Lipoprotein(a)
Lipoprotein(a) is an LDL-like particle whose level is mostly inherited and stays stable over years. US and European bodies place raised risk at 125 nmol/L (50 mg/dL) and above. Cohort and genetic studies tie higher levels to more heart attacks and aortic valve stenosis. In a 2026 trial, a drug that lowered it sharply did not reduce cardiovascular events.
Checked 2026-11-13
- Status
- A blood test ordered by a clinician and also sold direct to consumers by some US laboratories. FDA's product classification lists a lipoprotein(a) test system as a class I device under its lipoprotein test system regulation [1]. Assays report in two units that are not interchangeable, nmol/L and mg/dL [2].
- Measures
- The concentration of lipoprotein(a), an LDL-like particle that carries an extra protein called apolipoprotein(a), reported either as the number of particles (nmol/L) or as their mass (mg/dL) [2].
- Also called
- Lp(a), Lpa, LP(a), lipoprotein a, lipoprotein little a, lipoprotein (a), Lp little a, lipoprotein(a) mass, lipoprotein(a) particle concentration
- Tested for
- heart attack risk, stroke risk, aortic valve stenosis risk, inherited heart disease risk, family history of early heart disease, one-time cholesterol screening
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Linked in research3
- StrongLinked to more heart attacks and strokes at higher levels, about 11% more cardiovascular disease for each 50 nmol/L higher in 460,506 UK adults.
- StrongShown in genetic studies to track coronary heart disease: variants that raise lipoprotein(a) raised risk, about 22% more heart attacks for each doubling.
- ModerateLinked to more aortic valve stenosis in cohort and genetic studies, about 3 times more at levels above 90 mg/dL in 77,680 Danish adults.
Reported risks0
No risks sourced yet.
Reference ranges
Each range is the one its source published, in nmol/L. Where sources differ, each is shown.
National Lipid Association focused update, 2024
Adults · [3]
| Range | What the source calls it |
|---|---|
| below 75 nmol/L | "low risk" |
| 75 to 124 nmol/L | "intermediate risk" |
| 125 or above nmol/L | "high risk" |
The statement prints the bands as below 75 nmol/L (30 mg/dL), between 75 and 125 nmol/L (30 to 50 mg/dL), and 125 nmol/L (50 mg/dL) or above, so a result of exactly 125 nmol/L sits in its high risk band. It recommends measuring lipoprotein(a) at least once in every adult. The bands describe cardiovascular risk and are not a population reference interval [3].
European Atherosclerosis Society consensus statement, 2022
Adults · [4]
| Range | What the source calls it |
|---|---|
| below 75 nmol/L | "rule out" |
| 75 to 125 nmol/L | "grey zone" |
| above 125 nmol/L | "rule-in" |
The panel calls these pragmatic cut points and states that risk rises continuously with concentration, already below reported thresholds. In mg/dL it prints the same bands as below 30, 30 to 50, and above 50. It gives general statements in both units using an approximate interim factor of 2.5 and does not stand behind a standard conversion. The grey zone is described as relevant when weighing lipoprotein(a) together with other risk factors. An earlier European laboratory consensus published cut points in mg/dL only: 50 mg/dL or above as the value to flag, set at the 80th percentile of the assay in use, and above 150 mg/dL as the 99th percentile [5].
American Heart Association and American College of Cardiology cholesterol guideline, 2018, risk-enhancing factor
Adults aged 40 to 75 without diabetes, being assessed for risk of a first cardiovascular event · [6]
| Range | What the source calls it |
|---|---|
| below 125 nmol/L | No name given |
| 125 or above nmol/L | "elevated Lp(a)" |
The guideline lists lipoprotein(a) of 50 mg/dL or above, or 125 nmol/L or above, as a risk-enhancing factor, "especially at higher levels", and names a family history of premature cardiovascular disease as a relative indication for measuring it [6]. A 2026 guideline from the same bodies retires and replaces this one [7].
National Heart, Lung, and Blood Institute working group, 2018
Adults, as the threshold the working group describes as traditional · [8]
| Range | What the source calls it |
|---|---|
| 75 or below nmol/L | No name given |
| above 75 nmol/L | "elevated Lp(a)" |
The working group describes above 30 mg/dL or above 75 nmol/L as the traditional thresholds for elevated lipoprotein(a), approximating the 75th percentile in white populations. It notes that a European panel placed significant risk higher, at above the 80th percentile or above 50 mg/dL, which the working group glosses as about 100 to 125 nmol/L [8].
