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Lp(a) - an overlooked risk factor
Luke J Laffin1, Steven E Nissen1
1Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Insights
Lipoprotein(a) (Lp(a)) is a genetic risk factor for cardiovascular disease affecting up to 30% of people. Research is exploring therapies to lower Lp(a) and reduce cardiovascular events.
Area of Science:
- Cardiology
- Genetics
- Epidemiology
Background:
- Lipoprotein(a) (Lp(a)) is a significant risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis.
- Genetic and epidemiological studies confirm Lp(a)'s causal role in cardiovascular disease incidence.
- Elevated Lp(a) affects an estimated 20-30% of the global population.
Purpose of the Study:
- To review the genetics and pathophysiology of Lp(a).
- To discuss epidemiological data on Lp(a) and cardiovascular disease.
- To outline current screening recommendations and emerging pharmacotherapies for Lp(a) lowering.
Main Methods:
- Review of genetic and epidemiological studies.
- Analysis of pathophysiological mechanisms.
- Survey of ongoing and developing pharmacotherapies.
Main Results:
- Lp(a) levels are primarily genetically determined and resistant to lifestyle changes.
- Significant evidence supports Lp(a) as a causal factor in cardiovascular disease.
- Multiple pharmacotherapies targeting Lp(a) reduction are under development.
Conclusions:
- Lp(a) is a prevalent, genetically driven risk factor for cardiovascular disease.
- Effective screening and management strategies are crucial.
- Pharmacological Lp(a) lowering holds promise for reducing cardiovascular events.
Abstract:
Lipoprotein(a) (Lp(a)) is an increasingly discussed and studied risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis. Many genetic and epidemiological studies support the important causal role that Lp(a) plays in the incidence of cardiovascular disease. Although dependent upon the threshold and unit of measurement of Lp(a), most estimates suggest between 20 and 30% of the world's population have elevated serum levels of Lp(a). Lp(a) levels are predominantly mediated by genetics and are not significantly modified by lifestyle interventions. Efforts are ongoing to develop effective pharmacotherapies to lower Lp(a) and to determine if lowering Lp(a) with these medications ultimately decreases the incidence of adverse cardiovascular events. In this review, the genetics and pathophysiological properties of Lp(a) will be discussed as well as the epidemiological data demonstrating its impact on the incidence of cardiovascular disease. Recommendations for screening and how to currently approach patients with elevated Lp(a) are also noted. Finally, the spectrum of pharmacotherapies under development for Lp(a) lowering is detailed.
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