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Competing Interests: Conflict of interest: none declared.

Background: Therapeutic apheresis is a term used to describe a group of treatments where blood components are separated in real time, and one component is removed, exchanged, and/or treated to remove pathogenic substances from the circulation. Plasma exchange, which removed all plasma components, and lipid apheresis which selectively removes lipoproteins from circulation, have both been used to treat atherosclerotic vascular diseases., Methods: To review the literature regarding the application of therapeutic apheresis for atherosclerotic vascular diseases., Results: Primarily lipid apheresis is used to treat atherosclerotic vascular diseases, particularly familial hypercholesterolemia, lipoprotein (a) hyperlipoproteinemia and peripheral vascular diseases. Lipid apheresis can be used as first line or second line treatment with a strong evidenced-based recommendation. Its use has decreased atherosclerotic events., Conclusion: Lipid apheresis is an important therapy for the treatment of familial hypercholesterolemia, lipoprotein (a) hyperlipoproteinemia and peripheral vascular diseases. Lipid apheresis does more than remove low-density lipoproteins and other lipoproteins but also decreases inflammatory markers and improves blood flow.

Aims: The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies., Methods and Results: The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, ≥3% 10-year risk of fatal CVD according to European guidelines, and/or ≥10% 10-year risk of fatal + non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than ∼50 mg/dL). Treatment should primarily be niacin 1-3 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a)., Conclusion: We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.

The values of low-density lipoprotein cholesterol obtained according to the Friedewald formula (Clin Chem 1972; 18:499-502), or by the De Long transformation (J Am Med Assoc 1986;256:2372-7), were compared with the values obtained when the individual cholesterol/triglyceride ratio of very-low-density lipoprotein was used for estimating the contribution of this lipoprotein to the total cholesterol. We found that these formulas gave the greatest errors for individuals with a low serum cholesterol/triglyceride ratio. We propose criteria for deciding when the numerically calculated value of low-density cholesterol is appropriate, and when it is not.