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ApoB and Lp(a): The two cardiovascular numbers your standard German check-up does not measure

What the European cardiology guidelines (2019, updated 2025) recommend, what your Hausärztin orders by default, what the tests cost and what a high result really changes. No panic, no optimisation mania.

Updated 15 min read26 sources

The short answer

ApoB counts the particles that clog arteries, while Lp(a) is a particle whose level is more than 90% inherited, and the standard German check-up measures neither.[3, 5, 16] European guidelines recommend ApoB mainly with high triglycerides, diabetes or obesity, and European and US experts advise measuring Lp(a) once in every adult.[1, 5, 14] Your statutory health insurance (Kasse) pays when your doctor finds a test medically necessary.[11] Otherwise the self-pay lab fee is about 13 to 15 EUR for ApoB and 20 to 23 EUR for Lp(a), plus the draw and any consultation (as of October 2026).[12]

This content is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making changes to your diet, exercise routine, or supplement regimen.

Why ApoB can tell you more than LDL-C

ApoB can tell you more than LDL-C because it counts the artery-clogging particles themselves, while LDL-C only weighs the cholesterol inside them.[3] Your standard cholesterol panel reports LDL-C, the mass of cholesterol packed into LDL particles. Every LDL particle and every other plaque-forming fat carrier, from VLDL to Lp(a), carries exactly one ApoB molecule.[3] Your ApoB level therefore works as a particle count. That count matters because any particle, whatever its cholesterol load, can get stuck in the artery wall and start a plaque.[3]

For most people the particle count and the cholesterol mass tell the same story. They part ways most often in type 2 diabetes, belly fat, high triglycerides (another kind of blood fat) and metabolic syndrome, a cluster of heart risk factors.[3] In these conditions LDL particles tend to be small and low in cholesterol, so an ordinary LDL-C can hide a high particle count.[3] Researchers call this mismatch discordance, and it means LDL-C can understate a risk that ApoB picks up in the very people prevention is aimed at.[3]

Those discordant groups are exactly the ones the 2019 guidelines of the European cardiology and atherosclerosis societies (ESC/EAS) single out for an ApoB test.[1] They recommend it for risk assessment especially with high triglycerides, diabetes, obesity, metabolic syndrome or a very low LDL-C.[1] That advice carries Class I, their strongest grade.[1] Even so, LDL-C stays the main treatment target, with ApoB as a secondary one,[1, 15] and the 2025 focused update left the ApoB advice unchanged.[2] In the US, the cardiology societies ACC and AHA replaced their 2018 cholesterol guideline with a new dyslipidaemia guideline in 2026.[14] It, too, keeps ApoB as a selective test rather than one for everyone, used mainly once LDL-C is on target and especially with high triglycerides, diabetes or an LDL-C that treatment has already pushed low.[14, 15]

That selective role fits the strength of the evidence. The case for ApoB rests on large observational studies such as UK Biobank, which watch people rather than test a treatment.[4] It also rests on the biology of how particles get stuck in the artery wall.[3] No randomized trial has yet shown that treating to an ApoB target prevents more heart attacks and deaths than treating to an LDL-C target. So ApoB earns its place as the tiebreaker when your LDL-C and the rest of your picture do not match, which is the job both guidelines give it.

What is Lp(a), and why can't you change it much?

Lipoprotein(a), or Lp(a), is an LDL-like particle with one extra protein, apolipoprotein(a), attached to it, and more than 90% of your level is set by your genes.[5] Adult levels are usually reached by about age 5, though they can keep rising until adulthood, so children sometimes need more than one test.[5] Diet, exercise and statins barely move it, so the number you inherit is largely the number you keep.[5]

That inherited number is high in a lot of people. About one in five people has Lp(a) above 50 mg/dL.[2, 5] That level is linked to a higher risk of heart attack, stroke and a narrowed aortic valve, the heart's main outflow valve.[2, 5] Levels run much higher on average in people of African ancestry.[5] A large analysis pooling dozens of studies that followed people over time found a steady but modest link with coronary heart disease, independent of other risk factors.[7] Genetic studies later went a step further and showed that the link is causal, as a 2022 consensus of the European Atherosclerosis Society (EAS) summarises.[5]

Because the level is both inherited and causal, the EAS says every adult should have Lp(a) measured at least once.[5] It sees the test as part of a full heart-risk assessment.[5] Since 2026 the US guideline says the same, and it counts 50 mg/dL (125 nmol/L) or more as a factor that raises your risk.[14, 15] If your Lp(a) is normal, one test is usually enough, although a repeat can make sense with kidney or liver disease or after an acute infection.[5] Pregnancy can roughly double Lp(a) and an underactive thyroid raises it, so do not rely on a value taken at those times.[5]

