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Lipoprotein(a) and cardiovascular disease: sifting the evidence to guide future research
Pia R Kamstrup1,2, R Dermot G Neely3, Steven Nissen4
1Department of Clinical Biochemistry, Copenhagen University Hospital-Herlev and Gentofte, Borgmester Ib Juuls Vej 73, 2730 Herlev, Denmark.
Insights
Lipoprotein(a) (Lp(a)) is a key genetic risk factor for cardiovascular disease. This review proposes standards for Lp(a) data collection to improve risk assessment and cardiovascular disease prevention strategies.
Area of Science:
- Cardiology
- Genetics
- Epidemiology
Background:
- Lipoprotein(a) (Lp(a)) is a genetically determined causal risk factor for various cardiovascular diseases.
- Despite guideline recommendations, widespread Lp(a) assessment in clinical practice remains limited.
- Potent Lp(a)-lowering drugs are in clinical trials, necessitating better Lp(a) risk stratification.
Purpose of the Study:
- To review key findings from observational and genetic Lp(a) studies.
- To identify challenges in observational Lp(a) research.
- To propose requirements for harmonized Lp(a) data collection and improved clinical trial design.
Main Methods:
- Review of existing observational and genetic studies on Lp(a).
- Analysis of challenges in current Lp(a) data collection and interpretation.
- Formulation of recommendations for enhancing data quality and standardization.
Main Results:
- Lp(a) is a significant, genetically determined risk factor for cardiovascular diseases like coronary heart disease and stroke.
- Challenges in observational studies hinder accurate Lp(a) risk assessment.
- Standardized data collection is crucial for defining risk thresholds and informing clinical practice.
Conclusions:
- Enhanced quality and harmonization of Lp(a) data are essential for accurate cardiovascular risk assessment.
- Recommendations aim to improve the interpretation of clinical trial findings and patient care.
- Optimizing Lp(a) measurement and data collection will aid in cardiovascular disease prevention.
Abstract:
Lipoprotein(a) (Lp(a)) is a genetically determined causal risk factor for cardiovascular disease including coronary heart disease, peripheral arterial disease, ischaemic stroke, and calcific aortic valve stenosis. Clinical trials of specific and potent Lp(a)-lowering drugs are currently underway. However, in clinical practice, widespread assessment of Lp(a) is still lacking despite several guideline recommendations to measure Lp(a) at least once in a lifetime in all adults to identify those at high or very high risk due to elevated levels. The present review provides an overview of key findings from observational and genetic Lp(a) studies, highlights the main challenges in observational Lp(a) studies, and proposes a minimum set of requirements to enhance the quality and harmonize the collection of Lp(a)-related data. Adherence to the recommendations set forth in the present manuscript is intended to enhance the quality of future observational Lp(a) studies, to better define thresholds for increased risk, and to better inform clinical trial design. The recommendations can also potentially assist in the interpretation and generalization of clinical trial findings, to improve care of patients with elevated Lp(a) and optimize treatment and prevention of cardiovascular disease.
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