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Lipoprotein(a), a moving target: from the primary to secondary prevention of atherothrombotic events
  1. Josip A. Borovac1,2
  1. 1 Department of Pathophysiology, University of Split School of Medicine, 21000 Split, Croatia
  2. 2 Institute of Emergency Medicine, 21000 Split, Croatia
  1. Correspondence to Dr Josip A. Borovac, Department of Pathophysiology, University of Split School of Medicine, 21000 Split, Croatia; jborovac{at}

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Lipoprotein(a) [Lp(a)] is a cholesterol-rich modified low-density lipoprotein (LDL) with enhanced proinflammatory, proatherogenic and antifibrinolytic effects because it contains all atherogenic components of LDL in addition to apolipoprotein a [apo(a)], a particle with marked atherothrombotic potential. Namely, apo(a) inhibits plasminogen activation in vitro, promotes thrombosis and calcification, elicits inflammatory response through its content of oxidised phospholipids and upregulated monocyte trafficking and tightly adheres to lysine binding sites on denuded endothelium further penetrating subintimal spaces of arterial walls and aortic valve leaflets.1 A robust body of high-quality evidence corroborated from mechanistic animal experiments, prospective epidemiological studies, genome-wide association studies, meta-analyses and Mendelian randomisation studies demonstrated that increased plasma Lp(a) levels are independently and possibly causally associated with atherosclerotic cardiovascular (CV) disease (ASCVD) mortality, all-cause mortality, and ASCVD-related outcomes such as myocardial infarction (MI), ischaemic stroke, calcific aortic valve stenosis and peripheral artery disease.1 2 These observations are of importance because it is estimated that about 20% of the world population have elevated Lp(a) levels that are predominantly genetically determined; thus, adult Lp(a) levels mostly remain stable through an individual's lifetime regardless of dietary or environmental variables.3 Furthermore, relevant dyslipidaemia guidelines and consensus/scientific statements endorse Lp(a) testing in primary prevention and selected individuals with a personal or family history of premature CVD.1 3–5

While most of the available studies established the role of elevated Lp(a) levels regarding the risk for the first atherothrombotic event, there have been inconsistent findings in terms of elevated Lp(a) level impact on outcomes in patients with pre-existing CVD. These knowledge gaps are of clinical relevance because such population might be screened for Lp(a) levels and could benefit from therapeutic interventions that can reduce Lp(a) levels, thus mitigating the risk of subsequent events, independently of traditional lipid parameters.3

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  • 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.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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