  benefit from surgery is present only if the perioperative risk is < 6% or 3% (asymptomatic stenoses) → indications for revascularisation are discussed here
  • endovascular treatment (carotid angioplasty with stenting – CAS) is an alternative to carotid endarterectomy (CEA)
  • since 1994, there have been significant improvements in technology (including the controversial distal protection) and experience with stenting
  • new coated stents promise to bring additional safety see here
  • CAS and CEA equivalence regarding outcome was demonstrated by randomized trials  (e.g., SAPPHIRE and CREST)
  • studies were designed to demonstrate noninferiority and focused on patients at high operative risk (CAD,  cardiac failure, pulmonary disease, etc.)
    • CAS does not pose an increased risk compared to CEA and prevents at least the same number of strokes as CEA
  • in patients with extensive white matter lesions on CT/MRI (ARWMC score ≥ 7) prefer CEA (ICSS trial )
Carotid artery stenosis (ultrasound, CTA, MRA, DSA)
Trial n of patients
30 days m/m long term m/m
CARESS (2003) 397 2 vs 3%
CAVATAS (2001) 504 10 vs 10% 14.3 vs 14.2
SAPPHIRE (2004) 334 4.8 vs. 4.9% 12.2 vs 20.1
CREST (2010) 2502 5.2 vs 4.6% 7.2 vs 6.8% / 4 years


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  • significant tortuosity and/or profound atherosclerosis of the aortic arch or proximal CCA/brachiocephalic trunk preventing safe catheter insertion
  • the presence of large calcified plaques that prevent remodeling of the artery by CAS
  • distal ICA diameter < 3 mm making placement of a distal protection impossible (relative contraindication)
  • intracranial aneurysm > 5 mm or AV malformation (relative contraindication)


  • standard blood test (CBC, coagulation, basic metabolic panel included creatinin and urea)
  • insert intravenous cannula and urinary catheter
  • shave the groin (if transfemoral access is chosen)
  • sign the informed consent for anesthesia and for the CAS procedure
  • take measures to prevent contrast induced nephropathy (CIN) → see here


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Perioperative monitoring

  • the procedure is performed in cooperation of an experienced neuroradiologist, anesthesiologist, and a neurologist
  • analgosedation is preferred
  • basic monitoring:
    • ECG and blood pressure (every 5 minutes)
      • correct BP correction is necessary throughout the procedure (prevention of hyperperfusion syndrome) → parenteral antihypertensives
      • CAVE bradycardia, sometimes it is necessary to administer ATROPIN 0.5 mg i.v. , it can also be administered prophylactically
    • a pulse oximetry
    • patient’s neurological status  (level of consciousness, speech, visual field, acral motor skills)
  • TCD/TCCD monitoring
    • haemodynamic information   (hyperperfusion syndrome  is associated with a significant increase in blood flow velocity in the MCA during the procedure, with a concomitant decrease of PI and RI)
    • detection of embolization
      • microembolization (MES)
        • during the administration of contrast agent (dissolved air bubbles)
        • detection of particles released during critical phases of the procedure (distal protection filter insertion, pre-dilatation, stent deployment, post-dilatation, and protection withdrawal
        • increased risk of stroke  in case of > 5 series of microembolizations
      • macroembolization leads to transient or permanent flow restriction in the MCA (vessel occlusion)

CAS technique

Carotid angioplasty with stenting

CAS in patient with radiation-induced vasculopathy

Carotid angioplasty with stenting

Postoperative monitoring

  • extraction of the sheath and puncture closure on angio suite (e.g. angioseal)
  • the patient is observed in the ICU
  • continue monitoring of vital signs (BP measurement in the first hour every 15 min, then every 30 min for at least 24 h)
  • monitor complications and  neurological status (GCS, NIHSS)
  • doppler ultrasound within 24 h
    • record PSV in the stent middle section and distally
    • stent artifactually increases flow velocity
  • continue with dual antiplatelet therapy (DAPT) for ≥ 4 weeks (1-3 months)
Ultrasound follow up after CAS


