**2. Pathogenesis of atherosclerosis**

Atherogenesis starts early in life. Subintimal lipoprotein accumulation and leukocyte adhesion occurs as a result of increased endothelial permeability due to endothelial damage. Intimal neovascularization is seen with the migration of vasa vasorum into the intima. There is a structure in the luminal side of the atherosclerotic plaque that is called fibrous cap which contains molecules such as smooth muscle, collagen, and elastin. External elastic lamina is placed adjacent to the atherosclerotic plaque and tunica media and the lipid core is found between these two structures and it is made from the cholesterol crystals, smooth muscle cells, vascular structures, and foam cells.

Atherosclerotic plaques create luminal stenosis in the advanced stage. The first study in this subject was conducted by Glagov et al. in autopsy material of a patient with 136 left main coronary artery (LMCA) lesions. In this study, there is a positive correlation between internal elastic membrane area and plaque area, and luminal stenosis is prevented by expansion of the compensator at the atheromatous load of less than 40% [1]. In the REVERSAL trial, statin therapy was performed in patients with asymptomatic coronary artery disease. Atheroma volume, percentage of atheroma volume, and atheromatous change in the diseased segment were evaluated and progression of coronary atherosclerosis was observed in the pravastatin receiving group compared to baseline but no progression of atherosclerosis was observed in the atorvastatin group [2].
