At the end of the 20th century, the contribution of hyperlipoproteinemia (a) to early development and severity of coronary, cerebral and peripheral artery atherosclerosis was established, and its association with the development of aortic valve stenosis was shown. The results of epidemiological studies allow us to consider lipoprotein(a) (Lp(a)) as a new target for the diagnosis, prevention and pharmacotherapy of atherosclerotic cardiovascular diseases. The atherogenicity of Lp(a) is 6 times higher than that of low-density lipoproteins and can be the cause of early and rapid progression of atherosclerosis. The 2022 European Atherosclerosis Society statement stated that the threshold value of Lp(a) for "excluding" the risk of atherosclerotic cardiovascular diseases is less than 30 mg/dL. The range of Lp(a) values between 30 mg/dL and 50 mg/dL creates the so-called "grey zone" when the possible risks associated with Lp(a) and other cardiovascular risk factors should be considered. At Lp(a) values >180 mg/dL, the risk of cardiovascular diseases is equivalent to the risk of patients with heterozygous familial hypercholesterolemia. This review will discuss the genetic and pathophysiological properties of Lp(a), and the epidemiological data demonstrating its effect on cardiovascular morbidity. Extracorporeal methods for removing excess Lp(a) from blood serum are currently the only proven option to correct this dyslipidemia. Cascade plasmafiltration helps reduce LDLcholesterol and Lp(a) levels by more than 60%, as well as to decrease the level of oxidized phospholipids in plasma. It should be noted that according to 2023 domestic recommendations, the criteria for extracorporeal treatment are Lp(a) >50.0 mg/dl. The review provides recommendations for screening and treatment of patients with elevated Lp(a) levels, as well as a range of pharmacotherapeutic drugs being developed to reduce its level in the blood.