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Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 10, 2026
Reviewed October 10, 2026
26 sources · Measured in nmol/L

System: Metabolism & Metabolomics

Lp(a)Lipoprotein(a)

Lp(a) is set by genes, is usually measured once in a lifetime, and raises heart attack, stroke and aortic stenosis risk continuously with no floor found. Consensus statements read under 75 nmol/L (30 mg/dL) as lower risk, 75 to 125 nmol/L (30 to 50 mg/dL) as a grey zone, and 125 nmol/L (50 mg/dL) or more as high. Diet and exercise barely move it, so a high value is a reason to lower ApoB and blood pressure harder, earlier.

Lipoprotein(a) is an LDL-like particle with an extra protein, apolipoprotein(a), bolted on. Its level is more than 90 percent inherited, is reached by about age five, and stays put for life, so one measurement usually settles it. Laboratories flag it above about 75 nmol/L or 30 mg/dL; about one adult in five is above the consensus high line. The evidence that it causes disease is unusually strong; the evidence that lowering it helps does not yet exist.

01 · The scale

Where the laboratory range and the evidence sit.

Risk rose continuously with no threshold in 126,634 people across 36 prospective studies and in 460,506 UK Biobank adults; the genetic variants that raise Lp(a) raised heart attack and aortic stenosis risk in step, which makes it causal; a level of about 250 nmol/L (100 mg/dL) roughly doubled cardiovascular risk.

03075125150200250

  1. Common laboratory flag above 75 nmol/L (30 mg/dL)

    75 and above nmol/L · Typical US laboratories

  2. Rule-out zone: lower Lp(a)-attributable risk

    0 to 75 nmol/L · EAS 2022; NLA 2024

  3. Grey zone: read with other risk factors

    75 to 125 nmol/L · EAS 2022; NLA 2024

  4. High: a risk enhancer in every guideline

    125 and above nmol/L · EAS 2022; NLA 2024; ESC/EAS 2019

  5. 150 nmol/L and above: 50 percent higher risk in UK Biobank; about 250 doubles it

    150 and above nmol/L · Patel 2021; EAS 2022

  • Laboratory range
  • Evidence supports
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in nmol/L. Many US laboratories report mg/dL. The two units do not convert cleanly: roughly 1 mg/dL is 2 to 2.5 nmol/L, and the ratio depends on the assay and the person. This page gives both wherever a source does. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Lp(a) measures.

Lp(a) is an LDL particle with a second protein, apolipoprotein(a), covalently bound to its ApoB. Apolipoprotein(a) resembles plasminogen but has no clot-dissolving activity, and the particle preferentially carries oxidized phospholipids, which is thought to explain why it is more inflammatory and more calcifying, per particle, than LDL.1,2,3Grade A

The concentration is predominantly, more than 90 percent, determined by variation at the LPA gene, and 70 to 90 percent of the difference between people is genetic. The number of kringle IV type 2 repeats in the gene explains about 30 to 70 percent of that variation: fewer repeats make a smaller apolipoprotein(a) and a markedly higher level. The gene is fully expressed by age two, adult levels are usually reached by about age five, and the level then stays roughly constant through life in men, rising somewhat in women around menopause.3,4,5Grade A

Most people have low levels and a minority have very high ones. Among 460,506 UK Biobank adults the median was 19.6 nmol/L and the middle half of the population sat between 7.6 and 74.8; about 12 percent of those without heart disease were at 150 nmol/L or above. Medians differed by ancestry: 19 nmol/L in White, 31 in South Asian, 75 in Black and 16 in Chinese participants. Levels run about 5 to 10 percent higher in women than men. Worldwide about 1.4 billion people, roughly one adult in five, carry a level above the consensus high line.6,3,7Grade A

03 · The laboratory range

What a laboratory calls normal.

Flagged above about 75 nmol/L (30 mg/dL) by many US laboratories; some flag only above 125 nmol/L (50 mg/dL). Reported in nmol/L or mg/dL depending on the laboratory.

