Healthy human arteries are composed of three layers: the intima, the media, and the adventitia. Endothelial cells, which form the tunica intima, provide the physical interface between blood and surrounding tissue, regulate nutrient and blood component traffic, and participate in many physiologic events, such as hemostasis, inflammation, and angiogenesis. Within the tunica media, smooth muscle cells and extracellular matrix proteins, such as elastin, collagen, and proteoglycans, are quantitatively the largest components of the aortic vascular wall. The structural changes with atherosclerosis are currently considered degenerative phenomena, which primarily involve a sequence of reactions within the intima and include monocyte recruitment and macrophage formation, lipid deposition, smooth muscle cell migration, proliferation, and extracellular matrix synthesis. The molecular and cellular mechanisms underlying the disease cascade have been thoroughly investigated in experimental animals and cell culture, but the question of how these models can correctly mimic the human course of the disease remains open to debate. In the present review the basic structure of healthy human arteries and the pathological events occurring during the atherosclerotic process have been examined by both transmission and scanning electron microscopy. Human atherosclerotic lesions are presented and described in the following order: initial lesions, fatty dots and streaks, intermediate lesions, atheroma and fibrofatty plaques, and complicated lesions.