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Carotid stenting complications

An article from the e-journal of the ESC Council for Cardiology Practice

Carotid angioplasty and stenting (CAS) for the treatment of severe carotid obstructive disease is becoming more widely performed, and is now widely accepted as a less invasive technique that provides an attractive alternative for many patients, particularly those with significant co-morbidities. Complication rates range from 0.9% to 9.3% following the experience of different centres (1-10). It is of fundamental importance that physicians be able to recognise and manage the various possible complications of carotid angioplasty and stenting.

I - Introduction

The potential procedural and peri-procedural complications that may be related to carotid angioplasty and stenting may be categorised as minor or major complications:

A - Minor complications

  • Carotid artery spasm
  • Sustained hypotension / bradycardia
  • Carotid artery dissection
  • Contrast encephalopathy (very rare)
  • Minor embolic neurological events (TIAs)

B - Major complications

  • Major embolic stroke
  • Intracranial hemorrhage
  • Hyperperfusion syndrome
  • Carotid perforation (very rare)
  • Acute stent thrombosis (very rare)
  • Complications at the site of the vascular access

A- Minor Complicatons

1/ Carotid artery spasm

Spasm of the distal internal carotid artery (ICA) following distal deployment of a filter is a complication that usually resolves spontaneously after the filter-wire has been removed from the vessel. In our experience, a gentle approach as well as the use of soft-tipped filter-wires minimises the occurence of distal carotid artery spasm.
A flow-limiting spasm could be a potential hazard in the presence of occlusion of the contralateral ICA or in cases of incomplete circle of Willis.
Intra-arterial administration of 100 to 400 micrograms of nitroglycerin through the guiding sheath generally leads to a rapid resolution of the spasm.

2/ Transient bradycardia and hypotension

Transient sinus bradycardia or asystole are relatively common physiological responses to balloon dilatation of carotid bifurcation lesions, particularly during post-dilatation stenting (5). This phenomenon is less commonly observed with treatment of re-stenotic lesions following carotid endarterectomy (CEA) because the receptors may have been denervated by the surgical dissection.
These hemodynamic instabilities are effectively avoided by pretreatment with 0.5 to 1 mg of intravenous atropine. Large doses of atropine should be avoided in elderly patients, as they can result in confusion and make accurate neurological assessment more difficult.
Careful hemodynamic monitoring of all patients during the procedure and in the first hours following carotid artery stenting (CAS) is crucial for early recognition and management of the situation.

Note that in this clinical setting, there are other potential sources of hypotension which must be excluded:

  1. Volume depletion 
  2. Cardiac pathologies
  3. Bleeding from the site of vascular access.

Hypotension should be promptly corrected in the following situations:

  • Contralateral ICA occlusion
  • Significant vertebrobasilar disease
  • Additional intracranial stenosis
  • Periprocedural cerebral ischemia secondary to an embolic event.

Generally, hypotension responds well to intravenous hydration and/or small dose of intravenous vasopressors.

3/ Severe, sustained hypotension

Persistent hypotension has been reported to occur following 4 to11% of carotid stenting procedures and was not usually associated with any adverse clinical events in the hospital or during the 30-day follow-up period (5). Adverse events related to this phenomenon did, however, occur in two small series (11,12). The degree of hypotension appears to be more pronounced in patients with heavily calcified lesions.
Independent predictors of sustained hypotension following CAS (6,8) are:

  • Age
  • Transient hypotension during the balloon dilatation
  • The use of self-expanding stents
  • Severe calcifications

The mechanism of sustained hypotension following CAS may be explained on the basis of the carotid sinus reflex arc (13). Balloon dilatation and the radial force of the self-expanding stent result in increased radial pressure within the carotid sinus, leading to inappropriate activation of baroreceptors and subsequent development of sustained hypotension.
Careful hemodynamic monitoring in the 24 hours following CAS is crucial for proper management of patients with this complication.
Generally, this phenomenon responds well to intravenous hydration and prolonged administration of small doses of intravenous vasopressors.