The National Lipid Association's 2024 statement reads Lp(a) below 75 nmol/L (30 mg/dL) as low risk, 125 nmol/L (50 mg/dL) or above as high risk, and 75 to 125 as intermediate, and recommends measuring it at least once in every adult. It notes that about one person in five has an elevated level and that measurement rates are low.7Grade A

The 2022 European Atherosclerosis Society consensus uses the same lines, below 30 mg/dL (75 nmol/L) to rule out Lp(a)-attributable risk and above 50 mg/dL (125 nmol/L) to rule it in, with 30 to 50 mg/dL (75 to 125 nmol/L) as a grey zone to be read alongside other risk factors. It asks laboratories to report in molar units when possible and to name the assay, and it does not endorse a fixed conversion between mg/dL and nmol/L: 2 to 2.5 is a best guess, because assays differ.3Grade A

The European dyslipidaemia guideline says measurement should be considered at least once in each person's lifetime, in part to find the people who have inherited a level of 180 mg/dL (430 nmol/L) or more, whose lifetime risk approaches that of untreated familial hypercholesterolemia. The Canadian guideline recommends one lifetime measurement as part of the first lipid screen. The 2010 European consensus that started this practice set a desirable level below the 80th percentile, about 50 mg/dL.1,3,8,2Grade A

04 · The evidence

What the studies support.

The Emerging Risk Factors Collaboration pooled individual records from 126,634 people in 36 prospective studies, 9,336 coronary events among them. Coronary risk rose continuously with Lp(a): 1.13 times per 3.5-fold higher usual concentration after adjustment for lipids and other risk factors, with coronary event rates of 5.6 per 1,000 person-years in the top third against 4.4 in the bottom third. Ischemic stroke rose 1.10 times; cancer and other non-vascular deaths did not move at all. Lp(a) was also highly consistent within a person over several years.9Grade A

In the Copenhagen City Heart Study, 9,330 adults followed for 10 years, risk of heart attack climbed stepwise with no threshold: 2.6 times at 85 to 119 mg/dL and 3.6 (women) to 3.7 (men) times at 120 mg/dL or more, against under 5 mg/dL. In the highest-risk people, smokers with high blood pressure over 60, the absolute 10-year risk went from 10 to 20 percent in women and 19 to 35 percent in men across that span.10Grade B

Genetics show the relationship is causal, not a bystander. In the Copenhagen City Heart Study (8,637 people followed 16 years), the number of kringle IV repeats explained 21 percent of the variation in Lp(a) (27 percent in a second Copenhagen study of 29,388), people in the lowest-repeat quartile, who have the highest Lp(a), had 1.5 times the heart attack risk of the highest-repeat quartile, and genetically higher Lp(a) carried 1.22 times the risk per doubling. In 3,145 people with coronary disease and 3,352 controls, replicated in three further populations, two LPA variants raised coronary risk 1.70 and 1.92 times, 2.57 times when two or more were carried, and the association disappeared once the Lp(a) level was accounted for, which is what causation through the level itself looks like.5,11,3Grade A

Across 460,506 UK Biobank adults followed a median of 11.2 years, risk of a cardiovascular event rose linearly, 11 percent per 50 nmol/L, with no level below which it stopped. A level of 150 nmol/L or more carried 1.50 times the risk in people without prior disease. Risk per 50 nmol/L was similar in White, South Asian and Black participants (1.11, 1.10 and 1.07) even though their median levels differed four-fold.6Grade B

Lp(a) tracks with dying, not only with events. Among 69,764 Danes, a level above 93 mg/dL (199 nmol/L) carried 1.50 times the cardiovascular mortality and 1.20 times the all-cause mortality of a level under 10 mg/dL (18 nmol/L), and median survival was 83.9 against 85.1 years. Each 50 mg/dL (105 nmol/L) more carried 1.16 times the cardiovascular mortality observationally and 1.23 times by kringle-repeat genotype; for the same cholesterol content, Lp(a) was more strongly tied to mortality than LDL.12Grade B

