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Angioplasty and Stenting of Carotid Artery
Anil Karapurkar

Angioplasty and stenting of the carotid artery is slowly emerging as an alternate procedure to carotid endarterectomy. The incidence of complications in carefully chosen patients is low. The principal risk is that of stroke during the procedure.

Indications for angioplasty and stenting
Clinical indications are (i) TIA (transient ischaemic attack) is loss of function due to ischaemia in a vascular territory with complete recovery within 24 hours. In most instances the recovery is complete in 30 minutes. Loss of function includes amaurosis fugax, loss of vision with recovery within a few minutes. (ii) Minor stroke with complete recovery (iii) Major or minor stroke with partial or near total recovery; (iv) major stroke with no recovery but continuing TIAs.

Radiological indications are :
Symptomatic Patients i) Absolute : > 90% stenosis, unilateral or bilateral; ii) Absolute : 70 to 90% unilateral or bilateral stenosis; iii) Controversial : 50% unilateral or bilateral stenosis. Asymptomatic Patients : i) Absolute : > 90% stenosis; ii) 70% to 90% stenosis, especially if bilateral.

Contraindications for angioplasty and stenting
Absolute Contraindications : i) Thrombus inside lumen of artery; ii) Tortuous carotid artery below disease or beyond disease, iii) tortuous aortic arch; iv) difficult course of artery from arch, especially left common carotid artery; v) Recent large infarct. In patient having bilateral stenosis and major infarct on one side, the contra-lateral side may be stented immediately to improve collateral flow.

Relative Contraindications : i) Recent moderate size infarct, ii) Ulcerated plaque; iii) Calcified plaque.

In patients with large infarct and good recovery angioplasty and stenting may be carried out after 4 weeks.

Contraindications for Carotid Endarterectomy :
i) Disease above C2 (angle of mandible); ii) Hostile neck - short neck with previous surgery, iii) Stenosis following radiotherapy to the neck; iv) Relative contraindication - Bilateral severe stenosis.

Preparation of Patient : A detailed history is obtained and a detailed clinical examination is carried out when a procedure is contemplated. Usually multiple arteries are diseased. The patient may have associated contralateral carotid, vertebral, subclavian artery disease or cardiac, renal or peripheral vascular disease. Diabetes, hypertension and smoking are common, the latter especially amongst male patients. Diabetes and blood pressure are brought under control. The patient is started on aspirin 325 mg/day, clopidogrel 75 mg/day, and statin for at least 72 hours before stenting. If the serum lipids are normal 10 mg is given, if they are abnormal 20 mg. is prescribed. If the patient is getting multiple TIAs low molecular weight Heparin (LMWH) 0.6 mg 12 hly is added. If the patient is on anticoagulation, the drug (Warfarin or acetrom) is stopped and LMWH started. INR should not be more than 1,3 on the day of angiopgraphy.

Investigations : Haemogram, (particularly for polycythaemia), blood sugar, homocysteine, ECG, Chest X-ray, Echocardiogram are done. If the ejection fraction is low, stress test with adenosine is done to evaluate cardiac reserve. This is important because there is transient bradycardia and hypotension after stenting and angioplasty. This may be fatal if there is severe coronary or contralateral carotid or vertebral artery disease. As the contrast used for angiography is excreted in the kidneys renal function is assessed by BUN and creatinine. If the renal function is impaired mucomix is started 48 hours before procedure and continued for at least 3 days after the procedure. If renal impairment is severe, dialysis may be required. The patient is well hydrated with intravenous fluids and limited amount of iso-somolar, non-ionic contrast is used if the renal function is impaired.

Radiological : Doppler studies may show stensosis of the carotid artery but is observer dependent and there may be false positives and negatives. MRI of the brain shows fresh or old infarcts better than CT scan. MRA shows the arterial disease well. MRA using surface coils has been used to depict plaque morphology, especially for the “unstable plaque” and plaques with haemorrhage. Intracranial circulation and the circle of Willis are well visualized giving a good idea of the collateral circulation. However sometimes the stenosis may appear more severe or the artery may appear to be totally occluded when it is not. Intraluminal thrombus may be missed on MRA. CT angio, gives more information. It also shows the nature of the plaque and whether it is calcified.

