When should we measure lipoprotein (a)?

Kostner, Karam M., Maerz, Winfried and Kostner, Gerhard M. (2013) When should we measure lipoprotein (a)?. European Heart Journal, 34 42: 3268-3276c. doi:10.1093/eurheartj/eht053

Author Kostner, Karam M.
Maerz, Winfried
Kostner, Gerhard M.
Title When should we measure lipoprotein (a)?
Journal name European Heart Journal   Check publisher's open access policy
ISSN 0195-668X
Publication date 2013-11
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1093/eurheartj/eht053
Open Access Status DOI
Volume 34
Issue 42
Start page 3268
End page 3276c
Total pages 12
Place of publication Oxford, United Kingdom
Publisher Oxford University Press
Collection year 2014
Language eng
Abstract Recently published epidemiological and genetic studies strongly suggest a causal relationship of elevated concentrations of lipoprotein (a) [Lp(a)] with cardiovascular disease (CVD), independent of low-density lipoproteins (LDLs), reduced high density lipoproteins (HDL), and other traditional CVD risk factors. The atherogenicity of Lp(a) at a molecular and cellular level is caused by interference with the fibrinolytic system, the affinity to secretory phospholipase A2, the interaction with extracellular matrix glycoproteins, and the binding to scavenger receptors on macrophages. Lipoprotein (a) plasma concentrations correlate significantly with the synthetic rate of apo(a) and recent studies demonstrate that apo(a) expression is inhibited by ligands for farnesoid X receptor. Numerous gaps in our knowledge on Lp(a) function, biosynthesis, and the site of catabolism still exist. Nevertheless, new classes of therapeutic agents that have a significant Lp(a)-lowering effect such as apoB antisense oligonucleotides, microsomal triglyceride transfer protein inhibitors, cholesterol ester transfer protein inhibitors, and PCSK-9 inhibitors are currently in trials. Consensus reports of scientific societies are still prudent in recommending the measurement of Lp(a) routinely for assessing CVD risk. This is mainly caused by the lack of definite intervention studies demonstrating that lowering Lp(a) reduces hard CVD endpoints, a lack of effective medications for lowering Lp(a), the highly variable Lp(a) concentrations among different ethnic groups and the challenges associated with Lp(a) measurement. Here, we present our view on when to measure Lp(a) and how to deal with elevated Lp(a) levels in moderate and high-risk individuals.
Keyword Atherosclerosis
Myocardial infarction
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2014 Collection
School of Medicine Publications
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Citation counts: TR Web of Science Citation Count  Cited 22 times in Thomson Reuters Web of Science Article | Citations
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