Fig. 2.6.14 Monorail system follow cannulation of the CCA using a guide catheter or a guide sheath. Then procedure is continued - if necessary and always under protection - with predilatation of the lesion, stent implantation and (also if necessary) postdilatation of the stent. When insertion of a brain protection device is impossible, predilatation of the lesion using a coronary balloon can be done in order to help pass the protection device distally to the lesion. When the procedure is finished, the protection device is withdrawn.
Using a proximal occlusion device as a protection system is quite a different procedure. After inserting the guide catheter into the CCA, an occlusion balloon is inflated in the upper part of the CCA and, according to the type of system, a second occlusion balloon is inflated in the ECA and so reversed blood flow is created. The procedure is then continued with stenting and, if necessary, pre- or post-dilatation is done and the protection system is withdrawn.
184.108.40.206 Step 4: Control Angiography
Intervention is completed with angiographic control of the extra- and intracranial circulation.
Carotid angioplasty and stenting is performed using local anaesthesia under the anaesthetist's care, checking the patient's consciousness, motility and sensitivity levels during the whole procedure. Preoperatively, the patient is given salicylic acid and clopidogrel. During the procedure a bolus administration of 70-100 IU/kg unfrac-tionated heparin is given in order to raise their activated partial prothrombin time to 200-300 s. An intravenous bolus of atropine (0.6-1 mg) is administered before dilatation in order to decrease the risk of major bradycardia due to carotid sinus stimulation when the carotid bulb is dilated. In very rare situations a temporary pacemaker may be needed. During the intervention, monitoring of blood pressure, cardiac pulse, arterial blood oxygen saturation as well as roughly the neurological condition of the patient is essential. When possible a transcranial Doppler ultrasound is performed.
In most cases the procedure is successfully completed with a residual stenosis of <30%. In the early days, the rate of technical failure was up to 10%, but continuous improvement in materials and experience has reduced this rate to less than 2% [59, 60].
This is a rather rare complication involving patient confusion and neurological deficit. It is attributed to blood-brain barrier disturbance and extravasation of contrast agent. A CT scan can reveal signs of oedema and cortical enhancement which, however, soon vanish without leaving permanent neurological deficit .
The most common complication of this kind is haema-toma at the puncture site or in the retroperitoneal area. Rarely, a false aneurysm may develop. There are also reports of common femoral artery dissection, most likely secondary to closure-device misplacement leading to occlusion and needing surgical exploration .
220.127.116.11 Hyperperfusion Syndrome (Fig. 2.6.16)
Brain cells have the ability to autoregulate blood circulation in response to a large range of systematic arterial blood pressure values. The presence of high-grade stenosis in the ICA leads to maximal arterial vasodilatation in order to preserve cerebral perfusion. When stenosis is treated by CAS, blood flow is increased in dilated cerebral vessels. If autoregulation does not respond accordingly, there is the possibility of increased perfusion, oedema or even brain haemorrhage . The patient may suffer from headaches, seizures or even focal neurological symptoms and changes in their level of consciousness. The hyperperfusion occurrence rate ranges from 1.1% to 6.8% and is related to a high death rate (up to 40%) [1, 11]. It is associated with patients who have high-grade stenosis, a significant contralateral lesion and periproce-dural hypertension. Patients should therefore be closely monitored for their ability to maintain systemic arterial blood pressure at the level of 140 mmHg. Transcranial Doppler findings of increased velocities are indicative of the patient's high risk of developing the syndrome and may help in early diagnosis and treatment .
18.104.22.168 Hypotension and Bradycardia
Angioplasty and stenting of plaques located in the carotid bulb may result in haemodynamic alterations due to stimulation of the carotid sinus reflex. Stimulation of barore-ceptors leads to increased parasympathetic discharge and a reduction in the sympathetic discharge, which results in hypotension and bradycardia. Rates vary between 7% and 68% [14, 47]. This complication may develop late after angioplasty (after the first 24 h) and may last for up to 10 days, without however increasing the risk of neurological complications . Treatment initially involves fluid and atropine administration. Persistent hypotension may require the administration of vasoconstriction drugs and rarely a temporary pacemaker [21, 37].
