The risk of embolization during CAS may be influenced by a number of factors. Many studies have focused on the risk associated with catheterization maneuvers, experience of the physician, techniques and types of device used.1 Plaque characteristics had initially been considered one of the main determinants of embolization. Unstable plaques, ulcers of the lesion and sub-occlusive stenosis can be considered an important source of cerebral embolism during carotid stenting procedures (CAS).2 Uncomplicated plaque could theoretically carry a lower risk of surface fragmentation, with minor embolization potential. However, few data have been published about the association of carotid plaque characteristics with neurological complication in CAS procedures.2,3 In order to determine this possible association, we have analysed a series of CAS procedures performed in patients with different type of atherosclerotic lesions.
Material and Methods
From January 2005 to March 2007, all patients with an asymptomatic internal carotid stenosis > 80% or a symptomatic stenosis > 60%4 have been selected for CAS procedure. We have considered the following inclusion criteria: creatinine ≤ 2.0 mg/dl, no contraindication to antiplatelet therapy (aspirin and clopidogrel), no myocardial infarction (MI) in the last 30 days, patency of at least one iliac artery, and satisfactory cognitive capacities. Patients underwent either cerebral magnetic resonance imaging (RMI) or computed tomography (CT) scan and duplex scanning of carotid bifurcation. No exclusion criteria were set on the basis of plaque morphology or vessel tortuosity. Ultrasound was performed by GE scanner, with 12-MHz-linear probe. Images were stored and standardized using a dedicated software, (Adobe Photoshop 7.0), to calculate gray-scale median (GSM) score. The images were classified according to Beletsky and Gray-Weale5,6 scores divided in three stages: 1) soft plaques, organized thrombus, 2) intraplaque hemorrhage, fatty composition, 3) fibrosis, calcified plaque. This plaque composition corresponds to 1-echolucent, 2-echolucent with small areas of echogenicity, 3-echogenic or invisible for heavy calcifications. GSM levels were categorized as low < 25 and high > 25.
The grade of stenosis was considered 99% if PSV was > 400 cm/sec and the surface ulcerated if ulcers diameterwas > 2 mm. On the basis of morphology, we have created two groups of patients, in the first group, defined “ComP,” we have included all the patients with GSM < 25 and with subocclusive stenosis (99%). In the second group, “UncomP” all the patients with GSM > 25 and range of stenosis was 70–98%.
We have analyzed the difference in the two groups according to baseline characteristics (male gender, hypertension, ischemic heart failure, diabetes mellitus, dyslipidemia, chronic obstrusive pulmonary disease (COPD), chronic renal failure, as assested by specialist), preoperative neurological symptoms, type of aortic arch, presence of stenosis or occlusion of the contralateral carotid, cerebral CT, type of stent and protection system used, technical success (defined as correct stent deployment with residual stenosis < 30%), and the occurrence of neurological complications. All procedures were accomplished by a vascular surgeon with anesthesiologist support. Patients were premedicated with antiplatelet therapy (clopidogrel, 75 mg for 3 days) and heparinized (70 U/Kg). Percutaneous 8 Fr inguinal access was followed by placing a guiding catheter into the common carotid proximally to the target lesion through (40 degree or multipurpose 8 Fr (Boston Scientific, Natick, Massachusetts); hockey stick I or II (Medtronic) routine cerebral protection (Accunet Guidant or EZ Boston Scientific, Menlo Park, California), stenting of the lesion (Wallstent Boston Scientific or Acculink Guidant), and gentle postdilation.
Standard bivariate analyses were used to assess the differences between complicated and uncomplicated plaque patients (chi-square statistics for categorical variables; t-test for continuous ones). Two logistic regression models were fit to compute the odds ratio of neurological symptoms and technical failure in ComP versus UncomP patients, controlling age and gender.7
Statistical significance was defined as a two-sided pvalue < 0.05. All analyses were carried out using STATA statistical software, version 9.0 (Stata Corporation, College Station, Texas).
