Diabetes is associated with major life-threatening complications such as a markedly increased risk of cardiovascular disease, even in the presence of rigid glycemic control. Indeed, nearly 75% of diabetic patients eventually die of cardiovascular disease or cardiovascular complications. A striking feature of the diabetic cardiovascular phenotype is the appearance of accelerated atherosclerosis, which resembles atherosclerosis that may be encountered in the non-diabetic individual, except that it is more extensive, aggressive, and occurs at an earlier age. Atherosclerosis (or atherosclerotic vascular disease; ASVD), is a pathological syndrome affecting arterial vessels characterized by narrowing of the vascular lumen secondary to intravascular buildup of fatty material such as cholesterol, aggregated cellular debris, and inflammatory change in the vascular endothelium. Seemingly distinct, these two well-defined disorders are nevertheless, intimately and intricately linked. In fact, these two pathologies appear to be linked by common signaling pathways and shared regulatory systems that appear to go awry in an as yet poorly understood manner. In recent years, a body of evidence has been growing that suggests that inflammation peculiar to the vascular system, occurs in the diabetic patient. This review aims to present the empirical underpinning of the hypothesis that inflammatory change in the vasculature might be the integrated mechanism that connects a diabetic phenotype with its attendant vascular complications.