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Endothelial microparticles (EMPs) are complex submicron membrane-shed vesicles released into the circulation following endothelium cell activation or apoptosis. They are classified as either physiological or pathological, with anticoagulant or pro-inflammatory effects respectively. Endothelial dysfunction caused by inflammation is a key initiating event in atherosclerotic plaque formation. Athero-emboli, resulting from ruptured carotid plaques are a major cause of stroke. Current clinical techniques for arterial assessment, angiography and carotid ultrasound, give accurate information about stenosis but limited evidence on plaque composition, inflammation or vulnerability; as a result, patients with asymptomatic, or fragile carotid lesions, may not be identified and treated effectively. There is a need to discover novel biomarkers and develop more efficient diagnostic approaches in order to stratify patients at most risk of stroke, who would benefit from interventional surgery. Increasing evidence suggests that EMPs play an important role in the pathogenesis of cardiovascular disease, acting as a marker of damage, either exacerbating disease progression or triggering a repair response. In this regard, it has been suggested that EMPs have the potential to act as biomarkers of disease status. In this review, we will present the evidence to support this hypothesis and propose a novel concept for the development of a diagnostic device that could be implemented in the clinic.

IntroductionCarotid endarterectomy (CEA) should be performed within two weeks of symptoms for patients with carotid stenosis >50%. Whether these standards are being achieved and causes of delay between symptoms and CEA were investigated.DesignAn analysis of prospectively collected multi-centre data.MaterialsConsecutive data for patients undergoing CEA between January-2006 and September-2010 were collected. Asymptomatic patients and those with no details on the timing of cerebral symptoms were excluded.Methods‘Delay’ from symptom to CEA was defined as more than two weeks and ‘prolonged-delay’ more than eight weeks. Univariable and multivariable analyses were used to identify factors associated with these delays.ResultsOf 2147 patients with symptoms of cerebral ischaemia, 1522(70.9%) experienced ‘delay’ and 920(42.9%) experienced ‘prolonged delay’. Patients with ischaemic heart disease were more likely to experience ‘delay’ (OR = 1.56; 95% CI 1.11–2.19, p = 0.011), whereas patients with stroke (OR = 0.77; 95%CI 0.63–0.94, p = 0.011) and those treated at hospitals with a stroke-prevention clinic (OR = 0.57; 95%CI 0.46–0.71, p

Indium-111 labelled platelet scintigraphy permits simple, accurate evaluation of platelet kinetics and sites of deposition. The most meaningful results are obtained from serial scans, although these are clinically useful in only a few of the many applications that have been suggested, principally in studies of acute thrombosis, prosthetic graft thrombogenicity and antiplatelet medication. Key pitfalls are associated with selection of regions and patient variation.

Objectives: This study aimed to identify the risk factors that influence the healing process of venous leg ulcers treated with compression bandaging, with a view to predicting healing time. Method: A retrospective cohort study was performed on data collected prospectively on 325 consecutive patients presenting with 345 venous ulcers at the Salford Primary Care Trust leg ulcer clinic between January 1997 and December 1999. Use of an artificial neural network (ANN) technique accurately predicted the healing times for 68% of the patients. Results: The ANN demonstrated that healing was significantly related to a history of previous leg ulceration, ‘quite wet’ ulcer exudate, high body mass index, large initial total ulcer area, increasing age and male gender. Conclusion: The ability to identify at presentation ulcers that might be resistant to standard therapy would allow early consideration of more radical treatments such as hospitalisation, wound debridement or venous surgery. Declaration of interest: None.

Introduction Stroke is the third most common cause of death world wide. Most cases of stroke are caused by atherosclerotic plaque rupture. A challenge facing clinicians is identifying asymptomatic patients at risk of plaque instability. Locally released angiogenic growth factors may contribute to microvessel instability within plaques. Growth factors and inflammatory cytokines are potential serum biomarkers to identify patients at risk of stroke. Materials and methods Immunohistochemistry and quantitative PCR (Q-PCR) were used to establish localisation and expression of angiogenic growth factors within carotid endarterectomy specimens from symptomatic and asymptomatic patients. Stable or unstable microvessels were distinguished by CD31 and CD105 staining. Systemic levels of circulating angiogenic growth factors and inflammatory cytokines were measured in venous blood using Bio-Plex arrays. Results Hepatocyte growth factor (HGF) and its receptor c-Met were detected in CD31-positive endothelia, and α-SMA-positive cells, respectively. Q-PCR demonstrated upregulation of the angiogenic factors CD105, HGF (p Discussion Plaque instability may be mediated by HGF-induced formation of microvessels, and decreased PDGF. We will investigate the effects of inflammatory cytokines with a view to comparing symptomatic versus asymptomatic patients. Targeting surgery to those who will benefit would eliminate unnecessary risk.