HDL was reduced from 1.0 ± 0.2 mmol/L pre- to 0.5 ± 0.1 mmol/L post-apheresis (p = 0.03). It increased following apheresis and then remained constant throughout the evolocumab treatment. Lp(a) decreased from 484 ± 76 mg/L pre- to 142 ± 15 mg/L post-apheresis (P = 0.02), but there was a small increase from week 1 to week 7 (p < 0.01) during evolocumab therapy. There was a non-significant trend towards an increase in perceived health status (week 0; 57 ± 21, week three; 65 ± 9 and week seven; 77 ± 10).

The researchers reported that treatment with evolocumab was safe and well tolerated. Liver enzymes, bilirubin, liver function, creating kinase (CK), renal function, hematologic profile, and thyroid tests “were controlled at all sampling times, without deviations from normal values at any time.”

They noted that, on average, HDL cholesterol is reduced by 10% to 20% during apheresis. They acknowledge that there is no obvious explanation from this, but suggested that some patients with FH also have low levels of HDL and reduced cholesterol efflux capacity. In the current study, HDL cholesterol, which was reduced after LDL apheresis, returned to pre-apheresis levels in week 1 and remained at that level during evolocumab treatment. This could be “beneficial, with regards to cardiovascular disease,” they said. However, they cautioned, “this finding should be explored in further studies.”

One limitation of the study is that it is observational, the researchers noted. Moreover, the number of participants was low, which limited generalizability. And the effects observed when converting from LDL apheresis to PCSK9 inhibition “may not necessarily reflect effects in apheresis-naïve patients.” Nevertheless, they concluded that their study demonstrated reductions in LDL-C, triglycerides and Lp(a)when switching from LDL apheresis to evolocumab.

The researchers added that this was the first trial to study changes in lipoproteins during transitions from long-term LDL apheresis to self-administered PCSK9 inhibition.


1.      Moriarty PM, Hemphill L. Lipoprotein Apheresis. Endocrinol Metab Clin North Am. 2016 Mar;45(1):39-54.

2.      Hovland A, Marcovina S, Hardersen R, et al. Three different LDL apheresis columns efficiently and equally reduce lipoprotein(a) concentrations in patients with familial hypercholesterolemia and  small apolipoprotein(a) particles. Transfus Apher Sci. 2012 Feb;46(1):73-6.

3.      Lappegård KT, Enebakk T, Thunhaug H, Hovland A. Transition from LDL apheresis  to evolocumab in heterozygous FH is equally effective in lowering LDL, without lowering HDL cholesterol. Atherosclerosis. 2016 Jun 9;251:119-123. [Epub ahead of print]

4.      Wang A, Richhariya A, Gandra SR, et al. Systematic Review of Low-Density Lipoprotein Cholesterol Apheresis for the Treatment of Familial Hypercholesterolemia. J Am Heart Assoc. 2016 Jul 6;5(7) pii: e003294.

5.      Robinson JG, Farnier M, Krempf M, et al. Efficacy and safety of alirocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015 Apr 16;372(16):1489-99.

6.      Sabatine MS, Giugliano RP, Wiviott SD, et al. Efficacy and safety of evolocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015 Apr 16;372(16):1500-9.

7.      Koren MJ, Giugliano RP, Raal FJ, et al. Efficacy and safety of longer-term administration of evolocumab (AMG 145) in patients with hypercholesterolemia: 52-week results from the Open-Label Study of Long-Term Evaluation Against LDL-C (OSLER) randomized trial. Circulation. 2014 Jan 14;129(2):234-43.