Symptomatic Severe Carotid Stenosis Research Articles

Large artery atherosclerosis: carotid stenosis, vertebral artery disease, and intracranial atherosclerosis.

Large artery atherosclerosis is an important cause of ischemic stroke. Recent randomized clinical trials have helped clarify the treatment options for conditions such as carotid stenosis and intracranial atherosclerosis. This review outlines the primary findings of these trials and provides current recommendations for treatment. Carotid revascularization is preferred in patients with severe symptomatic carotid stenosis. Carotid endarterectomy achieves lower rates of stroke or death than carotid artery stenting. The risk of stroke or death with stenting is higher among older patients and women. Intensive medical therapy achieves low stroke and death rates in asymptomatic stenosis. Medical therapy and treatment of atherosclerotic risk factors are the mainstay of therapy for intracranial atherosclerosis, and medical therapy is recommended for patients with vertebral artery origin atherosclerosis. Contemporary medical therapy is paramount in large artery atherosclerosis. Patient demographics, comorbidities, and the periprocedural risks of stroke and death should be carefully weighed while choosing a revascularization procedure for carotid stenosis.

Impact of diabetes mellitus on characteristics of carotid plaques and outcomes after carotid endarterectomy

Published results for carotid endarterectomy (CEA) in symptomatic and asymptomatic severe carotid stenosis with diabetes mellitus (DM) are contradictory. To evaluate perioperative and long-term results of CEA in patients with DM, we retrospectively analyzed data of patients with or without DM who underwent CEA in our institute. Between January 2005 and December 2010, 281 consecutive CEAs were performed in 268 patients under general anesthesia. All patients were subject to cardiac work-ups before surgery, and coronary revascularization was performed prior to CEA if patients were diagnosed with significant coronary artery stenosis. Lesion characteristics were assessed by a duplex ultrasound scan, computed tomography angiography (CTA), and plaque imaging on magnetic resonance imaging (MRI) before surgery, and patients were followed-up by a duplex ultrasound scan at three, six, and 12months, then yearly, after surgery. Of 281 cases, 136 had DM (48%). Diabetic patients more frequently had a history of coronary artery disease than non-diabetic patients (48.5% vs. 36.6%, P = 0.042). Coronary intervention prior to CEA was more frequently performed in diabetic patients than in non-diabetic patients (22.1% vs. 11.0%, P = 0.013). The incidence of perioperative (30day) stroke (P = 1.000), death (P = 1.000), and cardiac complications (P = 0.484) did not differ among groups. Follow-up was available in 77.2% of patients, with a median duration of 50months (interquartile range, 32.1-67.2months). The incidence of ipsilateral stroke (P = 0.720), death (P = 0.351), and severe restenosis (peak systolic velocity > 230cm/sec) (P = 0.905) were not different between groups. DM does not increase the risk of perioperative complications and does not influence long-term outcomes after CEA if preexisting vascular risk factors and cardiac diseases are appropriately evaluated and treated before surgery.

The influence of vascular anatomy on carotid artery stenting: A parametric study for damage assessment

Carotid artery stenting is emerging as an alternative technique to surgery for the treatment of symptomatic severe carotid stenosis. Clinical and experimental evidence demonstrates that both plaque morphology and biomechanical changes due to the device implantation can be possible causes of an unsuccessful treatment. In order to gain further insights of the endovascular intervention, a virtual environment based on structural finite element simulations was built to emulate the stenting procedure on generalized atherosclerotic carotid geometries which included a damage model to quantify the injury of the vessel. Five possible lesion scenarios were simulated by changing both material properties and vascular geometrical features to cover both presumed vulnerable and stable plaques. The results were analyzed with respect to lumen gain and wall stresses which are potentially related to the failure of the procedure according to previous studies. Our findings show that an elliptic lumen shape and a thinner fibrous cap with an underlying lipid pool result in higher stenosis reduction, while large calcifications and fibrotic tissue are more prone to recoil. The shielding effect of a thicker fibrous cap helps to reduce local compressive stresses in the soft plaque. The presence of a soft plaque reduces the damage in the healthy vascular structures. Contrarily, the presence of hard plaque promotes less damage volume in the fibrous cap and reduces stress peaks in this region, but they seem to increase stresses in the media-intima layer. Finally the reliability of the achieved results was put into clinical perspective.