The LPA gene is the strongest genetic driver of calcific aortic stenosis. In a genome-wide study of 6,942 people with CT scans, one LPA variant doubled the odds of aortic valve calcification (2.05 per allele) and carried 1.68 times the risk of clinical aortic stenosis per allele in a Swedish cohort. In 77,680 Danes followed up to 20 years, Lp(a) above 90 mg/dL carried 2.9 times the risk of aortic stenosis, and the genetic estimate (1.6 times per 10-fold higher Lp(a)) matched the observational one (1.4). The European consensus notes the risk is about three-fold at the 80th percentile in people aged 45 to 54.13,14,3Grade A

The risk persists when LDL is treated. In 29,069 patients across seven statin trials, Lp(a) of 50 mg/dL or more carried 1.31 times the event risk at baseline and 1.43 times on statin, independent of LDL cholesterol, blood pressure, diabetes and smoking, and the relationship was stronger at younger ages. In the FOURIER trial, 25,096 patients with established disease on a statin, the top quartile of Lp(a) carried 1.22 times the coronary risk independent of LDL cholesterol.15,16Grade A

Put together, the European consensus reads a level of about 100 mg/dL (about 250 nmol/L) as roughly doubling cardiovascular risk whatever the baseline risk, which matters more in absolute terms when baseline risk is already high (20 to 40 percent rather than 5 to 10). Levels above 180 mg/dL (430 nmol/L) identify a lifetime risk equivalent to untreated heterozygous familial hypercholesterolemia.3,1Grade A

05 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Eating less saturated fat

    raises it modestly, while lowering LDL

    Lp(a) moves the opposite way to LDL on a diet change. In controlled feeding trials, cutting saturated fat from 16 to 5 percent of calories raised Lp(a) about 15 percent in healthy adults and 11 to 20 percent in people at metabolic risk, while LDL cholesterol fell 7 to 11 percent; across such trials the rise is 9 to 23 percent. A low-carbohydrate, higher-fat diet may lower Lp(a) 10 to 15 percent. The consensus still reads lifestyle as having minimal impact, because ApoB and LDL, not Lp(a), carry most of the diet's effect on risk.17,3Grade B

  • Exercise training

    changes it little or not at all

    Across short- and long-term training studies, including a four-year program in people with coronary disease, physical activity and fitness had no or minimal effect on Lp(a) while changing the other lipids. A 2025 meta-analysis of 25 randomized trials in 1,429 people found a pooled fall of 2.5 mg/dL, real but small next to the levels that carry risk.17,18Grade B

  • Menopause, kidney disease and an underactive thyroid

    raise it

    Across 15 studies of 4,686 premenopausal and 8,274 postmenopausal women, the postmenopausal women ran 3.8 mg/dL higher, though age-matched comparisons found no difference, so aging and menopause are hard to separate. Falling kidney function raises Lp(a) from early stages (median 11 mg/dL at a normal filtration rate to 24 at a rate under 45) and nephrotic syndrome raises it markedly; a kidney transplant largely restores the baseline. Overt hypothyroidism raises it, and treating it lowered Lp(a) by 5.6 mg/dL in a pooled analysis. These are the situations in which a repeat measurement is informative.19,17,3Grade B

  • Statins

    do not lower it; may raise it slightly

    Statins lower LDL by about 39 percent without lowering Lp(a). One pooled analysis of 5,256 trial participants found Lp(a) rose 8.5 to 19.6 percent on statins against a 0.4 to 2.3 percent fall on placebo; the seven-trial outcomes meta-analysis and a 147-trial review found no significant change. The consensus is clear that statins should not be stopped on this account, because their benefit in people with high Lp(a) outweighs any small rise.20,15,21,3Grade A

  • Lipid-lowering medications that do lower it

    lower it by about a fifth to a third

    Across 147 randomized trials in 145,314 people, PCSK9 antibodies lowered Lp(a) about 29 percent, inclisiran 22 percent and niacin 37 percent; ezetimibe, bempedoic acid, fibrates and omega-3 did nothing. None is approved for Lp(a) lowering, niacin is no longer recommended because two outcome trials showed no benefit, and whether a 20 to 30 percent fall in Lp(a) itself prevents events is unknown. People with higher Lp(a) did gain more absolute benefit from a PCSK9 antibody in FOURIER (2.49 against 0.95 percent over three years), but that drug lowers LDL cholesterol too. Whether and when to treat is a decision for a physician who knows the person's whole risk.21,3,16Grade A