4/ Distal embolisation (minor: TIAs; MAJOR: STROKES)

Symptomatic distal embolisation is the most frequent and important complication of CAS (1,2). It is caused by the release of material (thrombotic, necrotic, or atherosclerotic) from the site of the lesion during the intervention (7,8,14).
Extensive use of embolic protection devices has been demonstrated to reduce the incidence of this complication (6,10)

Risk factors for periprocedural distal embolizstion during CAS are the following:

Carotid lesion: a. Soft plaque, fresh thrombus.
Medical treatment: a. Poor pretreatment with double antiplatelet agents
b. Insufficient heparin during procedure (check active coagulation time!).
Stenting technique: a. Unprotected procedure
b. Aggressive manipulation of the guide wire
c. Aggressive balloon dilatation prior to or after stent deployment
d. Forceful introduction of a high-profile stent across a heavily calcified tight lesion
e. Prolonged, aggressive attempts to acess a highly atherosclerotic, tortuous common carotid artery

It is essential to monitor a patient's neurological status after each step of the procedure. If a significant change in neurological status appears and does not resolve within a short lapse of time, general care should be instituted with emphasis on maintaining normal blood pressure, expanding intravenous volume, stabilising the patient's heart rate, maintaining a viable airway, and administering oxygen as necessary. If the patient becomes uncooperative and agitated, particularly if he or she has a compromised airway, the assistance of an anesthesiologist should be sought.

Intracranial angiography is performed in anteroposterior and lateral projections. If possible, angiography of the contralateral carotid artery and at least one vertebral artery should be performed. Angiograms must be examined carefully to determine the site and extent of intracranial vessel embolism. The most likely sites of intracranial embolism are the distal ICA and the middle cerebral artery with its branches. Large vessel occlusion is usually easy to detect, but embolism in the smaller branches requires careful scrutiny. Acute occlusion of small branches may be detected only by comparing post- and pre-procedural angiograms. The availability of a good pre-procedural intracranial angiogram is, therefore, essential in all patients undergoing carotid stenting.

Given that "time is brain", once a distal embolisation of a large vessel has been recognised, attempts should be made to recanalise the occluded branch as soon as possible (with balloon angioplasty, mechanical devices for thrombus removal,  thrombolytic agents, IIb/IIIa inhibitors). 

If there is a neurological deficit and small branch occlusion, the patient can be hydrated, given heparin and his or her blood pressure raised.
It is important to remember that changes of neurological status can also be related to intracerebral bleeding or hyperperfusion syndrome. If there are signs of a localised, expanding phenomenon on angiography indicating intracerebral hemorrhage, anticoagulation should be reversed and computed tomography scanning of the brain performed.

B) Major Complications

1/ Intracranial hemorrhage

Cerebral hemorrhage is a life-threatening and usually fatal complication (15,17).
In the authors’ experience, it occurs in approximately 0.3% of endovascular carotid procedures.
Sudden loss of consciousness preceded by severe headaches in the absence of intracranial vessel occlusion should alert the operator to this life-threatening event.
If a cerebral hemorrhage is suspected, the procedure should be terminated. Anticoagulation should be reversed with protamine and emergency computed tomography performed.
In the literature, cerebral hemorrhage has been associated with a combination of excessive anticoagulation, poorly controlled hypertension, aggressive attempts at intracranial neurovascular rescue, presence of a vulnerable berry aneurysm, or CAS in the presence of a recent (less than 3 weeks previously) ischemic stroke.

2/ Hyperperfusion syndrome

The reported incidence of cerebral hyperperfusion syndrome following CEA ranges from 0.3% to 2.7% (18,20).

Clinical manifestations of this complication are varied and include:

  1. Ipsilateral headaches, nausea, vomiting
  2. Markedly elevated blood pressure
  3. Focal seizures and altered mental status
  4. Fatal intracranial hemorrhage

The syndrome typically occurs in patients with severe carotid stenosis and poor collateral circulation, particularly in those with complete occlusion of the contralateral ICA or patients with an underdeveloped circle of Willis. The mechanism is related to long-standing hypoperfusion that results in impaired autoregulation of the microcirculation (18).

Following revascularisation, the increased perfusion pressure overwhelms the ability of the dilated arterioles to constrict, resulting in the development of the clinical syndrome.
In the authors' experience, hyperperfusion syndrome occurs in approximately 0.5% of cases. Several factors may contribute to its development during CAS: severe carotid artery stenosis with contralateral ICA occlusion, recanalisation of a completely occluded carotid artery, concomitant bilateral carotid stenting during the same procedure (9).

Unlike the surgical hyperperfusion syndrome, in which symptoms usually develop within a few days following CEA, the endovascular hyperperfusion syndrome develops during the stenting procedure itself or in the immediate post-procedural aftermath (15,17). This is likely related to heparin administration and the use of antiplatelet agents, particularly intravenous glycoprotein IIB/IIIA antagonists. Given the lack of evidence for a beneficial effect of glycoprotein IIB/IIIA antagonists during CAS, we do not routinely administer these agents during carotid interventions.

Current management of the hyperperfusion syndrome consists of identification of patients predisposed to this complication, careful monitoring, and meticulous blood pressure control, since this last factor appears to be the most important one contributing to adverse outcome (18). It is, therefore, important to control blood pressure levels during the periprocedural period using intravenous antihypertensive agents if necessary.