What treatment can and cannot do yet

The test is simple, but acting on a high result is harder, because as of October 2026 no drug is approved specifically to lower Lp(a).[5, 10] The first large outcome trial has reported, and it disappointed. Lp(a)HORIZON tested pelacarsen, a gene-silencing drug, in more than 8,000 people who already had cardiovascular disease and high Lp(a).[10] Novartis announced topline results on 4 September 2026.[10] Compared with placebo, pelacarsen lowered Lp(a) but did not significantly cut a combined count of cardiovascular deaths, heart attacks, strokes and urgent procedures to reopen a heart artery.[10] The full data are still to be presented at a medical congress.[10]

Further outcome trials are running, and none has reported yet:

  • Olpasiran, another gene-silencing drug, is being tested in OCEAN(a)-Outcomes, which is expected to finish in 2028.[20]
  • Lepodisiran, which works the same way, is being tested in ACCLAIM-Lp(a), which is expected to finish in 2029.[21]
  • Muvalaplin, an Lp(a)-lowering tablet, is in a trial that is still recruiting.[22]

Until one of them succeeds, two existing treatments touch Lp(a) along the way. PCSK9 inhibitors, injectable drugs that lower LDL-C, also bring Lp(a) down by about a quarter on average.[9] They are not licensed for Lp(a) itself, though.[5] Niacin (vitamin B3), by contrast, is not recommended for lowering Lp(a), because it showed no clinical benefit in outcome trials.[5]

The second treatment is for a small group with very high Lp(a) and cardiovascular disease that keeps progressing despite optimal treatment. Lipoprotein apheresis is a weekly procedure in a specialist centre that filters Lp(a) and LDL out of the blood.[5] The evidence that it prevents events comes from uncontrolled studies.[5] In Germany statutory insurance covers it for isolated Lp(a) above 60 mg/dL with normal LDL-C, when the disease is shown to progress both clinically and on imaging.[23] Coverage also needs an assessment by a cardiologist and a lipid specialist and the Kasse's approval case by case.[23]

For almost everyone else, a high Lp(a) changes how strictly the rest of the risk picture is treated rather than the Lp(a) itself. The EAS recommends early, intensive management of the risk factors you can move, such as blood pressure, ApoB-carrying particles, smoking and blood sugar.[5]

How do you read ApoB and Lp(a) results?

You read ApoB against a goal set by your overall heart risk and Lp(a) against bands that rise with the value, after checking the unit.[1, 5] Units cause much of the confusion. ApoB shows up in g/L or mg/dL, while Lp(a) comes either in mass units (mg/dL) or in molar units (nmol/L), which the EAS prefers.[5] The EAS advises against converting between the two Lp(a) units with a fixed factor, because assays vary so much.[5]

For ApoB, the 2019 ESC/EAS guideline sets goals by risk category rather than one threshold, the same logic it uses for LDL-C.[1] The higher your risk, the lower the goal. Your category depends on your age, blood pressure, smoking, diabetes, family history and any existing heart disease. That is why a single number read off a screen cannot tell you your own target.

The table gives the guideline goals for ApoB and the EAS bands for Lp(a). Read the ApoB rows as targets for a given risk category and the Lp(a) rows as steps on a sliding scale.

Marker Value What it means
ApoB under 65 mg/dL (0.65 g/L) goal at very high risk
ApoB under 80 mg/dL (0.80 g/L) goal at high risk
ApoB under 100 mg/dL (1.00 g/L) goal at moderate risk
Lp(a) under 30 mg/dL (75 nmol/L) risk from Lp(a) unlikely
Lp(a) 30 to 50 mg/dL (75 to 125 nmol/L) grey zone
Lp(a) above 50 mg/dL elevated, adds to your overall risk
Lp(a) above 180 mg/dL (430 nmol/L) lifetime risk like familial hypercholesterolaemia

Sources: ApoB goals from ESC/EAS 2019,[1] Lp(a) bands from EAS 2022.[5]

Those Lp(a) bands are conventions on a continuous scale, because the EAS 2022 consensus calls the risk continuous and graded, with no point where danger suddenly starts.[5] Since no fixed conversion exists, the nmol/L figure for "elevated" differs between documents. EAS 2022 converts 50 mg/dL to 125 nmol/L,[5] while the 2025 ESC/EAS focused update uses 105 nmol/L.[2] At the top of the scale, values above 180 mg/dL (430 nmol/L) carry a lifetime risk similar to untreated heterozygous familial hypercholesterolaemia.[5] That is a high-cholesterol condition inherited from one parent.

