Mechanisms to explain the poor results of carotid artery stenting (CAS) in symptomatic patients to date and options to improve CAS outcomes

BackgroundCarotid artery stenting (CAS) is considered by many as an alternative to carotid endarterectomy (CEA) for the management of carotid artery stenosis. However, recent trials demonstrated inferior results for CAS in symptomatic patients compared with CEA. We reviewed the literature to evaluate the appropriateness of CAS for symptomatic carotid artery stenosis and to determine the pathogenetic mechanism(s) associated with stroke following the treatment of such lesions. Based on this, we propose steps to improve the results of CAS for the treatment of symptomatic carotid stenosis.MethodsPubMed/Medline was searched up to March 25, 2010 for studies investigating the efficacy of CAS for the management of symptomatic carotid stenosis. Search terms used were “carotid artery stenting,” “symptomatic carotid artery stenosis,” “carotid endarterectomy,” “stroke,” “recurrent carotid stenosis,” and “long-term results” in various combinations.ResultsCurrent data suggest that CAS is not equivalent to CEA for the treatment of symptomatic carotid stenosis. Differences in carotid plaque morphology and a higher incidence of microemboli and cerebrovascular events during and after CAS compared with CEA may account for these inferior results.ConclusionsCurrently, most symptomatic patients are inappropriate candidates for CAS. Improved CAS technology referable to stent design and embolic protection strategies may alter this conclusion in the future

How to identify which patients with asymptomatic carotid stenosis could benefit from endarterectomy or stenting

Offering routine carotid endarterectomy (CEA) or carotid artery stenting (CAS) to patients with asymptomatic carotid artery stenosis (ACS) is no longer considered as the optimal management of these patients. Equally suboptimal, however, is the policy of offering only best medical treatment (BMT) to all patients with ACS and not considering any of them for prophylactic CEA. In the last few years, there have been many studies aiming to identify reliable predictors of future cerebrovascular events that would allow the identification of patients with high-risk ACS and offer a prophylactic carotid intervention only to these patients to prevent them from becoming symptomatic. All patients with ACS should receive BMT. The present article will summarise the evidence suggesting ways to identify these high-risk asymptomatic individuals, namely: (1) microemboli detection on transcranial Doppler, (2) plaque echolucency on Duplex ultrasound, (3) progression in the severity of ACS, (4) silent embolic infarcts on brain CT/MRI, (5) reduced cerebrovascular reserve, (6) increased size of juxtaluminal hypoechoic area, (7) identification of intraplaque haemorrhage using MRI and (8) carotid ulceration. The evidence suggests that approximately 10%-15% of patents with asymptomatic stenosis might benefit from intervention; this will become more clear after publication of ongoing studies comparing stenting or endarterectomy with best medical therapy. In the meantime, no patient should be offered intervention unless there is evidence of high risk of ipsilateral stroke, from modalities such as those discussed here

The Impact of Lower Extremity Venous Ulcers due to Chronic Venous Insufficiency on Quality of Life

Lower extremity venous ulcers comprise a complex medical and social issue. The conservative and/or surgical management of venous ulcers is often inadequate. In addition, the psychosocial aspect of the disease is often overlooked and most often undertreated. Common symptoms such as pain, low self-esteem and patient isolation are usually not recognized and therefore not adequately managed

Increased Fluorodeoxyglucose Uptake Following Endovascular Abdominal Aortic Aneurysm Repair: A Predictor of Endoleak?

The main criterion for abdominal aortic aneurysm (AAA) repair is an AAA diameter ≥5.5 cm. However, some AAAs rupture when they are smaller. Size alone may therefore not be a sufficient criterion to determine rupture risk. Fluorodeoxyglucose (FDG) uptake is increased in the presence of inflammation and it was suggested that this may be a better predictor of rupture risk than AAA size. Furthermore, increased FDG uptake following endovascular AAA repair may be an indirect predictor of continuous AAA sac enlargement due to the presence of an endoleak (even if this is not detected by imaging modalities) and/or increased AAA rupture risk. The role of FDG uptake needs to be explored further in the management of AAAs