  • Lowering ApoB and blood pressure harder

    the lever the consensus actually recommends

    In the absence of an approved Lp(a)-lowering drug, the European and American statements both recommend early, intensive management of the other risk factors for anyone with a high Lp(a): LDL cholesterol (ApoB), blood pressure, glucose and lifestyle, scaled to the person's baseline risk and the Lp(a) level, with the aim of bringing total risk down by enough to offset what Lp(a) adds. Mendelian randomization suggests why the target is the rest of the picture: a 10 mg/dL lower Lp(a) carried 5.8 percent lower coronary risk, against 14.5 percent for 10 mg/dL of LDL, so roughly 100 mg/dL of Lp(a) lowering would be needed to equal 1 mmol/L (about 39 mg/dL) of LDL lowering.3,7,22Grade A

06 · Reading it well

Caveats, and what belongs with a physician.

The assay matters. Apolipoprotein(a) comes in genetically determined sizes, and most assays use antibodies that bind the repeated part of the protein, so they can under-read people with small isoforms (who tend to have high levels) and over-read those with large ones. The consensus asks laboratories to use isoform-insensitive assays traceable to reference material, report in nmol/L when possible, and name the assay on the report.23,3Grade A

mg/dL and nmol/L are not interchangeable. Against a reference molar method, the nmol-per-mg ratio ran from about 1.5 to 2.8 depending on the assay and the level, and from under 1 to over 5 for commercial assays. In 13,666 people screened for an outcome trial with both units measured, converting by the common factor of 2.5 agreed with the measured value in 92 percent of people at a 70 mg/dL cutoff and 85 percent at 90. Compare results in the unit they were measured in.24,25,3Grade B

One good measurement usually suffices. In 16,017 UK Biobank adults measured twice a median of 4.4 years apart, the two values correlated at 0.96, and the change between them added nothing to risk prediction once the later value was known. The consensus says repeat measurement is not needed except when something that changes Lp(a) has happened: kidney or liver disease, an acute infection, and, by the hormone data, menopause.26,3Grade A

Lp(a) is an ApoB particle, so it is already counted in ApoB, and its cholesterol, 30 to 45 percent of its mass, is counted inside the LDL cholesterol number. A very high Lp(a) can therefore inflate LDL cholesterol and mimic familial hypercholesterolemia; the consensus does not recommend routinely correcting LDL for it except when that diagnosis is in question. Very low Lp(a) may associate with a higher risk of type 2 diabetes, a finding the panel says merits further study.3Grade A

See a physician

  • An Lp(a) of 125 nmol/L (50 mg/dL) or more, and especially 430 nmol/L (180 mg/dL) or more, which the European guideline treats as a lifetime risk equivalent to familial hypercholesterolemia.
  • A parent, sibling or child with a heart attack, stroke, stent or aortic valve replacement before 55 (men) or 65 (women), whatever your own number; the consensus recommends measuring first-degree relatives of anyone with a high Lp(a).
  • A grey-zone or high Lp(a) alongside a high ApoB or LDL cholesterol, high blood pressure, diabetes, kidney disease or smoking, where the combination, not the single number, sets the plan.
  • A heart murmur, chest pressure, breathlessness on exertion or fainting with effort, which can be aortic stenosis, regardless of any lipid number.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

07 · Open questions

What the literature does not settle.

  • Whether lowering Lp(a) itself prevents events is not yet known. The first phase 3 outcome trial of a targeted Lp(a)-lowering drug reported topline results in September 2026 in a sponsor announcement, not yet peer-reviewed: the drug lowered Lp(a) but did not meet its primary endpoint. Until a trial shows otherwise, the benefit of lowering Lp(a) itself is unproven, and the case for measuring it rests on what a high value says about the rest of a person's risk.
  • How much Lp(a) would need to fall to matter is itself uncertain: Mendelian randomization puts it near 100 mg/dL for a benefit the size of 1 mmol/L of LDL lowering, far more than any current medicine achieves outside apheresis and the investigational RNA drugs.
  • The thresholds (75 and 125 nmol/L) are pragmatic lines drawn on a continuous risk curve, and they are assay-dependent; standardization work is in progress and the consensus suggests assay-specific cutoffs may be needed, as with troponin.
  • The thresholds were derived largely from European-ancestry cohorts. Risk per nmol/L looks similar across ancestries, but the median level in Black adults (75 nmol/L) sits on the laboratory flag, and whether the same cutoffs serve every population is unsettled.
  • Whether the modest statin-related rise in Lp(a) carries any cost, whether aspirin helps people with very high Lp(a), and whether very low Lp(a) raises diabetes risk are open; the consensus flags all three.