Carotid Stenting

Randomized clinical trials show higher 30-day risk of stroke or death after carotid artery stenting compared with surgery. We examined whether operator experience is associated with 30-day risk of stroke or death in the Carotid Stenting Trialists' Collaboration database. The Carotid Stenting Trialists' Collaboration is a pooled individual patient database including all patients recruited in 3 randomized trials of stenting versus endarterectomy for symptomatic carotid stenosis (Endarterectomy Versus Angioplasty in patients with Symptomatic Severe Carotid Stenosis trial, Stent-Protected Angioplasty versus Carotid Endarterectomy trial, and International Carotid Stenting Study). Lifetime carotid artery stenting experience, lifetime experience in stenting procedures excluding the carotid, and annual number of procedures performed within the trial (in-trial volume), divided into tertiles, were used to measure operator experience. The outcome event was the occurrence of any stroke or death within 30 days of the procedure. The analysis was done per protocol. Among 1546 patients who underwent carotid artery stenting, 120 (7.8%) had a stroke or death within 30 days of the procedure. The 30-day risk of stroke or death did not differ according to operator lifetime carotid artery stenting experience (P=0.8) or operator lifetime stenting experience excluding the carotid (P=0.7). In contrast, the 30-day risk of stroke or death was significantly higher in patients treated by operators with low (mean ≤3.2 procedures/y; risk 10.1%; adjusted risk ratio=2.30 [1.36-3.87]) and intermediate annual in-trial volumes (3.2-5.6 procedures/y; 8.4%; adjusted risk ratio=1.93 [1.14-3.27]) compared with patients treated by high annual in-trial volume operators (>5.6 procedures/y; 5.1%). Carotid stenting should only be performed by operators with annual procedure volume ≥6 cases per year.

Comparison of Carotid Artery Stenting and Carotid Endarterectomy in Patients with Symptomatic Carotid Artery Stenosis

PP-389 Large randomised trials have established carotid endarterectomy (CEA) as the standard treatment for symptomatic severe carotid artery stenosis. Carotid artery stenting (CAS) has been increasingly used for possible alternative treatment to CEA. In this study we aimed to compare the

Aggressive Medical Therapy Alone Is Not Adequate in Certain Patients With Severe Symptomatic Carotid Stenosis

The Case: A 59-year-old woman presents 4 weeks after a transient ischemic attack (left-sided weakness). Carotid ultrasound shows 80% right internal carotid artery stenosis. She takes aspirin 81 mg and atorvastatin 20 mg daily. The Questions: 1. Should the patient undergo carotid endarterectomy (CEA)? 2. Should clopidogrel be added to her therapy and the dose of atorvastatin increased to 80 mg instead of CEA? The Controversy: Aggressive medical therapy alone is not adequate in certain patients with severe symptomatic carotid stenosis? The results of the first European Carotid Surgery Trial (ECST) and the North American Symptomatic Carotid Endarterectomy Trial (NASCET) led to guidelines recommending carotid endarterectomy (CEA) for patients matching the trial characteristics, which are still current today. Thus, if you observe the guidelines, this patient should be referred for CEA. However, analysis of the trial data suggests that this is not necessarily the right decision. Rothwell et al1 developed a risk model using ECST data that predicted the future risk of stroke in patients allocated medical treatment alone and was validated in the NASCET dataset.1 The analyses showed that only patients with a 5-year risk of ipsilateral stroke of >20% benefited from CEA. The characteristics that predicted the risk of recurrent stroke included age, sex, symptom severity, time since symptoms, severity of stenosis, other vascular risk factors, and whether the stenosis was ulcerated, irregular, or smooth. A tool that uses this model is available online (http://www.stroke.ox.ac.uk/model/form1.html), and I have just used the tool to calculate the patient’s future risk of …