Central complications
Carotid angioplasty with stenting
1.1 Distal complications
  • distal micro/macro embolization
  • hyperperfusion syndrome (incl. hemorrhagic transformation)
  • hypoperfusion due to obturation of the distal protection filter with disloged thrombi
  • hypoperfusion during prolonged inflation of the angioplasty balloon
  • difficulty with retraction or intra-stent entrapment of the distal protection filter
1.2 In-stent complications
  • artery dissection or perforation
  • vasospasms  Vasospasms provoked by the distal protection
  • deformation, rupture, or migration of the stent
  • stent thrombosis
1.3 Proximal complications
  • aorta / CCA dissection or perforation
  • vasospasms
Peripheral (access-site) complications
Femoral arterial access is commonly used for CAS,  but radial or brachial approach can be considered. Complications range from asymptomatic to life-threatening conditions.
  • femoral artery thrombosis
  • dissecting pseudoaneurysm or A-V fistula in the groin
  • groin hematoma (treatment required in less than 0.5% of the cases)
  • retroperitoneal bleeding
    • an infrequent but life-threatening complication, with an incidence of 0.15%
    • hemodynamic instability up to a hemorrhagic shock are the typical signs
    • CT scan is mandatory
Systemic complications
  • hemodynamic instability with cerebral hypoperfusion
    • hypotension and bradycardia are common in CAS and are particularly worrisome in the high-risk patients
    • typically appearing after carotid sinus manipulation leading to parasympathetic activation
  • allergic reaction
  • contrast-induced nephropathy (CIN) and contrast-induced encephalopathy (CIE)

Distal embolisation

  • microembolization (mostly) x microembolization
    • responsible for a substantial portion of the 30-day mortality and morbidity
  • therefore distal protective devices were developed – placed distal to the stented area they should prevent cerebral embolization of particles released during the procedure
    • a meta-analysis of approximately 2400 patients showed that the 30-day mortality and morbidity without and with protection was 5.5% and 1.8%, respectively  [Kastrup, 2003]
  • the use of distal protection is debated; many centers have good results without protection
    • its insertion is associated with additional manipulation in carotid bifurcation, which itself increases the risk of embolization or vasospasm
    • other complications such as filter thrombosis, stent entrapment, stent damage are also a consideration
  • consider mechanical recanalization in case of symptomatic distal embolization

Stent thrombosis

  • the main mechanism of acute stent thrombosis is the platelet activation
    • the highest risk in the first 72h
    • the incidence of acute and subacute complete carotid stent thrombosis is 0.5-2%
  • in addition to occlusion, mural thrombi occur and can embolize to the brain
  • any change in the patient’s neurological status after the procedure should raise suspicion of acute stent thrombosis and urgent diagnosis (most easily by duplex ultrasound), and therapy with Ilb/IIIa receptor inhibitors is required
  • proper premedication (see above) and proper stent placement are the keys to the prevention of such complication
    • prophylactic add-on therapy with i.v. abciximab reduces the risk of ischemic complications but increases the risk of bleeding at the same time
  • therapy → abciximab iv. or i.a
Stent thrombosis on the ultrasound examination

Problems with distal protection extraction and its wedging in the stent

  • failure of distal protection retrieval is rarely impossible to overcome percutaneously
  • careful manipulation is crucial
  • it may be helpful to move the patient’s head, have the patient swallow or chose a higher torquability retrieval sheath. In case of filter fracture, it is recommended to  ‘jail’ the filter against the arterial wall with an additional stent

Stent deformation, rupture and migration

  • in case of stent migration, endovascular microsnare loops allow stent removal (stentectomy) in most cases  (Oh, 2012)
  • deformation is more common with balloon-expandable stents, with self-expandable stents the risk is low, uncorrectable stent deformation requires surgical revision
  • stent rupture may lead to a dissection with possible pseudoaneurysm formation   Stent rupture


  • early restenosis (intimal hyperplasia) < 2-3 years   Restenosis after CAS (CTA)
    • low risk of embolization
  • late restenosis (recurrence of atherosclerosis) > 3 years
    • lower risk of restenosis with stent use
    • higher risk with PTA alone and primary insufficient dilation of the artery
Restenosis after CAS on CTA


  • neurosonology – the 1st choice method, always examine velocities within the stent and in the proximal and distal segment Ultrasound follow up after CAS in a patient with carotid artery dissection Ultrasound follow up after CAS  Stent thrombosis on the ultrasound examination
  • MRA may be burdened by artifacts Stent on MRA follow-up
    • contrast-enhanced MRA (CE-MRA) is recommended rather than 3D-TOF
    • when a stent graft is used (e.g., for aneurysm treatment), contrast MRA is inconclusive, CTA should be performed   Artifact from the stentgraft on MRA Stentgraft on CTA
    • modern stents are MR compatible and should not migrate in the magnetic field
  • CTA   Patent carotid stent on CTA follow up
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