Arteriosclerosis is not an inevitable eonsequenee of age, as formerly supposed, but a reaetiv disease. It ean be prevented by elimination of the pathogenic faetors and regression of the lesions of the wall strueture by treatment is possible. Our experiments with animal models demonstrate that the aeeeierated metabolism of the arterial wall eells, indueed by very many kinds of pathogenic faetors, of risk faetors, is the real pathologie proeess, which produees a polymorphie pieture of deformations in the arterial wall. Today we have at our disposal a big preventive and therapeutical arsenal, the elimination of risk faetors, the treatment of basie diseases, such as arterial hypertension and hyperlipidemia, the applieation of lipidlowering drugs and antieoagulants. But the real pathologie proeess of arteriosclerosis, the aeeel­ erated metabolism of the arterial wall eells is influeneed by none of these therapeutical measures. Our experiments with animal models suggest that mesenchyme suppressive (antiphlogistie, antirheumatie) drugs will have these effeet. The result of a prospective double-blind-study (secondary prevention of myoeardial in­ faretion) in my clinic is reported.