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Published on: October 12, 2017
Lipoprotein(a): an important cardiovascular risk factor and a clinical conundrum
Marlys L Koschinsky1, Michael B Boffa1
1Department of Chemistry and Biochemistry, University of Windsor, 401 Sunset Avenue, Windsor, Ontario N9B 3P4, Canada.
Insights
Elevated lipoprotein(a) (Lp[a]) is a key risk factor for coronary heart disease (CHD). While its causal role is evident, Lp[a]
Area of Science:
- Cardiovascular Medicine
- Genetics
- Epidemiology
Background:
- Elevated lipoprotein(a) (Lp[a]) is increasingly recognized as a significant risk factor for coronary heart disease (CHD).
- Genetic and epidemiological studies strongly support a causal link between Lp[a] and CHD development.
- Despite growing interest, fundamental questions regarding Lp[a]'s role persist.
Purpose of the Study:
- To review the current understanding of lipoprotein(a) (Lp[a]) as a risk factor for coronary heart disease (CHD).
- To highlight the unresolved questions surrounding Lp[a]'s pathogenic mechanisms and clinical utility.
- To discuss the current therapeutic landscape for lowering Lp(a) levels.
Main Methods:
- Review of recent genetic and epidemiological data.
- Analysis of current clinical understanding and unanswered questions.
- Examination of existing and emerging therapeutic interventions.
Main Results:
- Strong evidence supports a causal role for Lp[a] in CHD.
- The precise pathogenic mechanisms of Lp[a] remain largely unknown.
- Uncertainty exists regarding the optimal clinical application of Lp(a) measurements.
- No specific therapies currently exist to lower Lp[a] concentrations, though some agents also reduce LDL.
Conclusions:
- Lipoprotein(a) is a confirmed causal risk factor for coronary heart disease.
- Further research is needed to elucidate Lp[a]'s pathogenic pathways and establish clear clinical guidelines.
- Development of targeted therapies to specifically reduce Lp[a] is an unmet clinical need.
Abstract:
Elevated plasma concentrations of lipoprotein(a) (Lp[a]) are an emerging risk factor for the development of coronary heart disease (CHD). Recent genetic and epidemiologic data have provided strong evidence for a causal role of Lp(a) in CHD. Despite these developments, which have attracted increasing interest from clinicians and basic scientists, many unanswered questions persist. The true pathogenic mechanism of Lp(a) remains a mystery. Significant uncertainty exists concerning the appropriate use of Lp(a) in the clinical setting. No therapeutic intervention remains that can specifically lower plasma Lp(a) concentrations, although the list of compounds that lower Lp(a) and LDL continues to expand.
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