Technique of angioplasty and Stenting
The patient is starved overnight. He/she receives all medications especially antihypertensives, antiplatelets and statins on the morning of the procedure. In diabetics a special schedule may have to be followed. The procedure is done under local anaesthesia with careful monitoring of pulse and blood pressure. A quick neurological exam is carried out after every step of the procedure. Some operators give a toy, usually a quacking duck, in the contralateral hand and the patient is asked to squeeze is contralateral occlusion some prefer to do the procedure under general anaesthesia as there is a high incidence of convulsions and transient cardiac arrest during the angioplasty. The author prefers to do the procedure under local anaesthesia. For brain protection diazepam, steroids and epsolin are injected just prior to plasty. Some position a pacing wire in the right atrium at the start of the procedure to counter severe bradycardia and cardiac arrest.

8F sheath is placed in the right femoral artery. 5000 or 6000 IU Heparin is injected as a bolus to keep the ACT (Activated Clotting Time) at 300. If required, a top up dose is given after 1 hour. 0.6 mg Atropine is injected just before the angioplasty. Complete diagnostic angiogram is done. This includes a study of the aortic arch to visualize the origins of the great vessels and their upper thoracic and lower cervical course. Bilateral carotid, bilateral subclavian and at least one vertebral angiogram are done. The common carotid bifurcation is studied in at least 2 if not 3 planes, lateral and oblique or AP. Every effort is made to separate the external carotid from the internal for proper visualization of the diseased segment. Subtracted and non-subtracted views are important to visualize the level of the disease in relation to the vertebral body and to look for intra-luminal thrombus. Views of the head are taken in at least 2 planes, lateral and towne, to visualize the ipsi-lateral branches of the anterior, middle and posterior cerebral arteries and collateral circulation via anterior and posterior communicating arteries, and via the branches of the external carotid artery to the ophthalmic artery and cortical pial arteries. If there is good collateral circulation the artery can be safely occluded for some seconds. If there is bilateral disease the symptomatic side is treated first. Both sides are almost never treated in the same sitting. The second side is treated after a gap of 3 weeks. If the patient tolerates angioplasty and stenting of the first side well, the second side may be treated after 3 days. After the angiography, a detailed discussion is held with the patient and his family regarding the pros and cons and risks of angioplasty and stenting and an informed consent is taken.

Stenting technique : 8F sheath is placed in the femoral artery. A large bore, 8F guiding catheter or 7F long sheath are placed in the common carotid artery below the disease. The stenosis is then crossed using a micro guide wire. If the stenosis is about 70% or less predilatation may not be required. 0.6 mg Atropine or 0.2 mg Glycopyrrholate is injected just before plasty. If the stenosis is severe angioplasty is done using a low profile, coronary, monorail, rapid-exchange balloon. A self expanding nitinol or steel stent of the appropriate diameter and length is then deployed from distal to proximal to cover the diseased segment. The diameter of the stent is 1 mm. more than the estimated diameter of the artery. The stent must extend from normal artery to normal artery. Nitinol stents have a good memory. They gradually expand after deployment. If the stent opens adequately 10 minutes after deployment the stent does not need to be dilated. If the stenosis is due to a heavily calcified or tough fibrous plaque it may not expand. The persistent hour-glass stenosis of the stent is dilated using 5 mm x 20 mm or 6 mm x 20 mm balloon. It is inflated to the nominal pressure. No effort is made to over dilate as there is risk of rupture of the carotid artery. One may have to accept a small residual stenosis, especially in heavily calcified plaques. Angiography of the head to show the intracranial circulation is performed. Attention is paid to all the major and minor branches of the anterior, middle and posterior cerebral arteries. If a branch is occluded by an embolus, it will not be seen and the late capillary-early venous phase, the so-called “cerebrogram phase”, will show a “bare area” corresponding to the territory of the occluded artery.

Post stenting the patient is carefully observed in the ICU for bradycardia, hypotension and neurological deficit. If the BP is around 80 mmHg no treatment is required if the patient is clinically well and there is no severe stenosis elsewhere. Otherwise low dose Noradrenaline, or Dopamine may have to be given for 24 to 48 hours. Aspirin 325 mg, clopidogrel 75 mg and antistatin are continued. If the plaque is heavily calcified LMWH is given for 3 to 5 days.