European Society of Cardiology and European Atherosclerosis Society guideline, 2019
Adults, to identify very high inherited levels · [9]
| Range | What the source calls it |
|---|---|
| below 430 nmol/L | No name given |
| 430 or above nmol/L | "extremely elevated" One to see a doctor about |
The guideline advises considering one measurement in each adult's lifetime to find people with an extremely elevated level, whose lifetime cardiovascular risk it compares to that of heterozygous familial hypercholesterolemia. It prints the level as 180 mg/dL (430 nmol/L), with "or above" in one passage and "above" in another. It names no bands below this level, so this block does not describe lower results [9].
What has been shown to move it
Tested, and not shown to change it1
Cholesterol and blood lipids
Shown to lower total and LDL cholesterol slightly, by about 0.3 mmol/L, with larger drops when more weight was lost.
Lipoprotein(a) did not change.
The numbers and sources
- Effect
- Orlistat lowered total cholesterol by 0.30 mmol/L and LDL cholesterol by 0.27 mmol/L. HDL cholesterol fell 0.034 mmol/L and triglycerides 0.09 mmol/L. Lipoprotein(a) did not change. LDL lowering was larger with more weight loss and shorter treatment [3]. An earlier systematic review also found greater falls in total and LDL cholesterol than with control [5].
- Population
- 33 RCTs [3]; 28 RCTs, 17 of them with 10,041 patients over a year [5].
- Sources
- [3], [5]
- Caveats
- The changes are small. The reviews do not separate the drug from the weight lost.
How it compares with the reference method
Matched the reference method2
Repeat testing in one person
Shown to stay stable over years: baseline and repeat lipoprotein(a) results 4.4 years apart correlated at 0.96 in 16,017 UK adults.
The numbers and sources
- Compared with
- A repeat measurement in the same person a median 4.4 years later
- Effect
- In the UK Biobank, baseline and follow-up molar concentrations had a Spearman correlation of 0.96 over a median 4.42 years, and the correlation was stable whether the gap was under 3 years or over 5. The change between the two measurements was not associated with coronary artery disease once the follow-up level was known, and the authors concluded that a single accurate measurement is an efficient way to inform risk [23]. In pooled cohorts, levels were highly consistent within individuals over several years [10]. An American Heart Association statement cites within-person variability of up to 20% in placebo-treated trial participants [2].
- Population
- 16,017 unrelated UK Biobank participants with two measurements [23].
- Sources
- [23], [10], [2]
- Caveats
- Statin use went with a rise in lipoprotein(a) among people starting at 70 nmol/L or above [23]. The study does not describe results from switching between assays.
Fasting against not fasting
Limited evidence: a European consensus statement drawing on Danish population data reports that lipoprotein(a) is not affected by fasting status.
The numbers and sources
- Compared with
- A fasting blood sample
- Effect
- A joint consensus statement of two European societies states that concentrations of lipoprotein(a) are not affected by fasting or non-fasting status, and uses the same flag value for both kinds of sample [5].
- Population
- The statement's comparison of fasting and non-fasting results draws on 92,285 people in the Copenhagen General Population Study [5].
- Sources
- [5]
- Caveats
- A statement in a consensus document, without a figure for lipoprotein(a) in its text. The underlying comparison is of people sampled at different times after eating, not the same people tested twice [5].
Did not match the reference method1
Results in mg/dL against results in nmol/L
Shown not to convert by one factor: the ratio of nmol/L to mg/dL ran from under 1 to over 5 across commercial assays and samples.
The numbers and sources
- Compared with
- Lipoprotein(a) molar concentration measured at a reference laboratory
- Effect
- One unit counts particles (nmol/L) and the other weighs them (mg/dL), and the apolipoprotein(a) protein varies widely in size between people, so the same particle count can weigh different amounts [2]. Comparing a reference molar assay with mass assays, the mean ratio of nmol/L to mg/dL was 2.42 (SD 1.25) against one laboratory's mass assay and 1.64 and 2.02 against two commercial assays. The ratios rose with the level: 1.82, 1.52 and 1.87 below 75 nmol/L, and 2.80, 1.89 and 2.24 above 125 nmol/L. For three other commercial assays the ratios ranged from under 1 to over 5. The authors concluded that a single conversion factor between assays is not appropriate [22]. A European panel does not recommend a standard factor and describes 2 to 2.5 as no more than a guess [4]. An American Heart Association statement says there is no unbiased conversion factor in either direction [2], and a US working group states that there is no conversion factor [8].
