Atherosclerosis is a multifactorial and polygenetic disease. In the scientific literature there are more than thousand risk-factors listed and many of them are causal. Here we focus only on the most prominent theories and pathophysiological pathways that are commonly accepted. Atherosclerosis is most abundant in the so called Western Civilized countries and the basis of coronary heart disease and stroke and thus the major cause of death. It starts already in infancy and progresses with age particularly if risk factors accumulate in a given individual. Major risk factors are high low-density lipoprotein (LDL) cholesterol, modified lipoproteins, lipoprotein (a) (Lp(a)), high blood pressure, smoking, oxidative stress, and diabetes mellitus. Pathophysiological pathways start with the damage of the endothelial layer of arteries caused by high plasma cholesterol or free radicals followed by the activation of hemostatic factors and platelet aggregation, the attraction and activation of immune cells, and the migration of lymphocytes and monocytes into the sub-endothelial layer. Monocytes and macrophages take up modified lipoproteins and are eventually transformed to foam cells and the formation of cholesterol crystals. Inflammatory immune cells secrete interleukins and cytokines that further activate the immune system and hemostatic factors. These processes trigger the growth of the atherosclerotic plaque. So-called vulnerable plaques are prone to rupture partly by mechanical stress, the attraction of thrombocytes, and to the occlusion of large vessels, causing myocardial infarction or stroke.