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Review
Lipoprotein(a): a risk factor for atherosclerosis and an emerging therapeutic target
  1. Stefania Angela Di Fusco1,
  2. Marcello Arca2,
  3. Pietro Scicchitano3,
  4. Alessandro Alonzo1,
  5. Francesco Perone4,
  6. Michele Massimo Gulizia5,6,
  7. Domenico Gabrielli7,
  8. Fabrizio Oliva8,
  9. Giuseppe Imperoli1,
  10. Furio Colivicchi1
  1. 1 Emergency Department, San Filippo Neri Hospital, Rome, Italy
  2. 2 Department of Translational and Precision Medicine, Sapienza University of Rome, Rome, Italy
  3. 3 Cardiology Department, Hospital “F Perinei”, Altamura, Italy
  4. 4 Rehabilitation Clinic "Villa delle Magnolie", Caserta, Italy
  5. 5 Cardiology Division, Garibaldi-Nesima Hospital, Garibaldi-Nesima Hospital, Catania, Italy
  6. 6 Heart Care Foundation, Florence, Italy
  7. 7 Cardiovascular Department, San Camillo Hospital, Rome, Italy
  8. 8 De Gasperis Cardio Center, Niguarda Hospital, Milan, Italy
  1. Correspondence to Dr Stefania Angela Di Fusco, Presidio Ospedaliero San Filippo Neri, 00135 Roma, Italy; doctstefania{at}hotmail.com

Abstract

Lipoprotein(a) (Lp(a)) is a complex circulating lipoprotein, and increasing evidence has demonstrated its role as a risk factor for atherosclerotic cardiovascular disease (ASCVD) and as a possible therapeutic target. Lp(a) atherogenic effects are attributed to several potential mechanisms in addition to cholesterol accumulation in the arterial wall, including proinflammatory effects mainly mediated by oxidised phospholipids. Several studies have found a causal and independent relationship between Lp(a) levels and cardiovascular risk. Furthermore, several studies also suggest a causal association between Lp(a) levels and calcific aortic valve stenosis. Available lipid-lowering agents have at best moderate impact on Lp(a) levels. Among available therapies, antibody proprotein convertase subtilisin/kexin type 9 inhibitors are the most effective in reducing Lp(a). Potent Lp(a)-lowering treatments that target LPA expression are under development. Lp(a) level measurement poses some challenges due to the absence of a definitive reference method and the reporting of Lp(a) values as molar (nanomoles per litre (nmol/L)) or mass concentrations (milligrams per decilitre (mg/dL)) by different assays. Currently, Lp(a) measurement is recommended to refine cardiovascular risk in specific clinical settings, that is, in individuals with a family history of premature ASCVD, in patients with ASCVD not explained by standard risk factors or in those with recurrent events despite optimal management of traditional risk factors. Patients with high Lp(a) levels should be managed with more intensive approaches to treat other modifiable cardiovascular risk factors. Overall, this review focuses on Lp(a) as an ASCVD risk factor and therapeutic target. Furthermore, it reports practical recommendations for Lp(a) measurement and interpretation and updated evidence on Lp(a)-lowering approaches.

  • atherosclerosis
  • pharmacology, clinical
  • biomarkers
  • hyperlipidemias

https://doi.org/10.1136/heartjnl-2021-320708

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    Footnotes

    • Twitter @doctstefania, @PeroneFrancesco

    • Contributors Conceptualisation: FC, MA; literature search: PS, AA, FP; writing original draft preparation: SADF, PS, AA, FP; review and editing: FC, MA; supervision and critical review; MMG, DG, FO, MA, GI, FC. All authors have read and agreed to the published version of the manuscript.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.