- Population
- Samples measured in molar units at one reference laboratory and in mass units by six assays, from 80 to 2,673 samples per assay [22].
- Sources
- [22], [4], [2], [8]
- Caveats
- This is why this page gives no conversion between the two units. A result in mg/dL cannot be placed in the nmol/L bands above, and each body's mg/dL cut points are given in the notes under its range. Assays based on antibodies that bind a repeated part of the protein can read high or low depending on the protein's size, and the European panel asks laboratories to name the assay on reports [4].
What studies tie it to
Linked in research3
Heart attack and stroke in cohort studies
Linked to more heart attacks and strokes at higher levels, about 11% more cardiovascular disease for each 50 nmol/L higher in 460,506 UK adults.
The numbers and sources
- Effect
- In 36 prospective studies, the risk ratio for coronary heart disease was 1.13 (95% CI 1.09 to 1.18) per 3.5-fold higher usual lipoprotein(a) after adjustment for lipids and other risk factors, and 1.10 (1.02 to 1.18) for ischemic stroke. It was 1.01 (0.98 to 1.05) for death from nonvascular causes [10]. In the UK Biobank, the relationship with atherosclerotic cardiovascular disease appeared linear, with a hazard ratio of 1.11 (95% CI 1.10 to 1.12) per 50 nmol/L. Median levels were 19, 31, 75 and 16 nmol/L in white, South Asian, black and Chinese participants, and the risk per 50 nmol/L was similar across groups. A level of 150 nmol/L or above was found in 12.2% of people without cardiovascular disease and went with a hazard ratio of 1.50 (95% CI 1.44 to 1.56) [11].
- Population
- 126,634 participants in 36 prospective studies, 1.3 million person-years [10]. 460,506 middle-aged UK Biobank participants, median follow-up 11.2 years, 22,401 events [11].
- Sources
- [10], [11]
- Caveats
- Observational. The pooled cohorts used many different assays [10]. A European panel states that risk rises continuously, with no level at which it begins [4].
Coronary heart disease in genetic studies
Shown in genetic studies to track coronary heart disease: variants that raise lipoprotein(a) raised risk, about 22% more heart attacks for each doubling.
The numbers and sources
- Effect
- In Danish studies, genetically elevated lipoprotein(a) went with a hazard ratio for heart attack of 1.22 (95% CI 1.09 to 1.37) per doubling, against 1.08 (1.03 to 1.12) for measured levels [12]. Two variants at the LPA gene had odds ratios for coronary disease of 1.70 and 1.92. Carrying one variant gave an odds ratio of 1.51 (95% CI 1.38 to 1.66) and two or more 2.57 (1.80 to 3.67), and the association disappeared after adjustment for the lipoprotein(a) level [13]. In a Mendelian randomization analysis, each 10 mg/dL lower genetically predicted lipoprotein(a) went with 5.8% lower coronary heart disease risk (OR 0.942, 95% CI 0.933 to 0.951). A difference of 101.5 mg/dL (95% CI 71.0 to 137.0) carried the same risk difference as 38.67 mg/dL of LDL cholesterol [14].
- Population
- 8,637, 29,388 and 2,461 white Danish participants in three studies [12]. 3,145 cases and 3,352 controls, replicated in 4,846 cases and 4,594 controls [13]. 20,793 coronary heart disease cases and 27,540 controls with individual data, plus summary data on 62,240 cases and 127,299 controls, all of European ancestry [14].
- Sources
- [12], [13], [14]
- Caveats
- Genetic studies estimate the effect of lifelong differences, which may not match what lowering later in life does. Participants were of European ancestry [12][14].
Aortic valve stenosis
Linked to more aortic valve stenosis in cohort and genetic studies, about 3 times more at levels above 90 mg/dL in 77,680 Danish adults.
