This study determined the effect of hyperglycemia-mediated inflammation on progression of atherosclerotic cardiovascular disease in type 2-diabetes. The exact mechanism leading to inflammation in diabetes remained obscure, until recently when it was demonstrated that hyperglycemia, a characteristic of poorly controlled type 2-diaebtes, mediates epigenetic reprograming (methylation and acetylation) in genes implicated in inflammation such as RELA. The RELA gene encodes for p65 subunit of NF-kB, a master switch that regulates the expression of pro-inflammatory cytokines.  It was further demonstrated that methylation of RELA was sensitive to glycaemic control, where transient spike in glucose levels induced persistent epigenetic changes in RELA gene. Therefore, this study is focused on research i) To measure epigenetic changes over time in RELA gene and its impact on expression of NF-kB in response to hyperglycemia, ii) measure the effect of hyperglycemia on inflammatory response in type 2-diabetes iii) evaluate the potential of pro-inflammatory cytokines and non-cytokine markers (C-reactive protein, and lipid profile) in determining the risk of CVD in those with diabetes.