Atherosclerosis is a vascular inflammatory disease resulting from lipid deposition within vascular wall and changes in structure and function of the vascular wall. Atherosclerosis is accelerated when total and LDL cholesterol are elevated and/or HDL is low. Free radical production is increased in hypercholesterolemia leading to oxidative transformation of both parts of LDL particles, protein and lipid part. Small, dense LDL particles have extreme atherogenic potential; they can be easily oxidized and strongly maintain vascular inflammation. Oxidized LDL particles (oxLDL) support further free radical production. OxLDL are removed by macrophages into sub epithelial space. During that process macrophages produce inflammatory cytokines and induce the production of adhesion molecules, which further cause adherences of new macrophages and further support inflammation. OxLDL also induce sinthesis of endothelial growth factor receptors, which enable transduction of different signals important for: vascular remodeling, cellular migration, mitosis and NF-kappaB activation and increased metalloproteinase activity. HDL particles have an important role in the reverse cholesterol path and protective effects in vascular inflammation and atherogenesis. The ratio of apoprotein AI and AII, amount of CETP, LCAT and paraoxsonase, determine the function of HDL particles. Increased levels of triglycerides in the morning and especially postprandial levels are an independent risk factor for coronary heart disease, and heighten the risk when associated with other lipid disturbances. An increased triglyceride level is associated with the increased PAI I and reduced fibrinolisis. The ratio of total cholesterol/HDL cholesterol, as well as the levels of markers of inflammation such as CRP or IL-6, have great predictive value for the development of ischemic heart disease and cardiovascular diseases.