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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
When should we measure lipoprotein (a)?
Karam M Kostner1, Winfried März, Gerhard M Kostner
1Associate Professor of Medicine, Mater Hospital, University of Queensland, St Lucia, QLD, Australia.
European Heart Journal
|June 6, 2013
Summary
Elevated lipoprotein (a) [Lp(a)] levels are causally linked to cardiovascular disease (CVD) risk. While new therapies show promise, routine Lp(a) measurement for CVD risk assessment is still debated due to intervention study gaps.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Biochemistry
Background:
- Epidemiological and genetic studies indicate a causal link between elevated lipoprotein (a) [Lp(a)] and cardiovascular disease (CVD).
- Lp(a) contributes to atherogenicity through molecular mechanisms including fibrinolytic system interference and interactions with cellular components.
- Apo(a) expression is influenced by factors like the farnesoid X receptor, though knowledge gaps persist regarding Lp(a) function and metabolism.
Purpose of the Study:
- To review the current understanding of lipoprotein (a) [Lp(a)] in cardiovascular disease (CVD) risk.
- To discuss the implications of Lp(a) atherogenicity and biosynthesis.
- To provide expert recommendations on measuring Lp(a) and managing elevated levels in at-risk individuals.
Main Methods:
- Review of recent epidemiological and genetic studies on Lp(a) and CVD.
- Analysis of molecular and cellular mechanisms of Lp(a) atherogenicity.
- Discussion of emerging therapeutic strategies targeting Lp(a) reduction.
Main Results:
- Strong evidence suggests elevated Lp(a) is an independent CVD risk factor.
- Several novel therapeutic agents demonstrating significant Lp(a)-lowering effects are in clinical trials.
- Despite progress, consensus on routine Lp(a) measurement is cautious due to limited intervention data and measurement challenges.
Conclusions:
- Expert opinion suggests specific scenarios for measuring Lp(a) and managing elevated levels in moderate to high-risk individuals.
- Further intervention studies are needed to confirm the clinical benefit of lowering Lp(a) for hard CVD endpoints.
- Addressing ethnic variations and measurement standardization is crucial for widespread Lp(a) assessment.
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