Many operators have felt that fragments of material from the plaque may break off during the procedure leading to embolism and stroke. Hits have been recorded by performing Doppler studies during the stenting. The shower of emboli is most prominent during dilatation of the stent. To reduce the risk of stroke a protection device is used. Protection devices are of three types : i) distal balloon; ii) proximal balloon with or without flow reversal, iii) umbrella or filter device. The 014 micro-wire has a balloon incorporated into it a few mm. from the tip. Once the wire is eased past the stenosis the balloon is inflated to occlude the artery and the angioplasty, stent deployment and plasty of the stent are carried out, after which the balloon is deflated and removed. The disadvantage is that the ICA is occluded for the entire duration of procedure and the wire being bulky may dislodge material as it traverses the stenosis. With the balloon occluding the ICA beyond the disease, embolic material may travel down the ICA and up into the ECA and from there into ophthalmic artery leading to loss of vision. As the balloon has to be inflated to tightly occlude the artery, arterial dissection and arterial aneurysms have been recorded at the site of balloon deployment. The proximal balloon with flow reversal, called Parodi technique, is a difficult technique and rarely used. Proximal balloon without flow reversal is also rarely used. Filters are of two types. They are attached to the micro guide-wire or they move on the wire. If they are to be effective the filter must appose the wall of the internal carotid artery closely. There are some problems with use of filter. The filter moves up and down with movements of the neck and with swallowing. There must be enough length of ICA beyond the diseased segment for safe deployment of the filter. In tortuous ICA this may not be possible. The complications of filter device are i) dissection, ii) occlusion of the ICA, iii) thrombus formation, iv) inability to close the device and retrieve it, v) fracture of the device.

The author does not use a protection device. All steps of the procedure are done under vision with a technique called road-mapping.

Transient bradycardia and hypotension occur almost everytime. These are due to pressure on baroreceptors in the carotid body which is located at the bifurcation of the CCA and origin of ICA. Hypotension could also be due to sudden loss of resistance after satisfactory angioplsty. For prevention of bradycardia, Atropine is injected before plasty. In old patients, Glycopyrrholate is preferred to Atropine, as there is no tachycardia and psychosis. To correct hypotension fluids are infused. Vasopressors are rarely required. They are given only if there is severe disease elsewhere, e.g. in coronary, renal or contralateral carotid artery. Noradrenaline, Midodrine or Dopamine are used in minimal doses. The blood pressure should be kept as low as is safe and sudden surges in BP should be prevented as there is a risk of “breakthrough haemorrhage” in the hitherto ischaemic tissue.

TIA, major or minor stroke is the most dreaded complication. The reported incidence varies between 3% and 9%. The patient may get restless, complain of headache, develop a neurological deficit or have a convulsion. The neurological deficit could be due to i) embolism and occlusion of a branch and infarct, 2) haemorrhage into ischaemic/infarcted brain, iii) reaction to contrast used during the procedure, iv) atropine psychosis, v) perfusion pressure breakthrough phenomenon.

If there is no flow across the filter this could be due to a large load of embolic material or fresh thrombus. A large bore catheter called “export catheter” is placed in the filter and strong aspiration is done to remove the material. If there is acute occlusion of the stent, ICA or a branch of a cerebral artery due to a fresh thrombus Reo-pro (Abciximab), Aggrastat (Tirofiban) or Integrilin (Eptifibatide) can be injected into the occluded artery through a micro-catheter or IV to dissolve the thrombus and restore flow through the artery. If the occlusion is due to lipid material little can be done. For break through changes Intravenous Mannitol, steroids and glycerol are used. Hemorrhage is a dreaded complication as Aspirin and clopidogrel have to be stopped and this can lead to thrombosis inside the stent. If the hemorrhagic clot is large, decompressive surgery may be required. In general conservative treatment is carried out with decongestants, Mannitol, Steroids, diamox and anticonvulsants. Hematoma at puncture site in the groin, or retroperitoneal hematoma is another uncommon complication. These are usually treated conservatively. Rarely blood transfusion may required.

Aspirin 325 mg and clopidogrel 75 mg and statins are continued for 6 months. After 6 months clopidogrel is stopped and aspirin reduced to 150 mg. which is continued for life. Statins are continued for life in appropriate doses.

Clinical follow up is done at 3 weeks, 3 months, 6 months and annually thereafter. Doppler studies are carried out at 3 months, 6 months and annually thereafter.

