Carotid intima-media thickness (IMT), indices of large artery stiffness and measures of endothelium function may be used as markers of early atherosclerosis in type 1 diabetes mellitus (T1DM). The aim of the present study was to compare the indices of large artery structure and function as well as endothelial function and regenerating capacity between adolescents with T1DM and healthy control of similar age. In addition, the associations of different vascular measures with endothelial progenitor cells (EPCs), glyco-metabolic control and serum levels of advanced glycation endproducts (AGEs), soluble receptors for AGEs (sRAGE) and adiponectin were evaluated.

Atherosclerosis is now generally accepted as an inflammatory disease, characterized by degenerative changes and extracellular accumulation of lipid and cholesterol. The evolving inflammatory reaction plays an important role in the initiation of atherosclerotic plaques and their destabilization, converting a chronic process into an acute disorder with an ensuing thrombo-embolism. Neovascularization has been, also, recognized as an important process for the progression of atherosclerotic plaques. In fact, vulnerable atherosclerotic plaque prone to rupture are characterized by an enlarged necrotic core containing an increased number of vasa vasorum, apoptotic macrophages, and more frequent intraplaque haemorrhage. Various functional roles have been assigned to intimal microvessels. This network of immature blood vessels is a viable source of intraplaque haemorrhage providing erythrocyte-derived phospholipids and free cholesterol. However, it is still challenging and controversial the relationship between the very process of angiogenesis and its causal association with the progression and complication of atherosclerosis. The selective targeting of neoangiogenesis poses a possible approach for the elimination of pre-existing and new growth of microvessels. The identification of target lesions is a critical issue, because current technologies have yet to achieve the goal of characterizing plaque morphology to the degree necessary to correctly identify rupture-prone lesions according to pathologic criteria. However, few imaging techniques can be used to detect the neovascularization within the atherosclerotic plaque in vivo. This review discusses the potential role of intraplaque angiogenesis as risk factor for plaque vulnerability.

Accumulating evidence indicates that circulating endothelial progenitor cells (EPCs) derived from bone marrow contribute to reendothelialization of injured vessels as well as neo-vascularization of ischemic lesions in either a direct or an indirect way. Moreover, the number and/or the functional activity of EPCs are inversely correlated with risk factors for cardiovascular disease. Among the different risk factors, cigarette smoking is a major cause of reducing the numbers and function of circulating EPCs. This review is a revision of recent literature on EPC alteration associated with smoking. In particular, we show the recent observation on the effects of active and second hand smoke (SHS) exposure on EPC number and functional activity. This review also considers the effects of nicotine and other smoke compounds on EPC number and activity, in in vitro and in vivo models.