ODYSSEY ESCAPE: is PCSK9 inhibition the Trojan Horse for the use of lipoprotein apheresis in familial hypercholesterolaemia?

This editorial refers to ‘Alirocumab in patients with heterozygous familial hypercholesterolaemia undergoing lipoprotein apheresis: the ODYSSEY ESCAPE trial’†, by P.M. Moriarty et al., on page 3588. Lipoprotein apheresis (LA) is a radical treatment for severe familial hypercholesterolaemia (FH) that entails the intermittent extracorporeal removal of atherogenic apolipoprotein B-100 containing lipoproteins from the circulation.1 Its use is well supported by international guidelines embodying clear evidence that LA improves coronary outcomes, progression of atherosclerotic cardiovascular disease (ASCVD), endothelial dysfunction, inflammation, and coagulation.1,2 Lipoprotein apheresis is indicated for patients with homozygous (Ho) or compound heterozygous (Hz) FH, as well as for those with classical HzFH who have progressive ASCVD and are refractory to maximally tolerated pharmacotherapy.1,2 Criteria, such as a reduction in LDL-cholesterol (LDL-Ch) of <50% or LDL-Ch >5 mmol/L on diet and maximally tolerated pharmacotherapy, for selecting FH patients for LA have been recommended, but in practice these are adjusted according to clinical context and availability of resources. FH patients with very high plasma lipoprotein(a) [Lp(a)] levels may also benefit from LA.3