Carotid Wars Episode VI: Return of the Standard

In modern medicine, a novel treatment or procedure typically needs decades to demonstrate efficacy compared with the previous standard and to make its way into routine clinical practice. More than 20 years ago, the young Challenger, carotid endarterectomy (CEA), defeated the old Standard, medical treatment, in the battlefields of North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Stenosis Trial (ECST). This victory established a new era of “The Surgical Empire,” and CEA was crowned as the treatment of choice for moderate and severe symptomatic carotid stenosis. However, despite the overall robust benefit from CEA, there were some fronts where the victory was less rotund. Subgroup analysis of pooled data from the large randomized controlled trials (RCTs) showed the lowest degree of benefit from surgery in women, patients 50%, the number needed to treat by CEA increased 4-fold in women, 3-fold in patients aged <65 years, and 25-fold in whom surgery was performed …

A Retrospective Study on Early Carotid Endarterectomy within 48 Hours after Transient Ischemic Attack and Stroke in Evolution

Large randomized controlled trials have shown that carotid endarterectomy (CEA) is beneficial in the treatment of recent severe symptomatic carotid stenosis. Data are lacking concerning the risks of early CEA (<48hours) for stroke in evolution (SIE) or crescendo transient ischemic attack (CTIA). The primary end point of this retrospective study was to evaluate the incidence of stroke, major adverse cardiac events (MACEs), and death within the first 30days after early CEA performed within 48hours in patients presenting with transient ischemic attack (TIA)/SIE. Between 2001 and 2010, we treated 3,023 carotid artery stenoses, 29.5% (891/3,021) of which were in symptomatic patients. Early CEA within 48hours after acute TIA/SIE was performed in 176 patients. Patients were divided into 3 groups for analysis of outcome after early CEA in symptomatic patients according to their initial neurologic deficit. Group 1 included 55 patients with TIA (single); group 2 included 55 patients with CTIA, and group 3 included 66 patients with SIE. Carotid artery stenosis was evaluated by duplex ultrasonography (DS). All patients were pre- and postoperatively visited by an experienced consultant neurologist who evaluated the neurologic status according to the modified Rankin Scale and the National Institutes of Health Stroke Scale (NIHSS). At admission, surgery was not performed on patients with disabling neurologic deficit (NIHSSscore: >6) except for 4 selected cases (NIHSS score range: 8-14), patients with cerebral lesions >3cm in diameter, patients with the presence or suspicion of parenchymal hemorrhage, patients with occlusion of the middle cerebral artery, and those who were deemed unfit for surgery. Clinical and DS follow-up examinations were performed after 6 and 12months and annually thereafter. The mean duration of follow-up was 29.4months (range: 0-120months). The cumulative TIA/stroke/myocardial infarction/death rate at 30days was 3.9% (7/176). TIA and stroke rates were 0% (0/176) and 3.4% (6/176), respectively. The stroke rate in groups 1, 2, and 3 was 1.8% (1/55), 0% (0/55), and 7.6% (5/66), respectively. No hemorrhagic strokes, TIAs, or MACEs were detected after surgery. Stroke risk was higher in group 3 than in groups 1 or 2, but the differences in the 3 groups were not statistically significant (group 1 vs. group 2: 1/55 vs. 0/55 events [P=0.3151]); group 1 vs. group 3: 1/55 vs. 5/66 events [P=0.3020]; and group 2 vs. group 3: 0/55 vs. 5/66 events [P=0.1039]. Thirty-day follow-up was available for all patients, while long-term follow-up (mean: 32.7±26.8months) was available only for 158 patients (1 patient died and 17 were lost to follow-up). CEA can be performed with an acceptable risk in properly selected symptomatic patients within 48hours after TIA or SIE. The benefits of early CEA in symptomatic patients include the prevention of recurrent stroke.

