Lipoprotein(a) – Lp(a) for short – is increasingly regarded as an independent and clinically relevant risk factor for cardiovascular disease. Several recent studies confirm this correlation. Among other things, the chosen measurement method is important for the interpretation.

Parameters such as LDL cholesterol (LDL-C), blood pressure or blood sugar are usually used to assess the risk of cardiovascular disease (CVD). Nevertheless, it is not uncommon for young patients to develop cardiovascular events even though they had no previous abnormalities in the classic risk factors(1).

Recent epidemiological and genetic studies emphasize the importance of Lp(a) as a biomarker: The studies were able to show that an increased Lp(a) serum concentration is associated with a higher cardiovascular disease rate and mortality. The risk of coronary heart disease and ischemic stroke increases, as does the risk of aortic valve stenosis or peripheral arterial occlusive disease.(2, 3, 4, 5) In people with type 2 diabetes, an undetected high Lp(a) level can further increase the risk of CVD.(6)

Lp(a): Determine at least once in a lifetime

Targeted therapies to lower Lp(a) levels are not yet available.(7) As the genetically determined Lp(a) level can hardly be influenced by lifestyle, it is nevertheless important to identify elevated levels at an early stage and to monitor other cardiovascular risk factors more closely. For this reason, professional societies such as the European Atherosclerosis Society (EAS) and the US National Lipid Association call for Lp(a) testing at least once in a lifetime.(4, 8, 9) The American Heart Association recommends Lp(a) screening for people who have experienced early cardiovascular events, either themselves or their first-degree relatives.(10)

The measurement method is crucial

The determination of the Lp(a) value is important for the assessment of the individual cardiovascular risk. There are two different methods to quantify Lp(a): the determination of particle mass (mg/dL) and the determination of particle concentration (nmol/L).(9, 10, 11) It is important to note that the size of Lp(a) particles differs between individuals, sometimes considerably, due to genetic factors. This is because one of the main components of the particles, the apolipoprotein [apo(a)], differs greatly in size between individuals and ethnic groups – up to a thousandfold. For this reason, the EAS guidelines, for example, also recommend determining the particle concentration, i.e. the number of Lp(a) particles per unit volume (nmol/L), whenever possible.(4) This method is independent of particle size. It therefore has a better correlation with the CVD risk than the conventional mass determination in mg/dL.(4, 9, 10, 11) A conversion from mg/dL to nmol/L is inaccurate because the ratio of mole to mass is not constant due to the variable apo(a) size.(4, 9, 10, 11) Such inaccuracies can lead to false-negative or false-positive results.(11, 12)

Indispensable today and in the future

High Lp(a) levels are not uncommon: in 2022, around 1.5 billion people worldwide showed elevated levels.(13) In the case of unremarkable lipid profiles, Lp(a) can help to identify residual cardiovascular risk. Patients with elevated Lp(a) levels could benefit from emerging Lp(a)-lowering therapies in the future(4).

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Literature:

1. Mayo J et al. Lipoprotein(a) as a unique primary risk factor for early atherosclerotic peripheral arterial disease. BMJ Case Rep. 2021 Jun 30;14(6)
2. Reuser A et al. Lipoprotein(a). Dtsch Med Wochenschr 2022; 147 (23): 1564-70
3. Reuser A et al. CHD patients with severely elevated Lp(a) levels, therapeutic consequences – today and in the future. Heart Medicine 2023; 5-2.
4. Kronenberg F et al. “Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement.” Eur Heart J. 2022;43(39):3925-3946.
5. Kronenberg F et al. “Frequent questions and responses on the 2022 lipoprotein(a) consensus statement of the European Atherosclerosis Society.” Atherosclerosis. 2023;374:107-120.
6. Shiyovich A et al. “Lipoprotein(a) as a cardiovascular risk factor among patients with and without diabetes mellitus: the Mass General Brigham Lp(a) Registry.” Cardiovasc Diabetol. 2023;22(1):147.
7. Thau H et al. “Targeting Lipoprotein(a): Can RNA Therapeutics Provide the Next Step in the Prevention of Cardiovascular Disease?” Cardiol Ther. 13(1), 39-67.
8. Pearson GJ et al. “2021 Canadian Cardiovascular Society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in adults.” Can J Cardiol. 2021;37(8):1129-1150.
9. Koschinsky ML et al. “A focused update to the 2019 NLA scientific statement on use of lipoprotein (a) in clinical practice.” J Clin Lipidol. 2024 May-Jun;18(3):e308-e319.
10. Reyes-Soffer G et al. Lipoprotein(a): a genetically determined, causal, and prevalent risk factor for atherosclerotic cardiovascular disease: a scientific statement from the American Heart Association. Arterioscler Thromb Vasc Biol. 2022;42(1):e48-e60.
11. Cegla J et al. HEART UK consensus statement on Lipoprotein(a): A call to action. Atherosclerosis. 2019 Dec;291:62-70.
12. Willeit P et al. “Discrimination and net reclassification of cardiovascular risk with lipoprotein(a): prospective 15-year outcomes in the Bruneck Study.” J Am Coll Cardiol. 2014;64(9):851-60.
13. Sosnowska D et al. “The year in cardiovascular disease – the year of Lipoprotein(a) – research advances and new findings.” Archives of Medical Science. 2025;21(2):355-73.

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