From January 2013 to June 2018, 97 patients who received CAS for carotid stenosis registered for the study from a single institution. Neurologists and vascular surgeons selected patients suitable for CAS. We performed digital subtraction angiography (DSA) to estimate the degree of stenosis. According to ECST criteria, the indications for CAS were more than 70% (n = 65 (63.16%) with symptom (transient ischemic attack (TIA) or stroke at the site supplied by the stenotic artery) or in asymptomatic cases, more than 70% (n = 32 (36.84%)) on DSA. Our institution's routine douplex ultrasound tests conducted follow-up management regularly six months after stent insertion. After CAS, neurological complications such as ipsilateral or contralateral stroke, resenosis, and hyperperfusion were recorded, analyzed. And the characteristics and conditions before and after procedure was also recorded and reviewed as well.

In Nov. 1999, our CAS program was started at the single neurovascular center. For internal quality control, we have created a computer-based database that includes all patients with carotid stenosis with CAS or carotid vascularization. Patient data was utilized until June 2018 for current analysis. All patients provided consent based on information on procedures and anonymous data collection and processing. All patients with or without symptoms were treated from the time of registration. The anatomical qualification criteria have been tested in all patients by CT angiography or MRA in our institution. If not already given with any anticoagulants, all patients were treated with 300 mg of clopidogrel and 500 mg of acetylsalicylic acid at least 24 hours prior to the procedure. After the procedure, 100 mg of acetylsalicylic acid and 75 mg of clopidogrel were given continuously for more than four weeks. Patients were then advised to take 100 milligrams of acetyl salicylate for life.

In our institution, only local anesthesia was used when performing CAS. Bolus of heparin (5000 IU) was administered in a standard manner. Whenever anatomically possible, we used an embolic protection device for periprocedural neuroprotection. All procedures were performed by a single neurointerventionist with at least 5 years of experience. Also, seven days before the procedure, patients received aspirin and Plavix for optimal treatment in addition to CAS. And within 24 hours prior to and after procedure, all patients were received neurological assessment by neurologist. An independent neurologist evaluated with the National Institutes of Health Stroke Scale and the modified Rankin Scale. First, entryways for angiography were secured through the right femoral artery and 5-F sheath was used. If you secure the fore-aft-side of the CCA through the catheter selection, and if stenosis is verified, we replaced it with guided-wire long enough that can reach the statistical CCA and ECA. Special care must be taken to avoid inappropriate contact between the stenosis and wire when the tip of the guided wired reaches near the CCA. If the Micro-wire and Microcatheter are successfully located in the stenosis, the delivery device must be over the microwire and past the stenosis. The length of the stent should be sufficient to extend from the CCA to the ICA in most cases to fully cover the stenosis. The diameter of the stent must match the CCA in order to properly match the wall adaptation of all carotid segments. The stent should be positioned slightly further than the desired stenosis position and should be pulled out before the position to be placed is reached, in order to reduce the possibility of a forward swivel movement. Atropine should be prepared for bradycardia at all times. Angiography should be performed on both cervical ICAs and intracranial circulation to evaluate stenosis, vasospasm, dissection, and cerebral blood flow. In this case, it is important to compare with the angiogram performed before the operation because the distal emboli are difficult to detect. After performing CAS through this procedure, it is necessary to pay attention to the complications that may arise from enlarging the diameter of the lesion by dilating the stent.

Data are expressed according to the properties of the variable. Continuous variables are presented as mean and standard deviation. Categorical variables are presented as frequency and percentage. In order to compare two groups, we performed the two-simple t-test or chi-square test (Fisher`s exact test) as appropriate. Logistic regression analysis was used to identify the factors to predict neurologic complications after CAS and the result were expressed as odds ratio (OR) with 95% confidence interval (CI). A p-value less than 0.05 was considered statistically significant and all statistical analyses were conducted using SPSS (version 24; IBM, Armonk, NY, USA).

Many authors have described CHS as a primary complication of carotid recanalization procedure.17) CHS is defined in several ways such as: 1) Severe headache, seizures, mental deterioration, and / or development of local neurological symptoms; 2) no additional ischemic lesion in imaging diagnosis of the brain; 3) Increased cerebral blood flow in the ipsilateral hemisphere, increased blood flow in the contralateral hemisphere, or increased cerebral artery flow rate value of > 100% compared with preoperative velocity, all postoperatively.7)14) According to Moulakakis et al, the incidence of CHS and ICH after CAS was 1.16% (range, 0.44% to 11.7%) and 0.74% (range, 0.36% to 4.5%), respectively and CHS may be fatal once an intracranial hemorrhage occurs.17) In this study, 13 cases (13.4%) were shown in all cases conforming to the above definition of HPS, but HPS with fetal ICH reported was 1 case (1.1%) in our institution. This increase in morbidity is associated with increased blood flow through the cerebral artery after the procedure and inadequate arterial blood pressure control.2) Although we found this phenomenon to be present after CEA for the first time, many authors have reported that post carotid angioplasty and stenting have similar results.7)21)