Aggressive Medical Therapy Alone Is Adequate in Certain Patients With Severe Symptomatic Carotid Stenosis

As clinicians, our responsibility is to be honest with our patients. To achieve the goal of an honest discourse with this patient, we must inform her that it is uncertain whether she would benefit from carotid endarterectomy (CEA). Although the landmark clinical trials that compared CEA plus optimal medical therapy (OMT) with OMT alone showed robust benefit for CEA in symptomatic patients with high-grade stenosis, we should acknowledge that studies such as the North American Symptomatic Carotid Endarterectomy Trial (NASCET) used what now would be regarded as “suboptimal” medical therapy. Furthermore, the 70% to 99% cohort of NASCET was published in 1991. It is shocking that clinicians are still making CEA decisions based on data that are 22 years old! What can we learn from more contemporary stroke prevention studies that have used aggressive medical therapy? A good place to start would be the Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis (SAMMPRIS) study1 …

Early Carotid Artery Endarterectomy after Intravenous Thrombolysis Therapy

Carotid endarterectomy reduces the risk of stroke in patients with recently symptomatic stenosis.It is also well established that there is a reduction in benefit from CEA with time from the presenting event. Therefore, the procedure should be done early within two-weeks in neurologically stable patients (3,4). According to our results and the small data available in the medical literature, surgery of recently symptomatic severe carotid stenosis previously treated by IVT should not be delayed. There seems to be no higher haemorrhagic risk once this surgery is applied to patients with a stable neurological status and good clinical recovery after lysis. As large series of patients will be difficult to

Treatment of Symptomatic Carotid Stenosis: Carotid Stent Placement Versus Endarterectomy

The mainstay of treatment options for symptomatic carotid stenosis is focused around medical management, carotid endarterectomy, and carotid angioplasty and stent placement. The International Carotid Stenting Study (ICSS), also called Carotid and Vertebral Artery Transluminal Angioplasty Study 2 (CAVATAS 2), the Stent-Supported Percutaneous Angioplasty of the Carotid Artery Versus Endarterectomy (SPACE) trial, the Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial, the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, and the Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST) were five major trials which compared carotid endarterectomy and carotid angioplasty and stent placement. We review the results of the trials and incorporation of the results into clinical decision making.

Increased platelet activation in early symptomatic vs. asymptomatic carotid stenosis and relationship with microembolic status: results from the Platelets and Carotid Stenosis Study

Cerebral microembolic signals (MES) may predict increased stroke risk in carotid stenosis. However, the relationship between platelet counts or platelet activation status and MES in symptomatic vs. asymptomatic carotid stenosis has not been comprehensively assessed. University teaching hospitals. This prospective, pilot observational study assessed platelet counts and platelet activation status, and the relationship between platelet activation and MES in asymptomatic vs. early (≤4weeks after TIA/stroke) and late phase (≥3months) symptomatic moderate or severe (≥50%) carotid stenosis patients. Full blood count measurements were performed, and whole blood flow cytometry was used to quantify platelet surface activation marker expression (CD62P and CD63) and circulating leucocyte-platelet complexes. Bilateral simultaneous transcranial Doppler ultrasound monitoring of the middle cerebral arteries was performed for 1h to classify patients as MES positive or MES negative. Data from 31 asymptomatic patients were compared with 46 symptomatic patients in the early phase, and 35 of these patients were followed up to the late phase after symptom onset. The median platelet count (211 vs. 200×10(9) L(-1) ; P=0.03) and the median percentage of lymphocyte-platelet complexes was higher in early symptomatic than asymptomatic patients (2.8 vs. 2.4%; P=0.001). The percentage of lymphocyte-platelet complexes was higher in early symptomatic than in asymptomatic patients with ≥70% carotid stenosis (P=0.0005) and symptomatic patients recruited within 7days of symptom onset (P=0.028). Complete TCD data were available in 25 asymptomatic, 31 early phase symptomatic and 27 late phase symptomatic patients. Twelve per cent of asymptomatic vs. 32% of early phase symptomatic (P=0.02) and 19% of late phase symptomatic patients (P=0.2) were MES positive. Early symptomatic MES-negative patients had a higher percentage of lymphocyte-platelet complexes than asymptomatic MES-negative patients (2.8 vs. 2.3%; P=0.0085). Recently, symptomatic carotid stenosis patients have had higher platelet counts (potentially reflecting increased platelet production, mobilization or reduced clearance) and platelet activation status than asymptomatic patients. MES were more frequently detected in early symptomatic than asymptomatic patients, but the differences between late symptomatic and asymptomatic groups were not significant. Increased lymphocyte-platelet complex formation in recently symptomatic vs. asymptomatic MES-negative patients indicates enhanced platelet activation in this early symptomatic subgroup. Platelet biomarkers, in combination with TCD, have the potential to aid risk-stratification in asymptomatic and symptomatic carotid stenosis patients.

