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104 | Chapter 7 Lipoprotein apheresis Lipoprotein apheresis can lower LDL-C 60-70% by removal of lipoproteins from the circulation. It is used in patients with severe hypercholesterolemia such as homozygous familial hypercholesterolemia (FH) [22]. Another indication for lipoprotein apheresis is Lp(a)-hyperlipoproteinemia (Lp(a) > 0,6g/L) with progressive CVD [23]. In these patients, who are adequately treated with statins, lipoprotein apheresis reduces Lp(a) by 70% directly post-treatment [22, 23], this led to a decrease of major adverse coronary events by 78% [22]. However, it is uncertain whether the reduced event rate is due to Lp(a) lowering per se, because lipoprotein apheresis also lowers other lipoproteins, and may as well reduce other unknown risk factors. Disadvantages of lipoprotein apheresis include it’s time expenditure and costs. Furthermore apheresis is not reimbursed in all countries. Despite the limited indication and availability, lipoprotein apheresis is a sound method to reduce CVD events in Lp(a)-hyperlipoproteinemia patients who have progressive CVD, although it is unknown if this effect is due to Lp(a) lowering per se. Niacin Niacin (Vitamin B3 or nicotinic acid) has multiple effects on different lipoproteins; it lowers LDL-C and triglycerides (TG), and it increases HDL-C. Since 1990 it is being reported that niacin can also lower Lp(a) although the mechanism is unclear [24]. In the AIM-High (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides) trial patients were treated with high dose extended release niacin (1,5-2,0 g/day) or placebo, on top of statins. Baseline Lp(a) and on-study Lp(a) predicted CVD events in both arms [25]. This suggest that Lp(a) still contributes to residual risk. In the extended release niacin group Lp(a) was 19% lower than in the placebo group. Despite this reduction in Lp(a), extended release niacin did not lead to a reduction in CVD events [25]. The criticism regards this trial include the fact that patients were at low LDL-C levels (1.97 mmol/L), and critical differences in terms of LDL-C, HDL-C and TG levels were very small between treatment arms. The observed event rate was lower than expected, and the overall study was seriously underpowered [25, 26]. In addition, the recent HPS-2- THRIVE (Heart Protection Study-2-Treatment of HDL to Reduce the Incidence of Vascular Events) trial also failed to show benefit on CVD outcome, despite an Lp(a) reduction of 24% [27]. In this trial Tredaptive (niacin 2g/laropiprant 40mg, MSD, Whitehouse Station, NJ, USA) was compared to placebo, on top of statin therapy. LDL-C , HDL-C and TG levels were optimal and it is questionable whether 2g of nicotinic acid is the correct therapy in that situation. It is also possible that the addition of lapopiprant, a prostaglandin D2

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