ISCHEMIC STROKE / PREVENTION

Carotid angioplasty with stenting (CAS)

Created 27/01/2022, last revision 04/02/2023

  • approx. 10-20% of ischemic strokes are caused by significant carotid stenosis (TOAST 1)
    • the risk of stroke or vascular death with symptomatic ICA stenosis >70% is up to 26%/2 years, depending on symptoms, gender, and severity of the stenosis  [Rothwell, 2005]
    • risk of stroke in asymptomatic carotid stenosis of >60%  is ~11%/5 years
    • high-risk plaque characteristics and a higher degree of stenosis are associated with an increased risk    Five-year actuarial risk of ipsilateral carotid territory ischemic stroke by decile of symptomatic carotid stenosis. Patients with 70% to 99% stenosis and narrowing of the poststenotic ICA are grouped separately. Numbers above error bars represent the number of patients in each decile (Rothwell, 2000)
  • revascularization procedures reduce the risk of stroke; the benefit is only present when the perioperative risk is < 6% (symptomatic) or 3% (asymptomatic stenosis) → indications for revascularization are discussed here
  • endovascular treatment (carotid angioplasty and stenting – CAS) is an alternative to carotid endarterectomy (CEA)
  • since 1994, there have been significant improvements in technology (including proximal and distal embolic protection devices – EPD) and experience with stenting
  • new coated stents promise additional safety → see here
  • randomized trials showed similar efficacy/safety of CAS and CEA  (e.g., SAPPHIRE and CREST)
  • trials were designed to demonstrate non-inferiority and focused on patients with high surgical risk due to comorbidities (CAD, heart 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
  • patients with extensive white matter lesions on CT/MRI (ARWMC score ≥ 7) should undergo CEA (ICSS trial)
Carotid artery stenosis (ultrasound, CTA, MRA, DSA)

Trials comparing CEA and CAS

Trial N of patients
 30 days mortality/morbidity
 long-term mortality/morbidity
CARESS (2003) 397 2 vs. 3% –
CAVATAS (2001) 504 10 vs 10% 14.3 vs. 14.2
SAPPHIRE (2004) 334 4.4 vs. 9.9%
(stroke+MI+death)
 12.2 vs. 20.1
CREST (2010) 2502 5.2 vs. 4.6% (CEA)
(stroke+MI+death)
4.1% vs 2.3% (CEA)
(perioperative stroke)
 primary endpoint:  7.2 vs 6.8% / 4 years
stroke+death 6.4 (CAS) vs 4.7% (CEA)

Indications

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Contraindications

  • significant tortuosity and/or severe atherosclerosis of the aortic arch or proximal CCA/BCT, that prevent safe catheter insertion
  • elongated aortic root, bovine arch
  • tortuous iliac artery
  • large calcified plaques preventing the artery remodeling
  • distal ICA diameter < 3 mm preventing the use of distal protection (relative contraindication, proximal protection can be used)
  • intracranial aneurysm > 5 mm or AV malformation (relative contraindication)

Procedure

  • order standard laboratory tests (CBC, coagulation test, basic metabolic panel) and other examinations required by an anesthesiologist
  • insert IV cannula and short-term urinary catheter and shave the groin  (if transfemoral access is chosen)
  • educate the patient about the risks, benefits, and alternatives of the procedure; the patient must sign an informed consent

Premedication

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Periprocedural monitoring

  • the procedure is performed in cooperation with an experienced neuroradiologist, anesthesiologist, and a neurologist
  • analgosedation is preferred
  • basic monitoring:
    • ECG and blood pressure (every 5 minutes)
      • correct BP correction is critical throughout the procedure (prevention of hyperperfusion syndrome) → parenteral antihypertensives
      • if bradycardia occurs, it may be necessary to administer ATROPIN 0.5 mg IV  (which may also be given prophylactically)
    • a pulse oximetry
    • patient’s neurological status  (level of consciousness, speech, visual field, acral motor skills)
  • TCD/TCCD monitoring (optional)
    • hemodynamic 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 contrast administration (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 with > 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