During the study period, 298 consecutive patients underwent CAS, 77 with ComP (25.8%) (Figure 1) and 221 with UncomP (74.2%) (Figure 2). At bivariate analysis, the two groups were not significantly different in terms of baseline characteristics (excluding age), preoperative symptoms, presence of stenosis or occlusion of the contralateral carotid, cerebral CT positivity for ischemic lesions and type of aortic arch (Table 1).
Overall, technical success was achieved in 272 cases (91.2%), and postoperative neurological symptoms occurred in 23 cases (7.7%). All symptoms were temporary — 19 TIA and 4 minor stroke — with complete regression of symptoms within 1 month from the procedure. No acute death occurred in this series.
In the ComP group, technical success was achieved in 70 cases (90%). In these patients, reasons for technical failure were excessive angulation of the aortic arch (bovine arch, type III arch) (n = 6) and uncrossable stenosis (n = 1). Neurological complications occurred in 6 cases (7.8%). The onset of symptoms was in 2 cases during the procedure and in 4 cases from 1 to 6 hours after the procedures. The complete regression of the neurological symptoms occurred in 5 cases after a few hours and in 1 case within two weeks.
In the UncomP group, technical success was achieved in 202 cases (91.4%). The reason for technical failure was, in all cases, excessive angulation of the aortic arch or excessive vessel tortuosity of the common carotid artery. Neurological complications occurred in 17 cases(7.7–11% TIAs, and 6 minor strokes). Symptoms occurred during the procedure in 6 cases, from 1 to 6 hours after the procedures in 9 patients and after 7 hours or more in 2 cases. The complete regression of the neurological symptoms occurred in 11 cases in a few hours and in 6 cases within four weeks.
There were no significant differences between the two groups regarding neurological events (ComP 7.8% vs. UncomP 7.7%, P = 0.98) and technical failure (9.1% vs. 8.6%, respectively, P = 0.97). These results were confirmed in multivariate logistic regression, which showed a significant increase in the risk of technical failure with aging (P = 0.002) (Table 2).
During the follow-up, there were 2 cases of asymptomatic occlusion of the internal carotid at 3 months and at 1 year after the procedure. Two patients died due to MI 6 and 8 months after the intervention.
Our results reveal an absence of correlation between the characteristics of carotid plaques and CAS outcome. Although the risk of surface disruption is theoretically higher in the ComP group, the treatment did not show a greater rate of neurological complications or technical failure. Several studies indicate that plaque echolucency is related to the histological structure and, in particular, thatlow echolucency is associated with a lipid structure or with hemorrhage content, the so-called soft tissue.8 In addition, plaque echolucency is associated with higher incidence of brain infarcts as assessed with CT scans.9 Other studies showed that echolucency is associated not only with silent cerebral ischemia, but also with a higher risk of stroke.9–13 Some authors suggest the use of “closed cells” stents to prevent plaque fragmentation and embolization,14 however, our study failed to show a correlation between the type of device used and neurological complications, even in the UcomP group.
The results of the study by Reiter et al are similar to our data.3 In their single-center registry, with characterization of plaque morphology by GSM scores, plaque echolucency did not predict the risk of peri-interventional neurological complications. In contrast, in the nonrandomized multicenter registry by Biasi et al,2 the degree of stenosis and the plaque composition are independent predictors of stroke. The findings that carotid plaque characteristics are not the only determinant of outcome are supported by other works showing bilateral or contralateral cerebral embolic lesions after CAS.1 Even though the majority of those embolic events did not induce neurological deficit,1,15 it is clear that the mechanism of cerebral embolization is not dependent uniquely on plaque fragmentation. Timing of neurological symptom onset, however, does not help in a clear vision of the mechanism. The only factor associated with an increased number of technical failures is the aortic arch anatomy, a finding described in other works.16
Thus, one can only postulate that catheterization and dilation maneuvers disrupt plaques, either in the aortic arch or in the carotid bifurcation, with subsequent detachment of embolic material immediately, or at a later time.
Carotid plaque characteristics are not associated with the risk of neurological complication or technical failure in CAS procedure. An indication to CAS can be given irrespective of plaque morphology.
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