Bivalirudin for Carotid Artery Stenting

In the past decade, carotid artery stenting (CAS) has been carefully studied as a treatment for symptomatic and asymptomatic carotid artery stenosis. In the Carotid Revascularization Endarterectomy vs. Stenting Trial (CREST) trial, it was shown that the composite outcome of death, stroke, or myocardial infarction is similar for CAS versus carotid endarterectomy when performed by experienced operators.1 During this time period, significant advances have been made with regards to patient selection and procedural techniques.2 In addition, there have been improvements in embolic protection and stent technology. With these advancements, CAS outcomes have continued to improve with a low rate of periprocedural adverse events observed in numerous single-center and multicenter studies.3–5 Article see p 131 In comparison with recent advances in CAS technology, intraprocedural anticoagulation during CAS has been relatively understudied. The initial randomized studies of CAS, including Stenting and Angioplasty with Protection in Patients at High-Risk for Endarterectomy, Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S), Stent-Supported Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy (SPACE), and the International Carotid Stenting Study (ICSS). all used heparin for adjunctive pharmacotherapy.6–9 In the CREST trial, patients randomized to CAS could be treated with either heparin (86%) or bivalirudin (14%).1 Most of the current evidence for CAS is, therefore, based on using heparin as the intraprocedural anticoagulant. The current societal guidelines for CAS do not make a specific recommendation regarding periprocedural anticoagulation but state that either heparin or bivalirudin may be used.10 A direct thrombin inhibitor, such as bivalirudin, could have significant advantages as an anticoagulant during CAS. Bivalirudin can be administered as weight-based infusion with minimal intraprocedural monitoring and predictable pharmacokinetics. In comparison, heparin has variable between-person pharmacokinetics, and the correct dose of heparin for the goal level of …

Enhanced Thrombin Generation Potential in Recently Symptomatic Versus Asymptomatic Moderate and Severe Carotid Artery Stenosis – Results from the Platelets and Carotid Stenosis (PACS) Study (P03.154)

Enhanced Thrombin Generation Potential in Recently Symptomatic Versus Asymptomatic Moderate and Severe Carotid Artery Stenosis – Results from the Platelets and Carotid Stenosis (PACS) Study (P03.154)

Increased von Willebrand Factor Propeptide Levels in Symptomatic Versus Asymptomatic Moderate and Severe Carotid Artery Stenosis – Results from the Platelets and Carotid Stenosis (PACS) Study (S42.007)

Increased von Willebrand Factor Propeptide Levels in Symptomatic Versus Asymptomatic Moderate and Severe Carotid Artery Stenosis – Results from the Platelets and Carotid Stenosis (PACS) Study (S42.007)

Abstract WP137: Improvement of Cerebrovascular Reactivity After Carotid Stenting is Greater in Non-Diabetic than in Diabetic Patients: a Bold-FMRI Study.

Background: Cerebrovascular reactivity (CVR) has been suggested as an independent predictor of stroke in patients with severe carotid stenosis. Functional-MRI (fMRI) can be used to assess CVR by comparing latency parameters of the neurovascular coupling, i.e. BOLD response at baseline and during hypercarbic challenge. We aim to compare BOLD amplitude and latency parameters in the ipsilateral (IH) and contralateral hemispheres (CH) induced by auditory stimulus, under different hypercapnia levels in diabetic and non-diabetic patients with symptomatic carotid stenosis, before and after carotid stenting. Methods: seven diabetic and eight non-diabetic patients with unilateral severe symptomatic carotid stenosis and similar clinical characteristics were evaluated. The protocol was undertaken one week before and three months after the endovascular intervention. Subjects were submitted to auditory stimulus (3s) under normocapnia and EtCO2 increase of 5 and 10mmHg. The images were acquired with a 3T MRI-scanner, preprocessed and BOLD response amplitude and latency parameters were analyzed. Results: We observed decreased BOLD amplitude in the IH compared to the CH (p&lt;0.05) in non-diabetic patients in hypercapnic conditions, and was compromised bilaterally in diabetic patients before the stenting. In diabetic patients the mean change on BOLD latency parameters were not significant with CO2 increment. After carotid stenting, BOLD amplitude (p&lt;0.05) under hypercapnic conditions and area under the curve (P&lt;0.05) were increased for non-diabetic patients but not for diabetic patients. Conclusions: diabetic patients have diffuse baseline compromise of CVR and their cerebrovascular reactivity measured on BOLD fMRI does not respond to carotid stenting as non-diabetic patients.