08 · In practice

How Dr. Tagge reads it in his own practice.

I measure Lp(a) once on everyone, usually with the first lipid panel, and I like to see it under 75 nmol/L (30 mg/dL), which is where the consensus statements draw their rule-out line. When it is higher I do not chase the number, because nothing I can prescribe has yet been shown to help by lowering it. I read it as a reason to get ApoB and blood pressure lower, earlier, than the general targets would ask, and to look for calcium in the coronary arteries and the aortic valve sooner than age alone would suggest. I also ask that parents, siblings and adult children be measured once, because the level is inherited and the measurement is cheap. The rest is judgment, and I say so.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

09

Questions

10 · Sources

26 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    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. PMID 31504418. DOI 10.1093/eurheartj/ehz455.

    Guideline · Lp(a) measurement should be considered at least once in each person's lifetime; 180 mg/dL (430 nmol/L) or more marks a lifetime risk near familial hypercholesterolemia.

  2. 2.

    Nordestgaard BG, Chapman MJ, Ray K, et al.; European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. European Heart Journal. 2010. PMID 20965889. DOI 10.1093/eurheartj/ehq386.

    Consensus statement · Elevated Lp(a) is causally related to premature cardiovascular disease, continuously and without a threshold; measure once with an isoform-insensitive assay; desirable level below the 80th percentile, about 50 mg/dL.

  3. 3.

    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. PMID 36036785. DOI 10.1093/eurheartj/ehac361.

    Consensus statement · Measure once in adults; rule out below 30 mg/dL (75 nmol/L), rule in above 50 (125), grey zone between; about 100 mg/dL doubles risk; no fixed unit conversion; manage other risk factors intensively.

  4. 4.

    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. PMID 34647487. DOI 10.1161/ATV.0000000000000147.

    Consensus statement · About 70 to 90 percent or more of the variation in Lp(a) between people is genetically determined; Lp(a) remains a risk factor even when LDL cholesterol and ApoB are well controlled.

  5. 5.

    Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA. 2009. PMID 19509380. DOI 10.1001/jama.2009.801.

    Mendelian randomization · Kringle IV repeats explained 21 to 27 percent of Lp(a) variation; genetically higher Lp(a) carried 1.22 times the heart attack risk per doubling, consistent with causation.

  6. 6.

    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. PMID 33115266. DOI 10.1161/ATVBAHA.120.315291.

    Prospective cohort · 460,506 adults: median 19.6 nmol/L; risk linear, hazard ratio 1.11 per 50 nmol/L; 150 nmol/L or more in 12.2 percent, hazard ratio 1.50; medians 19, 31, 75 and 16 nmol/L by ancestry with similar risk per unit.

  7. 7.

    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. PMID 38565461. DOI 10.1016/j.jacl.2024.03.001.

    Consensus statement · Below 75 nmol/L (30 mg/dL) low risk, 125 (50) or above high, between intermediate; measure at least once in every adult; about one in five elevated.

  8. 8.

    Pearson GJ, Thanassoulis G, Anderson TJ, et al.. 2021 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in Adults. Canadian Journal of Cardiology. 2021. PMID 33781847. DOI 10.1016/j.cjca.2021.03.016.

    Guideline · Lipoprotein(a) measurement recommended once in a patient's lifetime as part of initial lipid screening.

  9. 9.

    Emerging Risk Factors Collaboration; Erqou S, Kaptoge S, et al.. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA. 2009. PMID 19622820. DOI 10.1001/jama.2009.1063.

