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Background and aims Diabetes is traditionally associated with vascular calcification, but the molecular mechanisms are largely unknown. We herein explored the relationships among carotid plaque calcification, composition and gene expression, and how these are modified by diabetes. Methods We collected carotid endoarterectomy specimen from 59 patients, of whom 23 had diabetes. We analysed histology with pentachromic staining, calcification with Alizarin red and Von Kossa's staining, chemical calcium extraction and quantification, as well as gene expression by quantitative PCR. Results We detected no differences in the extent of plaque calcification and in plaque composition between diabetic and non-diabetic patients. In non-diabetic plaques, calcium content was directly correlated with the area occupied by muscle/fibrinoid tissue and inversely correlated with collagen, but such correlations were not seen in plaques from diabetic patients. While consistent correlations were found between calcium content and RUNX2 (direct), as well as Osteopontin (inverse), diabetes modified the association between plaque calcification and inflammatory gene expression. Only in diabetic plaques, calcium content was inversely correlated with MCP1 and IL1b, whereas the direct correlation with TNF-alpha expression seen in non-diabetic plaques was lost in diabetes. Conclusions Though plaque composition and calcification were not quantitatively affected, diabetes modified the relationships between plaque calcium, composition and inflammation. These results suggest that the mechanisms and the clinical significance of atherosclerotic calcification in diabetic may be different than in non-diabetic patients.

Occlusion of the contralateral internal carotid artery (ICA) is considered to have a significant impact on the outcome of carotid endarterectomy (CEA). The purpose of this study was to review one center's experience concerning CEA opposite an occluded ICA, to see whether results differed from those obtained in patients with patent contralateral ICA in terms of relevant neurologic complication rate (RNCR, fatal + disabling stroke), stroke-free rate, and survival rate. From January 1997 to December 2002, 1,381 patients underwent a total of 1,445 CEAs at the Department of Vascular Surgery of Padua University. Patients were divided into two groups: group A included 144 patients with occlusion of the contralateral ICA and group B consisted of 1,237 patients with a patent contralateral ICA. There was no postoperative mortality in patients of group A, while in group B, two patients died as a result of myocardial infarction and cardiac failure and one died as a direct result of perioperative stroke. Postoperative disabling strokes occurred in one (0.7%) patient in group A and 10 (0.8%) patients in group B (p > 0.5). At 72 months, there were no statistical differences between the two groups in terms of RNCR, stroke-free rate, and late death. Our results show that contralateral carotid occlusion does not reduce the safety of CEA. The efficacy in terms of RNCR, stroke-free rate, and late survival is no different in patients with contralateral carotid occlusion.

OBJECTIVES We sought to establish whether a reduction in endothelial progenitor cells (EPCs) has a putative role in peripheral vascular disease (PVD) of type 2 diabetic patients. BACKGROUND Peripheral vascular disease is a common and severe complication of diabetes mellitus. Impaired collateralization of diabetic vasculopathy has been extensively shown, but causes leading to its pathogenesis are not fully understood. Recently, EPCs have been found to contribute to vascular repair and angiogenesis. Diabetes has been associated with low levels of circulating EPCs, but no data are available in the literature on the relationship between EPCs and PVD in diabetes. METHODS Flow cytometric analysis was used to quantify circulating progenitor cells (CPCs, CD34+) and EPCs (CD34+KDR+) in 51 patients and 17 control subjects. RESULTS The CPCs and EPCs from diabetic patients were reduced by 33% and 40%, respectively, compared with healthy subjects (p < 0.001). An inverse correlation was found between the number of EPCs and the values of fasting glucose (r = -0.49, p = 0.006). Peripheral vascular disease was associated with a 47% reduction in EPCs (p < 0.0001) and EPC levels directly correlated with the ankle-brachial index (r = 0.70, p = 0.01). The subgroup of diabetic patients with PVD also had reduced CPCs by 32% (p = 0.037), whereas patients with ischemic foot lesions had the lowest levels of both EPCs and CPCs (p = 0.02). CONCLUSIONS Our data demonstrate decreased EPC levels in diabetic patients and, for the first time, show that PVD is associated with an extensively low number of EPCs. Depletion of circulating EPCs in diabetic patients may be involved in the pathogenesis of peripheral vascular complications.

A new endovascular procedure is reported to treat bilateral common iliac artery (CIA) aneurysms extending to both iliac bifurcations.The left internal iliac artery (IIA) was first embolised, two overlapped Viabahn endografts were delivered from the right IIA to the distal aorta and, finally, CIA aneurysms excluded using iliac contralateral leg and extension endografts from the distal aorta to both external iliac arteries, applying a combined 'chimney-graft/double-barrel' technique.This procedure may extend the limits of conventional iliac endografting by preserving blow flow to at least one IIA using off-label commercially available devices, avoiding associated open surgical procedures. © 2010 European Society for Vascular Surgery.