Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries Endorsed by: the European Stroke Organization (ESO) The Task Force for the Diagnosis and Treatment of Peripheral Arterial Diseases of the European Society of Cardiology (ESC) and of the European Society for Vascular Surgery (ESVS)

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AAAs. There were 28 deaths (6.1%) following elective repair of 459 incidentally detected AAAs (OR, 0.37; 0.24 to 0.68).Comment: The risk of death in a male patient Ͼ65 years operated for an incidentally detected aneurysm is approximately three times more than one operated on for a screened detected AAA. The data do not permit a "drill down" for why patients operated on for screened AAAs have lower operative mortality than those operated on for incidentally detected AAAs. Reasons could include lower ages and decreased comorbidities of screened patients. Also, screened patients may have smaller aneurysms and/or less complex anatomy permitting a higher proportion of endovascular repairs. Overall, however, the author's data provid another bit of evidence to encourage screening in patients at risk at for AAA. Proposed Chronic Cerebrospinal Venous Insufficiency Criteria Do Not Predict Multiple Sclerosis Risk or SeverityCentonze D, Floris R, Stefanini M, et al. Ann Neurol 2011;70:51-8. Conclusion: Chronic cerebrospinal venous insufficiency (CCSVI) has no role in either multiple sclerosis (MS) risk or MS severity. Summary: Anatomic abnormalities of major neck and chest veins are proposed to impair central nervous system venous drainage. Zamboni has proposed that CCSVI has a strong association with multiple sclerosis (J Neurol Neurosurg Psychiatry 2009;80:382-99). His results indicate MS is caused by CCSVI and that CCSVI plays a substantial role in MS progression. Endovascular interventions directed to correct abnormalities of venous drainage reportedly characteristic of CCSVI could potentially improve the clinical course of MS (Zamboni P, et al. J Vasc Surg 2009;50:1348-58). However, some question the very existence of CCSVI (Doepp F et al. Ann Neurol 2010;68:173-83).It has been suggested that studies failing to demonstrate a significant association between CCSVI and MS use alternative approaches to define CCSVI than those utilized by Zamboni et al. The authors, therefore, utilized an experimental protocol they feel is identical to that developed by Zamboni and coworkers. This protocol was applied to an independent population of MS patients and healthy controls by operators specifically trained by Dr Zamboni in CCSVI identification.The Zamboni method for CCSVI identification was studied in 84 MS patients and 56 healthy subjects. There were no significant differences (P ϭ .12) in CCSVI frequency between MS and control subjects. No differences were found between CCSVI-positive and CCSVI-negative patients with respect to MS duration, time between MS onset and first relapse, relapsing progressive MS, and risk of secondary progression. There were no statistical differences found between CCSVI-positive and CCSVI-negative MS subjects by analyzing measures of disability such as the mean expanded disability status scale (P ϭ .07) mean progressive index (P Ͼ .1) and mean MS severity score (P Ͼ .1). The percentage of subjects who reached expanded disability status scale 4.0 and 6.0 was not different among CCSVI-negative and CCSVI-p...

whether grade of stenosis, or also treatment delay, or all three criteria (gender, delay and grade of stenosis) were considered. When 150 (17.7%) asymptomatic patients were added to the most precise calculation, the SPP of CEAs decreased from 201.4 to 181.5. Increasing proportion of asymptomatic patients up to 50% or 75% would have decreased the corresponding SPP down to 145.0 or 116.9 for our cohort. The SPP for symptomatic patients (including all subgroups) was 140.8, 159.9 and 179.1 with theoretical 6%, 3% and 0% complication rates, respectively. When the figures for asymptomatic patients on statin treatment at the time of randomization in ACST-1 were used, the SPP for our cohort was 169.5, but if the proportion of asymptomatic patients would have increased to 50% or 75% the SPP would have gone down to 111.2 or 66.7, respectively. Conclusion-From the same cohort of operated patients strokes prevented per 1000 operations in 5 years varied between 145.9 and 201.4 depending on which factors were taken into account. We recommend that grade of stenosis, gender and delay be all considered when the stroke preventing power of CEA services are reported. This may be particularly important when national and international comparisons are made from registered data. References 1. Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJM. Sex-difference in effect of time from symptoms to surgery on benefit from carotid endarterectomy for TIA and non-disabling stroke. Stroke. 2004;35:2855e2861 2. Naylor AR. An update on the randomized controlled trials of interventions for symptomatic and asymptomatic carotid artery disease.