The numbers and sources
- Effect
- Against levels below 5 mg/dL, adjusted hazard ratios for aortic valve stenosis were 1.6 (95% CI 1.1 to 2.4) at 20 to 64 mg/dL, 2.0 (1.2 to 3.4) at 65 to 90 mg/dL and 2.9 (1.8 to 4.9) above 90 mg/dL. Genetic analysis gave a relative risk of 1.6 (95% CI 1.2 to 2.1) for a 10-fold higher lipoprotein(a) [15]. In a genome-wide study, one LPA variant was associated with aortic valve calcification (odds ratio per allele 2.05), with incident aortic stenosis (HR per allele 1.68, 95% CI 1.32 to 2.15) and with aortic valve replacement (HR 1.54, 95% CI 1.05 to 2.27) [16].
- Population
- 77,680 Danish adults followed for up to 20 years, 454 diagnosed with aortic valve stenosis [15]. 6,942 people with CT scans in the discovery cohorts, with replication in further cohorts [16].
- Sources
- [15], [16]
- Caveats
- The cohort reported mass units (mg/dL), which do not convert to nmol/L by a fixed factor. The cohort analysis is observational, and the genetic analyses estimate the effect of lifelong differences [15][16].
Mixed results1
Cardiovascular events in trials that lowered lipoprotein(a)
Mixed results: a trial designed to test lowering took lipoprotein(a) from 236 to 64 nmol/L with no fewer cardiovascular events, while PCSK9 inhibitor trial analyses tied lowering to fewer.
The numbers and sources
- Effect
- In a placebo-controlled trial of monthly pelacarsen in patients with cardiovascular disease and lipoprotein(a) of at least 70 mg/dL, the median baseline level was 236 nmol/L. At 12 months it was 64.4 nmol/L on pelacarsen and 233.4 nmol/L on placebo. Over a median 4.7 years, a major adverse cardiovascular event occurred in 12.3% and 12.1% (HR 1.02, 95% CI 0.90 to 1.15). Among patients starting at 90 mg/dL or above the hazard ratio was 1.00 (0.87 to 1.15) [17]. Further analyses by treatment exposure, by the level reached at 3 months and by subgroup also found no association with fewer events [18]. Adding niacin to a statin lowered lipoprotein(a) 21% and did not reduce cardiovascular events [19]. Evolocumab lowered lipoprotein(a) by a median 26.9%, and reduced coronary events by 23% (HR 0.77, 95% CI 0.67 to 0.88) in patients with baseline levels above the median against 7% (HR 0.93, 0.80 to 1.08) at or below it, an interaction with a P value of 0.07 [20]. With alirocumab, each 1 mg/dL reduction in lipoprotein(a) went with a hazard ratio of 0.994 (95% CI 0.990 to 0.999) for major cardiovascular events, independent of the fall in LDL cholesterol [21].
- Population
- 8,350 patients with cardiovascular disease randomized and 8,322 analyzed, mean age 59.7, 27.0% women [17]. Patients with cardiovascular disease and low HDL cholesterol in a niacin trial [19]. 25,096 patients with cardiovascular disease, median follow-up 2.2 years [20]. 18,924 patients after an acute coronary syndrome, median follow-up 2.8 years [21].
- Sources
- [17], [18], [19], [20], [21]
- Caveats
- A marker that tracks risk is not always one whose lowering changes it. The pelacarsen trial enrolled people who already had cardiovascular disease, was funded by Novartis and was published in November 2026 [17]. The PCSK9 inhibitor findings are secondary analyses of drugs that mainly lower LDL cholesterol [20][21]. The sources for this page include no outcome results for other drugs built to lower lipoprotein(a).
