Diabetes and atherosclerosis Figure 26 Chronic hyperglycemia leads to accumulation of glycated proteins in the blood. This causes an increase in vascular permeability which, in turn, increases the level of oxidized LDL. There is also a release of cytokines, which increases the level of vascular inflammation.

Tobacco and atherosclerosis Figure 27 Smoking increases the formation of oxidative free radicals, which raises the level of oxidized LDL. Nicotine has several direct effects, which include: increased cytokine production (which raises the level of vascular inflammation); direct cytotoxicity; vasospasm.

Dyslipidemia and atherosclerosis Figure 28 Atherogenic lipoproteins (e.g. LDL, apo B-rich particles like Lp-B:C-III) penetrate the arterial wall and induce: expression of adhesion molecules (which capture monocytes which then migrate into the intima); differentiation of macrophages (which release inflammatory cytokines); increased lipoprotein capture and penetration.

HTN, hemodynamic factor and atheroclerosis Figure 29 Hypertension creates areas of low shear stress within arteries, which in turn results in: increased endothelial permeability; increased duration of lipoprotein contact with the endothelium; increased lipoprotein penetration; decreased endothelium-dependent vasodilation.

How to reduce plaque formation Intervention on risk factors Figure 30 Risk factor modification is a key therapeutic target in patients with and without clinically manifested atherosclerotic disease.