    Systematic review and meta-analysis · 126,634 participants in 36 studies: coronary risk ratio 1.13 per 3.5-fold higher Lp(a) after adjustment, continuous, with no association with non-vascular deaths.

  10. 10.

    Kamstrup PR, Benn M, Tybjaerg-Hansen A, Nordestgaard BG. Extreme lipoprotein(a) levels and risk of myocardial infarction in the general population: the Copenhagen City Heart Study. Circulation. 2008. PMID 18086931. DOI 10.1161/CIRCULATIONAHA.107.715698.

    Prospective cohort · Stepwise rise in heart attack risk with no threshold; 3.6 to 3.7 times at 120 mg/dL or more; absolute 10-year risks of 20 and 35 percent in high-risk women and men.

  11. 11.

    Clarke R, Peden JF, Hopewell JC, et al.; PROCARDIS Consortium. Genetic variants associated with Lp(a) lipoprotein level and coronary disease. New England Journal of Medicine. 2009. PMID 20032323. DOI 10.1056/NEJMoa0902604.

    Mendelian randomization · Two LPA variants raised coronary odds 1.70 and 1.92 times, 2.57 with two or more; the association vanished after adjusting for the Lp(a) level.

  12. 12.

    Langsted A, Kamstrup PR, Nordestgaard BG. High lipoprotein(a) and high risk of mortality. European Heart Journal. 2019. PMID 30608559. DOI 10.1093/eurheartj/ehy902.

    Prospective cohort · Above 93 mg/dL (199 nmol/L): hazard ratio 1.50 for cardiovascular and 1.20 for all-cause mortality; median survival 83.9 versus 85.1 years; genetic estimate by kringle repeats concordant.

  13. 13.

    Thanassoulis G, Campbell CY, Owens DS, et al.; CHARGE Extracoronary Calcium Working Group. Genetic associations with valvular calcification and aortic stenosis. New England Journal of Medicine. 2013. PMID 23388002. DOI 10.1056/NEJMoa1109034.

    Mendelian randomization · LPA variant rs10455872: odds ratio 2.05 per allele for aortic valve calcification and hazard ratio 1.68 per allele for incident aortic stenosis, supporting a causal role.

  14. 14.

    Kamstrup PR, Tybjærg-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. PMID 24161338. DOI 10.1016/j.jacc.2013.09.038.

    Mendelian randomization · 77,680 Danes: Lp(a) above 90 mg/dL carried 2.9 times the aortic stenosis risk; genetic relative risk 1.6 per 10-fold increase matched the observational 1.4.

  15. 15.

    Willeit P, Ridker PM, Nestel PJ, et al.. Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials. Lancet. 2018. PMID 30293769. DOI 10.1016/S0140-6736(18)31652-0.

    Systematic review and meta-analysis · 29,069 patients in seven statin trials: Lp(a) of 50 mg/dL or more carried hazard ratios of 1.31 at baseline and 1.43 on statin, independent of LDL cholesterol; statins did not change Lp(a) significantly.

  16. 16.

    O'Donoghue ML, Fazio S, Giugliano RP, et al.. Lipoprotein(a), PCSK9 Inhibition, and Cardiovascular Risk. Circulation. 2019. PMID 30586750. DOI 10.1161/CIRCULATIONAHA.118.037184.

    Randomized trial · In FOURIER (25,096 patients) the top Lp(a) quartile carried hazard ratio 1.22 independent of LDL cholesterol; evolocumab lowered Lp(a) a median 26.9 percent, with greater absolute benefit above the median Lp(a).

  17. 17.

    Enkhmaa B, Berglund L. Non-genetic influences on lipoprotein(a) concentrations. Atherosclerosis. 2022. PMID 35606076. DOI 10.1016/j.atherosclerosis.2022.04.006.

    Review · Reducing saturated fat raises Lp(a) 9 to 23 percent in feeding trials while lowering LDL; exercise has no or minimal effect; kidney disease and hypothyroidism raise it; hormone therapy lowers it.

  18. 18.

