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. 2023 Oct;33(10):1866-1877.
doi: 10.1016/j.numecd.2023.07.019. Epub 2023 Jul 19.

Consensus document on Lipoprotein(a) from the Italian Society for the Study of Atherosclerosis (SISA)

Giulia Chiesa  1 , Maria Grazia Zenti  2 , Andrea Baragetti  3 , Carlo M Barbagallo  4 , Claudio Borghi  5 , Furio Colivicchi  6 , Aldo P Maggioni  7 , Davide Noto  4 , Matteo Pirro  8 , Angela A Rivellese  9 , Tiziana Sampietro  10 , Francesco Sbrana  10 , Marcello Arca  11 , Maurizio Averna  12 , Alberico L Catapano  3
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Free article

Consensus document on Lipoprotein(a) from the Italian Society for the Study of Atherosclerosis (SISA)

Giulia Chiesa et al. Nutr Metab Cardiovasc Dis. 2023 Oct.
Free article

Abstract

Aims: In view of the consolidating evidence on the causal role of Lp(a) in cardiovascular disease, the Italian Society for the Study of Atherosclerosis (SISA) has assembled a consensus on Lp(a) genetics and epidemiology, together with recommendations for its measurement and current and emerging therapeutic approaches to reduce its plasma levels. Data on the Italian population are also provided.

Data synthesis: Lp(a) is constituted by one apo(a) molecule and a lipoprotein closely resembling to a low-density lipoprotein (LDL). Its similarity with an LDL, together with its ability to carry oxidized phospholipids are considered the two main features making Lp(a) harmful for cardiovascular health. Plasma Lp(a) concentrations vary over about 1000 folds in humans and are genetically determined, thus they are quite stable in any individual. Mendelian Randomization studies have suggested a causal role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis and observational studies indicate a linear direct correlation between cardiovascular disease and Lp(a) plasma levels. Lp(a) measurement is strongly recommended once in a patient's lifetime, particularly in FH subjects, but also as part of the initial lipid screening to assess cardiovascular risk. The apo(a) size polymorphism represents a challenge for Lp(a) measurement in plasma, but new strategies are overcoming these difficulties. A reduction of Lp(a) levels can be currently attained only by plasma apheresis and, moderately, with PCSK9 inhibitor treatment.

Conclusions: Awaiting the approval of selective Lp(a)-lowering drugs, an intensive management of the other risk factors for individuals with elevated Lp(a) levels is strongly recommended.

Keywords: Antisense oligonucleotides; Aortic valve stenosis; Atherosclerotic cardiovascular disease; Familial hypercholesterolemia; Lipoprotein(a); Mendelian randomization; Oxidized phospholipids; Small interfering RNA.

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Conflict of interest statement

Declaration of competing interest APM received personal fees from AstraZeneca, Bayer, Novartis for the participation in study committees, outside the present work. M Arca has received research grant support and lecturing fees from Alfasigma, Amarin, Amgen, Amryt, IONIS/Akcea Therapeutics, Daiichi Sankyo, Novartis, Pfizer, Regeneron and Sanofi, SOBI. ALC in the last three years has received honoraria, lecture fees or research grants from Aegerion, Akcea Therapeutics, Amarin, Amgen, Amryt Pharma, AstraZeneca, Daiichi Sankyo, Esperion, Ionis Pharmaceutical, Medscape Education, Menarini, Merck, Mylan, Novartis, PeerVoice, Pfizer, Recordati, Regeneron, Sanofi, The Corpus, Viatris. GC, MGZ, AB, CMB, CB, FC, DN, MP, AAR, TS, FS, M Averna declare no competing interest.