The risk of carotid artery stenting compared with carotid endarterectomy is greatest in patients treated within 7 days of symptoms

Among patients with symptomatic carotid artery stenosis, carotid artery stenting (CAS) is associated with a higher risk of periprocedural stroke or death than carotid endarterectomy (CEA). Uncertainty remains whether the balance of risk changes with time since the most recent ischemic event. We investigated the association of time between the qualifying ischemic event and treatment (0-7 days, 8-14 days, and >14 days) with the risk of stroke or death within 30 days after CAS or CEA in a pooled analysis of data from individual patients randomized in the Endarterectomy vs Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial, the Stent-Protected Angioplasty versus Carotid Endarterectomy (SPACE) trial, and the International Carotid Stenting Study (ICSS). Data were analyzed with a fixed-effect binomial regression model adjusted for source trial. Information on time of qualifying event was available for 2839 patients. In the first 30 days after intervention, any stroke or death occurred significantly more often in the CAS group (110/1434 [7.7%]) compared with the CEA group (54/1405 [3.8%]; crude risk ratio, 2.0; 95% confidence interval, 1.5-2.7). Patients undergoing CEA within the first 7 days of the qualifying event had the lowest periprocedural stroke or death rate (3/106 [2.8%]). Patients treated with CAS in the same period had a 9.4% risk of periprocedural stroke or death (13/138; risk ratio CAS vs CEA: 3.4; 95% confidence interval, 1.01-11.8; adjusted for age, sex, and type of qualifying event). Patients treated between 8 and 14 days showed a periprocedural stroke or death rate of 3.4% (7/208) and 8.1% (19/234), respectively, for CEA and CAS. The latest treatment group had 4% complications in the CEA group (44/1091) and 7.3% in the CAS group (78/1062). The increase in risk of CAS compared with CEA appears to be greatest in patients treated within 7 days of symptoms. Early surgery might remain most effective in stroke prevention in patients with symptomatic carotid artery stenosis.

Platelet Activation, Function, and Reactivity in Atherosclerotic Carotid Artery Stenosis: A Systematic Review of the Literature

An important proportion of transient ischemic attack or ischemic stroke is attributable to moderate or severe (50-99%) atherosclerotic carotid stenosis or occlusion. Platelet biomarkers have the potential to improve our understanding of the pathogenesis of vascular events in this patient population. A detailed systematic review was performed to collate all available data on ex vivo platelet activation and platelet function/reactivity in patients with carotid stenosis. Two hundred thirteen potentially relevant articles were initially identified; 26 manuscripts met criteria for inclusion in this systematic review. There was no consistent evidence of clinically informative data from urinary or soluble blood markers of platelet activation in patients with symptomatic moderate or severe carotid stenosis who might be considered suitable for carotid intervention. Data from flow cytometry studies revealed evidence of excessive platelet activation in patients in the early, sub-acute, or late phases after transient ischemic attack or stroke in association with moderate or severe carotid stenosis and in asymptomatic moderate or severe carotid stenosis compared with controls. Furthermore, pilot data suggest that platelet activation may be increased in recently symptomatic than in asymptomatic severe carotid stenosis. Excessive platelet activation and platelet hyperreactivity may play a role in the pathogenesis of first or subsequent transient ischemic attack or stroke in patients with moderate or severe carotid stenosis. Larger longitudinal studies assessing platelet activation status with flow cytometry and platelet function/reactivity in symptomatic vs. asymptomatic carotid stenosis are warranted to improve our understanding of the mechanisms responsible for transient ischemic attack or stroke.