    Downes D, Goodman S, van der Touw T, et al.. Effect of Exercise Training on Apolipoproteins: Meta-analysis and Trial Sequence Analysis. International Journal of Sports Medicine. 2025. PMID 40203891. DOI 10.1055/a-2580-0722.

    Systematic review and meta-analysis · Across 25 randomized trials (1,429 participants), exercise training lowered Lp(a) by a mean 2.52 mg/dL.

  19. 19.

    Anagnostis P, Antza C, Trakatelli C, Lambrinoudaki I, Goulis DG, Kotsis V. The effect of menopause on lipoprotein (a) concentrations: A systematic review and meta-analysis. Maturitas. 2023. PMID 36302338. DOI 10.1016/j.maturitas.2022.09.012.

    Systematic review and meta-analysis · Postmenopausal women ran 3.77 mg/dL higher than premenopausal across 15 studies (12,960 women); age-matched comparisons showed no difference.

  20. 20.

    Tsimikas S, Gordts PLSM, Nora C, Yeang C, Witztum JL. Statin therapy increases lipoprotein(a) levels. European Heart Journal. 2020. PMID 31111151. DOI 10.1093/eurheartj/ehz310.

    Systematic review and meta-analysis · In 5,256 trial participants, Lp(a) rose 8.5 to 19.6 percent on statins against a 0.4 to 2.3 percent fall on placebo (ratio of geometric means 1.11).

  21. 21.

    Xie S, Galimberti F, Olmastroni E, et al.; META-LIPID Group. Effect of lipid-lowering therapies on lipoprotein(a) levels: a comprehensive meta-analysis of randomized controlled trials. Atherosclerosis. 2025. PMID 40618457. DOI 10.1016/j.atherosclerosis.2025.120420.

    Systematic review and meta-analysis · 147 trials, 145,314 people: statins, ezetimibe, bempedoic acid, fibrates and omega-3 did not change Lp(a); PCSK9 antibodies lowered it 29 percent, inclisiran 22, CETP inhibitors 46, niacin 37.

  22. 22.

    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. PMID 29926099. DOI 10.1001/jamacardio.2018.1470.

    Mendelian randomization · A 10 mg/dL lower Lp(a) carried 5.8 percent lower coronary risk versus 14.5 percent for 10 mg/dL of LDL cholesterol; about 100 mg/dL of Lp(a) lowering would equal 1 mmol/L of LDL lowering.

  23. 23.

    Marcovina SM, Albers JJ. Lipoprotein (a) measurements for clinical application. Journal of Lipid Research. 2016. PMID 26637278. DOI 10.1194/jlr.R061648.

    Laboratory method study · Apolipoprotein(a) size heterogeneity causes isoform-dependent inaccuracy in immunoassays and blocks common cut points until measurement is standardized.

  24. 24.

    Tsimikas S, Fazio S, Viney NJ, Xia S, Witztum JL, Marcovina SM. Relationship of lipoprotein(a) molar concentrations and mass according to lipoprotein(a) thresholds and apolipoprotein(a) isoform size. Journal of Clinical Lipidology. 2018. PMID 30100157. DOI 10.1016/j.jacl.2018.07.003.

    Laboratory method study · nmol/L-to-mg/dL ratios ran from about 1.5 to 2.8 depending on level and assay, and from under 1 to over 5 for commercial assays; no single conversion factor is appropriate.

  25. 25.

    Cho L, Nordestgaard BG, Chang B, et al.. Concordance of Lipoprotein(a) measurements in mg/dL and nmol/L: Insights from the Lp(a)HORIZON trial. Atherosclerosis. 2026. PMID 42250319. DOI 10.1016/j.atherosclerosis.2026.120796.

    Laboratory method study · In 13,666 people with both units measured, converting by 2.5 agreed with the measured nmol/L value in 92 percent at a 70 mg/dL threshold and 85 percent at 90 mg/dL.

  26. 26.

    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. PMID 35177190. DOI 10.1016/j.jacc.2021.11.055.

    Prospective cohort · In 16,017 adults measured twice a median 4.4 years apart, values correlated at 0.96 and the change added nothing to coronary risk prediction; a single accurate measurement suffices.

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