The most common time period for occurrence of CHS is several hours to several days after the procedure.20) Ogasawara suggested that the onset time of CHS among patients who received CAS reached its peak within 12 hours after the procedure. Mental deterioration, confusion, and headache are the most common symptoms of CHS, among which headache usually occurs on the ipsilateral side of the arterial artery, often degree of moderate to severe, and characterized by pulsatile and migraine symptoms.4) Cerebral edema is a neurological deficit of secondary CHS, which is usually transient. These are mostly derived from the cerebral cortex, including hemiplegia, hemiparesis, hemianopsia, aphasia, and obtundation, and also epileptic disorders such as generalized or focal seizures. Other symptoms such as movement disorders, visual impairment, cognitive impairment, and psychotic disorders are rare, but have reported in CHS patients as well.19) And some of the untreated patients may die.17)

The pathogenesis and risk factors of CHS are not fully known, but uncontrolled hypertension seems to be the most important cause of CHS.5) It stimulates the occipital-parietal region more noticeably because of the sympathetic nerves that innervate very little on the vertebrobasilar circulation.22) This suggests that impaired cerebral autoregulation, baroreceptor-reflex breakdown, and an axon-like trigeminovascular reflex contribute to the pathogenesis of CHS.16)17) Another serious concern is the intake of antiplatelet and statins, which is recommended for patients with carotid stenosis before and after procedure.5) These drugs can increase the risk of cerebral hemorrhage and CHS, especially after carotid stenting.20)

ICH is the most disasteric event secondary to hyperperfusion, which is also associated with CAS.17) ICH can cause vomiting or change of mentality because of increased pressure in the cranium.1)

It is important to note that ICH after CAS is difficult to prevent because it appears to occur within few hours without symptoms and mostly unavoidable and even fatal.17) There are several risk factors, including preoperative hypertension, bilateral carotid disease or contralateral carotid occlusion as well as impaired cerebrovascular reserve, which were associated with the formation of ICH after the procedure.7) It is known that ICH, which appears immediately after CAS, is caused by the rupture of the perforating artery in the basal ganglia hence the sudden exposure of normal perfusion pressure pathophysiologically.17) Rate of morbidity and mortality are high in both patients who treated with open surgery or endovascular repair, therefore it is crucial to prevent such a catastrophic event after the procedure.3)7)

Stroke occurs more commonly after CAS than after CEA. The periprocedural strokes in CREST were most commonly minor, ipsilateral to the treated artery, and ischemic in type and occurred twice as frequently in the CAS arm.9) Major stroke occurred in 0.6% (13/2272), indicative of the very low overall complication rate observed in the trial.8)9) According to Michael et al, complications that occurred during the carotid stent placement or within a 30-day period following placement were recorded and the definitions were defined as follows: (1) TIA, any neurological deficit (either ocular or cerebral) that resolved completely within 24 hours; (2) minor stroke, any new neurological deficit (either ocular or cerebral) that persisted for 24 hours and that either resolved completely within 7 days or increased the National Institutes of Health stroke scale 3 points; (3) major stroke, any new neurological deficit that persisted after 30 days and increased the National Institutes of Health stroke scale by 3 points.12)

There is evidence of a higher risk of stroke and mortality after CAS in patients with symptomatic patients than in asymptomatic patients, but it has not yet been studied how certain symptoms affect previously symptomatic patients after CAS procedure.12)

In this study, we analyzed all patients who underwent CAS to identify potential clinical risk factors for neurologic complications after CAS procedure. The significance of this study is that no previous studies analyzing the effects of CAS on post-procedural results have been reported, particularly in Asia, and based on evidence that the risk of stroke and death after CEA depends not only on symptoms but also on the type of presenting event.11)12) In some studies, age was identified as an independent risk factor for neurologic complications after CAS procedure, but DM and preoperative NIHSS were found to be related to our study. Hyperlipidemia has also been described as a risk factor in patients with complication after CAS in a number of studies. Comparable with recent studies in Qureshi et al., with that in univariate analysis, we found no association between the hyperlipidemia and postprocedural neurological deficit. Diabetes (DM) is an independent risk factor for cardiovascular disease and stroke and has a high incidence of diabetes among people undergoing carotid revascularization.12)13)15) However, it is well known that the risk of morbidity and mortality or the risk of late stroke is not greater after CAS in diabetic patients.12) Renato et al. reported that the presence of diabetes was associated with an increased periprocedural risk, but did not show any additional risk as a result of long-term follow-up and had a higher rate of restenosis in diabetic patients.18) Therefore, these studies are not comparable to our results. Studies suggesting that post-surgical risk for DM patients may be higher after CEA.6) And this may be helpful in selecting the appropriate technique for carotid revascularization in patients best suited to the procedure type. In some studies, clinical symptoms have also been known to be potential risk factors for periprocedural complications following CAS, but not in accord with our study. However, this association is reported to be consistently insignificant in other studies as well, therefore we could come to a conclusion that it is not significant.10) The cause of this conflicting result may be a small number of patients.

Several limitations should be pointed out. There may be some neurological complications that the even patient has not noticed would have been missed. The size of the data was small. Without a randomized control group, no clear comparison of CEA or other medical treatment can be made. Since the current data is collected as a single center experience, the results cannot be generalized in a simple way.