Sources
- US Food and Drug Administration. 21 CFR 862.1475, Lipoprotein test system. Electronic Code of Federal Regulations, with the FDA product classification entry for lipoprotein(a) test systems (product code MSM). https://www.ecfr.gov/current/title-21/section-862.1475
- Reyes-Soffer G, Ginsberg HN, Berglund L, et al. Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association. Arteriosclerosis, Thrombosis, and Vascular Biology. 2022. https://doi.org/10.1161/ATV.0000000000000147
- Koschinsky ML, Bajaj A, Boffa MB, et al. A focused update to the 2019 NLA scientific statement on use of lipoprotein(a) in clinical practice. Journal of Clinical Lipidology. 2024. https://doi.org/10.1016/j.jacl.2024.03.001
- Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. European Heart Journal. 2022. https://doi.org/10.1093/eurheartj/ehac361
- Nordestgaard BG, Langsted A, Mora S, et al. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points. A joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. European Heart Journal. 2016. https://doi.org/10.1093/eurheartj/ehw152
- Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019. https://doi.org/10.1161/CIR.0000000000000625
- Blumenthal RS, Morris PB, Gaudino M, et al. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2026. https://doi.org/10.1161/CIR.0000000000001423
- Tsimikas S, Fazio S, Ferdinand KC, et al. NHLBI Working Group Recommendations to Reduce Lipoprotein(a)-Mediated Risk of Cardiovascular Disease and Aortic Stenosis. Journal of the American College of Cardiology. 2018. https://doi.org/10.1016/j.jacc.2017.11.014
- Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. European Heart Journal. 2020. https://doi.org/10.1093/eurheartj/ehz455
- Emerging Risk Factors Collaboration. Lipoprotein(a) Concentration and the Risk of Coronary Heart Disease, Stroke, and Nonvascular Mortality. JAMA. 2009. https://doi.org/10.1001/jama.2009.1063
- Patel AP, Wang M, Pirruccello JP, et al. Lp(a) (Lipoprotein[a]) Concentrations and Incident Atherosclerotic Cardiovascular Disease: New Insights From a Large National Biobank. Arteriosclerosis, Thrombosis, and Vascular Biology. 2021. https://doi.org/10.1161/ATVBAHA.120.315291
- Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction. JAMA. 2009. https://doi.org/10.1001/jama.2009.801
- Clarke R, Peden JF, Hopewell JC, et al. Genetic Variants Associated with Lp(a) Lipoprotein Level and Coronary Disease. New England Journal of Medicine. 2009. https://doi.org/10.1056/NEJMoa0902604
- Burgess S, Ference BA, Staley JR, et al. Association of LPA Variants With Risk of Coronary Disease and the Implications for Lipoprotein(a)-Lowering Therapies: A Mendelian Randomization Analysis. JAMA Cardiology. 2018. https://doi.org/10.1001/jamacardio.2018.1470
- Kamstrup PR, Tybjaerg-Hansen A, Nordestgaard BG. Elevated Lipoprotein(a) and Risk of Aortic Valve Stenosis in the General Population. Journal of the American College of Cardiology. 2014. https://doi.org/10.1016/j.jacc.2013.09.038
- Thanassoulis G, Campbell CY, Owens DS, et al. Genetic Associations with Valvular Calcification and Aortic Stenosis. New England Journal of Medicine. 2013. https://doi.org/10.1056/NEJMoa1109034
- Cho L, Nicholls SJ, Frndak S, et al. Pelacarsen and Cardiovascular Outcomes in Patients with High Lipoprotein(a). New England Journal of Medicine. 2026. https://doi.org/10.1056/NEJMoa2610159
- Nissen SE, Cho L, Frndak S, et al. Extended Analyses of Pelacarsen and Cardiovascular Outcomes in Patients with High Lipoprotein(a). NEJM Evidence. 2026. https://doi.org/10.1056/EVIDoa2600373
- Albers JJ, Slee A, O'Brien KD, et al. Relationship of Apolipoproteins A-1 and B, and Lipoprotein(a) to Cardiovascular Outcomes: The AIM-HIGH Trial (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglyceride and Impact on Global Health Outcomes). Journal of the American College of Cardiology. 2013. https://doi.org/10.1016/j.jacc.2013.06.051
- O'Donoghue ML, Fazio S, Giugliano RP, et al. Lipoprotein(a), PCSK9 Inhibition, and Cardiovascular Risk. Circulation. 2019. https://doi.org/10.1161/CIRCULATIONAHA.118.037184
- Bittner VA, Szarek M, Aylward PE, et al. Effect of Alirocumab on Lipoprotein(a) and Cardiovascular Risk After Acute Coronary Syndrome. Journal of the American College of Cardiology. 2020. https://doi.org/10.1016/j.jacc.2019.10.057
- Tsimikas S, Fazio S, Viney NJ, et al. Relationship of lipoprotein(a) molar concentrations and mass according to lipoprotein(a) thresholds and apolipoprotein(a) isoform size. Journal of Clinical Lipidology. 2018. https://doi.org/10.1016/j.jacl.2018.07.003
- Trinder M, Paruchuri K, Haidermota S, et al. Repeat Measures of Lipoprotein(a) Molar Concentration and Cardiovascular Risk. Journal of the American College of Cardiology. 2022. https://doi.org/10.1016/j.jacc.2021.11.055