The incidence of in-stent stenosis is low. It varies between 2 and 5%. Early thrombosis of the stent has been reported in patients who are resistant to aspirin and clopidogrel. In such patients ticlopidine or dipyridamole may be used. Tests are available to determine resistance to each of the drugs, aspirin, ticlopidine, clopidogrel, LMWH and heparin. If there is stenosis angioplasty is done if clinically warranted.

Fig. 1 : DSA showing intraluminal thrombus- an absolute
Carotid Stenting
Fig. 2 : Operative specimen of plaque showing intraluminal
thrombus, absolute contraindication.

Material and Methods
This is an analysis of 140 patients treated from 1997 to December 2004. Subsequently 55 more stents have been inserted.

The youngest patient was 42 years old and the oldest was 82. There were 90 males and 50 female patients. 128 patients had presented with TIA or stroke. Two patients had presented with a flurry of TIAs and were stented in emergency. In 2 patients with bilateral stenosis and large infarcts contralateral stenting was done immediately and ipsilateral after 3 weeks. Bilateral stenting was done in 10 patients, in 2 after 3 weeks and in 8 patients after 3 days. The contralateral ICA was occluded in 12 patients. In 5 patients carotid endarterectomy was done on one side either because of tortuosity or intraluminal thrombus and stenting was done on the other side. In 2 patients carotid and subclavian stenting was done in the same sitting. CABG was done in 2 patients 3 days after carotid stenting. Pre-stent dilatation was required in 135 patients and poststent dilatation was performed in 105, most of these were after stenting with the steel (Wall) stent. After nitinol stent dilatation was done only if the plaque was heavily calcified or if it was tough fibrous plaque. Transcranial Doppler recording was done in 4 during the stenting and no hits were recorded. The lumen was restored 100% in 95, 95% in 45 and 90% in the rest. The complications were persistent bradycardia, persistent severe hypotension, convulsions and stroke. Two patients with contralateral carotid disease in 2 and coronary disease in 1, needed vasopressors for 2 days, Noradrenaline in 1 and Dopamine in the other 2. One patient had minor weakness of the contralateral hand which recovered over 3 weeks. One patient had minor stroke 3 weeks later with almost complete recovery in dysphasia and hemiparesis. Two patients with occlusion of the contralateral carotid artery had convulsions on dilating the stent. As this was early in our experience we had not taken preventive action. In subsequent patients, Diazepam, steroids and Epsolin are injected before the angioplasty. There was no death or major disability. There was no case of perfusion pressure breakthrough or haemorrhage.

On follow up 1 patient presented 6 months after stenting with recurrent TIAs due to restenosis of a calcified plaque. She was treated with balloon angioplasty and hasn’t had any further TIA on follow up for 2 years. 2 patients who did not report for follow up presented 1 year later with occluded stents. One had a TIA, the other was asymptomatic. Both had uncontrolled diabetes and the serum lipids were severely raised. 2 patients had retroperitoneal haematoma which was treated conservatively, with ice packs, analgesics and anti-inflammatory drugs.

Fig. 3 : Tortuous arteries: absolute contraindication.

Fig. 4 : MRI showing multiple fresh infarcts.

Fig.5 : Same patient MRA neck showing occlusion of right cervical ICA.

Fig. 6 : Same patient MRA no trace of intracranial right ICA.

Fig. 7 : Same patient DSA showing severe stenosis
suggestive of occlusion of ICA on MRA.

Fig. 8 : Same patient balloon angioplasty.

Fig. 9 : Same patient stent being deployed, note waist
in stent.

Fig. 10 : Same patient dilatation of stent; post dilatation
mild persistent defect in posterior wall of ICA.

Fig. 11 : Same patient; before stent, note prominent ECA
and poor MCA and branches.

Fig. 12 : Same patient ; post stenting good MCA and
branches, poor filling of ECA and branches.

Fig.13 : a) DSA showing severe stenosis, b) balloon
angioplasty under roadmapping, c) stent deployment
under fluoroscopy using bone landmarks, d) poststenting.

Fig. 14 : Same patient.
Pre stenting ACA not seen Post stent ACA seen well.

Fig. 15 : Occlusion right ICA, pre- and post- Stenting left ICA

Fig. 16 : Bilateral stenting, pre- above, post- below.

In carefully selected patients angioplasty and stenting with or without protection is a safe procedure. It is effective in preventing further stroke or TIA. The rate of restenosis is low.

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Consultant Neurosurgeon, Department of Endovascular Neurosurgery, Bombay Hospital Institute of Medical Sciences, Mumbai