Atherosclerosis is characterized by chronic inflammation of an injured intima. The pathological processes are initiated by accumulation of morphologically distinct, modified forms of LDL, and followed by cellular infiltration and foam cell formation. Activated intimal cells secrete enzymes and agents capable of modifying LDL, and the modified lipids of LDL, in turn, are able to activate intimal cells and to trigger various inflammatory signals. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression. In this review, we focus on the LDL modifications relevant to the initial lipid accumulation and discuss their pro-inflammatory effects.