Preliminary report of carotid endarterectomy versus stenting treatment in patients with severe symptomatic carotid stenosis

Objective To compare stenting treatment with endarterectomy in patients with symptomatic carotid stenosis (at least 60％ ).Methods We conducted a center randomized controlled noninferiority trial for comparing stenting treatment to endarterectomy in 195 patients with severe symptomatic atherosclerotic carotid artery stenosis.The primary end point of this hospital - based study was ipsiateral ischaemic stroke or death from time of randomisaion to 90 days after the proceduce.The secondary end point was the related complications of either intervention,or severe restenosis at 90 day after operation.Results 195 patient were induded in the analysis.The rate of death or ipsiateral ischaemic stroke frow randomization to 90 days after stenting procedure was 3.1％ and 3.1％ after carotid endarterectomy.The one - sided p value for non - inferiority is 0.08.The secondary end point occurred in 8 patients randomly assigned to undergo endarterectomy (cumulative incidence,8.3％ ) and 5 patients randomly assigned to undergo stenting (cumulative in cadence,5.1％ ).The difference was not significant.Cranial - nerve injury was more commonly seen after endarterectomy than that after stenting.Conclusions There is no difference in the risks of stenting treatment compared with carotid endarterectomy.The risk of stroke or death after 90 days of treatment is almost identical in both groups. Key words: Endarterectomy; Angioplasty; Randomized controlled trials; Carotid stenosis

Increased Platelet Count and Lymphocyte-Platelet Complex Formation in Patients with Recently Symptomatic Versus Asymptomatic Carotid Stenosis: Results from the Platelets and Carotid Stenosis (PACS) Study (P01.026)

Objective: We hypothesised that patients with recently symptomatic moderate or severe carotid stenosis would have excessive platelet activation compared with asymptomatic carotid stenosis patients. Background The precise mechanisms responsible for the disparity in stroke risk between asymptomatic and symptomatic carotid stenosis patients are unclear. We hypothesised that recently symptomatic patients would have excessive platelet activation compared with their asymptomatic counterparts. Design/Methods: We performed an observational analytical study to compare haematological parameters and platelet activation status in asymptomatic versus early (≤4 weeks after TIA or stroke onset) and late phase (≥3 months) symptomatic moderate or severe (≥50%) carotid stenosis patients. The sensitive and specific technique of whole blood flow cytometry was used to quantify platelet surface CD62P and CD63 expression, and the % circulating leucocyte-platelet complexes. Unpaired non-parametric comparisons were performed with the Wilcoxon rank sum test. Results: Data from 31 asymptomatic carotid stenosis patients were compared with those from 46 symptomatic patients in the early phase, and 35 of these patients in the late phase after symptom onset, 23 of whom underwent intervention. Median platelet count was higher in early symptomatic than asymptomatic carotid stenosis patients (211 vs. 200 x 109/L; p=0.03), but the differences between the late symptomatic and asymptomatic groups were not significant (219 vs 200 x 109/L, p=0.1). The median % lymphocyte-platelet complexes was higher in early symptomatic than asymptomatic patients (2.8 vs. 2.4%, p=0.001; Figure 1). There were no significant differences in the expression of other activation markers between the groups. Conclusions: These findings improve our understanding of the haemostatic/thrombotic profile in carotid stenosis. Increased platelet count and leucocyte-platelet complex formation could predispose to recurrent ischaemia or infarction in patients with recently symptomatic carotid stenosis. Longitudinal studies are warranted to assess the prognostic value of these biomarkers in asymptomatic and symptomatic carotid stenosis. Disclosure: Dr. Kinsella has nothing to disclose. Dr. Tobin has nothing to disclose. Dr. Tierney has nothing to disclose. Dr. Feeley has nothing to disclose. Dr. Egan has nothing to disclose. Dr. Collins has nothing to disclose. Dr. Coughlan has nothing to disclose. Dr. O9Neill has nothing to disclose. Dr. Harbison has nothing to disclose. Dr. Doherty has received personal compensation for activities with UCB Pharamaceuticals, Eiasi, and Jansen-Cilag. Dr. Madhavan has nothing to disclose. Dr. Moore has nothing to disclose. Dr. O9Neill has nothing to disclose. Dr. Murphy has nothing to disclose. Dr. Hamilton has nothing to disclose. Dr. Mccabe has nothing to disclose.