Neurological events due to emboli are one of the most severe and life-threatening complications. Emboli production is possible in nearly all phases of angioplasty. Neurological event rates are decreasing as materials improve and experience grows. The combined 30-day stroke and death rate in various reports range between 4% and 10%. Brain protection systems have improved angioplasty results in such a way that recent reports estimate 30-day combined stroke and death rate at 1.8-3.3% [2, 13, 16, 19, 24, 25, 27, 29, 42, 48].
22.214.171.124 Complications Involving Brain Protection Devices
The use of brain protection devices is now considered almost mandatory in carotid artery angioplasty procedures. However, their use is also linked with certain complications. These complications refer to the introduction and deployment of the devices as well as to tolerance, effectiveness and, most commonly, to device retrieval.
Balloon occlusion devices are not always tolerated and filters can be the cause of spasm and dissection of the artery . Debris may well end up in the brain, being transferred by the collateral circulation of the ECA . Also they may not be captured by the filter device or slip out as the withdrawal catheter is being retrieved [43, 44, 58]. Finally brain protection systems increase the duration, technical difficulty and the cost of the procedure.
Patients who do not suffer from any kind of complication after angioplasty may safely leave hospital on the first or second postoperative day, while in some cases patients can leave hospital in the evening of the day of operation .
It is necessary that patients undergo an examination of their neurological condition at regular periods as well as Duplex ultrasound control for possible asymptomatic restenosis, which in several trials is reported to be 5-20% after 5 years [30, 50, 53]. Complete physical and neurological examination along with Duplex control of the carotid arteries in 6 and 12 months and then yearly is considered a sufficient postoperative follow-up. In cases where Duplex control reveals gradient restenosis, pa
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tients should be examined more frequently. If restenosis becomes haemo dynamically important and over 70%, a new DSA of the carotid arteries will be necessary in order to verify Duplex findings and determine the need for a possible new angioplasty.
2.6.10 Carotid Angioplasty and Stenting (CAS): Present and Future
Carotid endarterectomy (CEA), having good results for symptomatic and asymptomatic patients [4, 40], was considered the gold standard for carotid occlusive disease. It is therefore for CAS plus brain protection systems to prove that it is at least as effective as endarterectomy.
There are two main questions to be answered:
• Endarterectomy or angioplasty?
• Use brain protection systems or not?
The question of whether to use stents or not with carotid angioplasty does not exist.
The CAVATAS trial  showed equal results regarding major complications (stroke and death) for CAS and CEA, while there was a statistically significant difference in favour of angioplasty regarding lesser complications such as cranial nerve injury or haematomas. The 1-year follow-up showed an increased rate of restenosis for the endovascular treatment but the 3-year follow-up, however, did not reveal any difference in stroke events between the two methods.
The SAPHIRE trial , focusing on mortality as well as stroke and myocardial infarction rates in the 1-year follow-up, showed results such as 12.2% and 20.1% for
CAS and CEA respectively (p=0.004). Reoperation rates in the 1-year follow-up were 0.6% and 4.3% for CAS and CEA, respectively (p=0.04).
The CARESS trial  revealed the same 30-days stroke- and myocardial ischaemia-related mortality rate (2%) for both methods.
Based on these results carotid angioplasty and stent-ing with the use of brain protection systems seem to have equally good results as endarterectomy, and have the additional advantage of being minimally interventional.
Furthermore, materials are being improved and have become less traumatic, more flexible and have a smaller cross-sectional profile. Drug-eluting stents have already given good results in coronary interventions by reducing the restenosis rate, while implementation of biodegradable stents is thought to produce natural remodelling of the vessels [5, 39, 52]. There is also significant progress in the study of plaques, which will enable better patient selection, while progress in drugs research has produced agents capable of reducing stroke rates [23, 46].
Bearing in mind that CAS is a new method, with continuous evolution of materials and technique it seems that the treatment of carotid occlusive disease is entering a new era. Results from new and larger clinical trials will answer our questions. Reports showed that CAS represented 8% of all interventions for carotid stenosis in Europe for the year 2000 . It is estimated that this percentage will grow to 60% by the year 2006.
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