 Post-procedural management

  • retrieve filter (aspirate filter prior to retrieval if slow flow occurs)
  • remove the sheath and secure the groin  (use Angioseal or other devices)
  • observe the patient in the ICU
  • continue monitoring of vital signs with careful BP control (check it every 15 minutes in the first hour, then every 30 minutes for at least 24 hours)
  • check for complications and monitor neurological status (GCS, NIHSS)
  • perform control Doppler ultrasound (neurosonography) within 24 hours
    • record PSV in the proximal, mid, and distal portions of the stent and in the segment distal to the stent
    • stent artifactually increases flow velocities
  • after the procedure, continue dual antiplatelet therapy (DAPT; aspirin 100 mg + clopidogrel 75 mg) for at least 4 weeks (1-3 months)
  • then switch the patient to monotherapy (either ASA or CLP)
Ultrasound follow up after CAS

Complications

Central complications
Carotid angioplasty with stenting
1.1 Distal complications
  • distal micro/macro embolization
  • hyperperfusion syndrome (incl. hemorrhagic transformation)
  • hypoperfusion (slow-flow) due to distal protection filter occlusion with dislodged thrombi and plaque debris
  • 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
  • stent deformation, rupture, or migration
  • 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 approaches may be considered. Complications range from asymptomatic to life-threatening conditions
  • femoral artery thrombosis
  • dissecting pseudoaneurysm or groin AV fistula (shunt)
  • groin hematoma (requires treatment in less than 0.5% of cases)
  • retroperitoneal bleeding
    • a rare 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 of concern in the high-risk patients
    • typically occurs after carotid sinus manipulation leading to parasympathetic activation
  • contrast-related complications

Distal embolization

  • microembolization (most common) x microembolization
    • responsible for a substantial portion of the 30-day mortality/morbidity
  • distal and proximal protection devices prevent cerebral embolization
    • a meta-analysis of approximately 2400 patients showed that the 30-day mortality and morbidity were 5.5% and 1.8% (without and with protection)  [Kastrup, 2003]
  • use of distal protection is debated; many centers have comparable results without it
    • 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, and damage must be considered
  • mechanical recanalization or intraarterial thrombolysis may be performed in the 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 carotid stent thrombosis is 0.5-2%
  • besides 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 requires urgent diagnosis (most easily by duplex ultrasound) and therapy with Ilb/IIIa receptor inhibitors
  • proper premedication (see above) and stent placement are key to the prevention of such complication
    • prophylactic add-on therapy with IV abciximab reduces the risk of ischemic complications while increasing the risk of bleeding
  • therapy →  IV or IA abciximab
Stent thrombosis on the ultrasound examination

Vasospasms

  • most vasospasms are transient and resolve after catheter removal  Rozvoj vazospazmů v průběhu stentingu ACI  Vazospazmus ACI na DSA
  • if hemodynamically severe vasospasm persists, PTA or vasodilators (local/systemic) may be used

Stent deformation, rupture or migration

  • endovascular microsnare loops have been developed to remove the migrated stent (stentectomy)   (Oh, 2012)
  • deformation is more common with balloon-expandable stents compared to self-expandable stents
  • uncorrectable stent deformation may require surgical revision
  • stent rupture may result in dissection with possible pseudoaneurysm formation  Ruptura stentu

Problems with distal protection extraction and its wedging in the stent

  • difficulties with distal protection retrieval can usually be resolved percutaneously
  • careful manipulation is crucial
  • it may be helpful to move the patient’s head, have the patient swallow, or choose a more torquable retrieval sheath. In case of filter fracture, it is recommended to ‘jail’ the filter against the arterial wall with an additional stent

Restenosis

  • early restenosis (intimal hyperplasia) < 2-3 years   Restenosis after CAS (CTA)
    • low risk of embolization
  • late restenosis (recurrent atherosclerosis) > 3 years
    • lower risk of restenosis with stenting compared to angioplasty alone
Restenosis after CAS on CTA

Follow-up

  • neurosonology – method of choice; always examine the velocities within the stent and in proximal and distal segments Ultrasound follow up after CAS in a patient with carotid artery dissection Ultrasound follow up after CAS  Stent thrombosis on the ultrasound examination
  • MR angiography may be subject to artifacts Stent on MRA follow-up
    • contrast-enhanced MRA (CE-MRA) is recommended instead of 3D-TOF
    • when a stent graft is used (e.g., for aneurysm treatment), contrast-enhanced MRA is inconclusive and 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
  • CT angiography   Patent carotid stent on CTA follow up

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Carotid angioplasty and stenting (CAS)
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