3/ Carotid artery dissection

Carotid artery dissection is a rare but important complication of CAS.
Factors which may predispose to this complication include:

(a) Severe "bends" or "kinks" in the ICA
(b) Aggressive hardware (guide wires, balloon catheters, stents) within the ICA
(c) Postdilatation of the distal stent edge within the ICA
(d) Aggressive manipulation of the guiding sheath tip, which is usually located in the common carotid artery

Stenting of lesions that are adjacent to severe distal kinks or bends can be a technical challenge and predispose to the development of vascular dissections.
Spasms, pseudo-spasms, and distally displaced kinks should be recognised, and stenting of these side effects must be avoided.
Generally, dissections are treated by additional stenting prior to removal of the guiding catheter/sheath. When there is suspicion of a carotid dissection, it is essential mandatory to maintain the guide wire position until the final angiographic assessment has been completed and the presence or absence of dissections has been ascertained.

4/ Carotid artery perforation

Carotid artery perforation during CAS is an extremely rare event. In the authors' experience of over 1,150 stented carotid arteries, a single case was observed. This perforation occurred following aggressive balloon dilatation of the middle part of the stent using a 6.0-mm diameter balloon in order to optimise the final result in a post-radiation carotid stenosis  (9).
We now appreciate that residual luminal narrowing of less than 25%, parietal irregularities, and residual ulcerations external to the stent are of no prognostic significance in terms of immediate or late results.

5/ Acute stent thrombosis

Acute stent thrombosis is a remarkably rare event after CAS. The use of appropriate doses of adjunctive double antiplatelet therapy (1, 2) has lowered the rates of stent thrombosis and periprocedural embolic events.
Beside the antiplatelet regimen, stenting techniques can play a positive role in preventing acute stent thrombosis. The stenting strategies that minimise the risk of acute stent thrombosis include:

  1. Proper stent sizing and careful stent opposition to the arterial wall,
  2. Stenting from an angiographically "normal" proximal segment to an angiographically “normal” distal segment.

Late in-stent thrombosis is possible, but it is actually very difficult to determine its real frequency because only symptomatic late occlusion is clinically detectable. As a general rule, based mostly on common sense, we treat patients referred for non-atherosclerotic lesions or with sub-optimal results with double antiplatelet agents (aspirin + ticlopidine/clopidogrel) indefinitely.

6/ Contrast agent encephalopathy

Contrast encephalopathy is very rare (< 0.1%), and is defined as a transient neurological syndrome mostly related to a prolonged procedure in which a large volume of contrast medium is used. The patient can develop profound neurological deficits related to the involved hemisphere, with marked contrast enhancement "staining" in the basal ganglion and the cortex, but no radiographic brain abnormalities on computed tomography. Usually no angiographic vascular abnormalities are detected by intracranial angiography.
Given that contrast medium does not pass through the blood-brain barrier, this phenomenon may be caused by fine particulate embolisation and/or excessive local contrast injection (21,22).
Patients typically recover completely within 24 hours without a permanent neurological deficit.
From a clinical stand point, the interventionist must differentiate this phenomenon from a massive cerebral infarction or hyperperfusion syndrome.

Complications at the site of the vascular access
Puncture site complications can be minimised with :

  • Careful anterior wall puncture of the femoral artery
  • Adequate periprocedural anticoagulation
  • The use of vascular closure devices at the end of the procedure to achieve immediate hemostasis

It should be taken into account that early ambulation and discharge can counteract the activated carotid sinus reflex and the occasionally observed post-procedural hypotension (23).
If a manual technique of sheath removal is used, the sheath should be removed by experienced personnel under additional local anesthesia 2 to 4 hours after the procedure has been completed when the activated coagulation time has shortened to 150 seconds or less. Patients are usually kept on bed rest for 4 to 6 hours following removal of the sheath.


It is of fundamental importance that physicians can recognise and manage the various possible complications of carotid angioplasty and stenting.


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Vol8 N°17

Notes to editor

Fausto Castriota1, Alberto Cremonesi1, Luigi Tavazzi2

GVM Hospitals of Care and Research
1 Interventional Cardio-Angiology Unit, 2 Research Unit
- Villa Maria Cecilia Hospital –
Cotignola (RA) – Italy

Corresponding author:
Fausto Castriota, MD
Co-Director, Interventional Cardio-Angiology Unit
Department of Medical and Surgical Cardiology
Villa Maria Cecilia Hospital
Via Corriera 1, 48010 Cotignola (RA) - Italy
Tel. +39 0545 37202
Fax +39 0545 37208

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.