Any value in those bands still needs its context. Read both markers with a full lipid panel, blood pressure, glucose or HbA1c (your average blood sugar over about three months) and a documented family history. It also matters whether you have already had a heart attack or stroke.[1] Preventing a first event is called primary prevention and preventing another one secondary prevention, and your doctor weighs the same value differently in each.[1]

Why doesn't your GP order ApoB or Lp(a)?

Your Hausärztin (GP) usually skips ApoB and Lp(a) because the statutory check-up she offers does not include them.[16] Statutory insurance pays for this general check-up (Gesundheitsuntersuchung, popularly called Check-up 35) once between 18 and 34, and every three years from 35.[16] From 35 its blood tests are a lipid panel (total cholesterol, LDL-C, HDL-C, triglycerides) and fasting glucose, plus a urine strip.[16] Under 35, blood is drawn only with a risk profile such as a family history, obesity or high blood pressure.[16] ApoB, Lp(a), the inflammation marker hs-CRP and HbA1c are not part of it.[16]

That focus on LDL-C is not a German quirk. Most treatment trials were built on lowering LDL-C, so primary care anchors on it. The European risk calculator SCORE2 also uses total and HDL cholesterol rather than ApoB or Lp(a).[18] ApoB and Lp(a) only joined the guidelines later, as tools that refine a risk estimate.[1, 5] The German panel may still change. In October 2026 the G-BA, the committee that decides what statutory insurance pays, began reviewing the check-up, with a deadline of end 2027.[17]

Until then, your Kasse (statutory health insurer) still pays for both tests outside the check-up when there is a medical reason. Both have their own codes in the statutory fee catalogue (EBM 32452 for ApoB, 32456 for Lp(a)), and the EBM attaches no fixed list of indications.[11] Your doctor bills the Kasse whenever the test is medically necessary in your case.[11] For ApoB, typical reasons from the guidelines are high triglycerides, diabetes, obesity, metabolic syndrome or a very low LDL-C.[1] For Lp(a), they include known cardiovascular disease, a high overall risk, early heart disease in the family, and known or suspected familial hypercholesterolaemia.[1, 5] Pure screening without such a reason is IGeL (Individuelle Gesundheitsleistung, a self-pay extra).

A documented family history, with who had what at which age, is one of the most useful things you can bring to that decision. If your GP still sees no medical reason, she is following the rules, and you have two routes. You can ask her to add both markers as a self-pay line on your next blood draw. Or you use a Selbstzahler (self-pay) service that orders from a large lab such as Synlab, Limbach or Sonic Healthcare. Both routes end up in the same kind of lab, so the price is what you compare.

What do ApoB and Lp(a) tests cost in Germany, Austria and Switzerland?

In Germany, testing without a medical reason costs about 13 to 15 EUR in lab fees for ApoB and about 20 to 23 EUR for Lp(a).[12] The blood draw and any consultation come on top (as of October 2026).[12] Either your Hausärztin bills you privately under the German fee schedule for doctors (GOÄ), or a Selbstzahler (self-pay) service ships your blood to a large lab.

The price range is that narrow because the GOÄ caps lab fees in its section M at 1.3 times the base rate, with 1.15 times as the usual rate.[12] It also rules out fee agreements above that cap.[12] The table shows the lab fee per marker at the usual rate and at the legal maximum.

Marker Usual fee (1.15x) Maximum (1.3x) Statutory insurance
ApoB (GOÄ 3725) 13.41 EUR 15.16 EUR if medically necessary
Lp(a) (GOÄ 3730) 20.11 EUR 22.74 EUR if medically necessary

Blood draw (GOÄ 250) about 5 EUR, consultation extra. As of October 2026.[12]

Online services sell package prices that include the draw, shipping and service, so compare the total rather than the lab fee alone. If you have private insurance (PKV) or Beihilfe, ask your insurer before ordering whether it pays for these tests without a medical reason.

In Austria the cost depends on who orders the test. If a doctor with a contract with the public insurer (a Kassenarzt) finds a medical reason, the test goes through a contract lab.[25] You then pay nothing or only a small co-payment.[25] At a Wahlarzt (a doctor without a Kassen contract) or a private lab, you pay first.[19] You then claim back 80% of what the Kasse would have paid a contract partner.[19] That is rarely 80% of your invoice, because Wahlarzt prices are usually higher.[19] Tests without a medical need, and extras not foreseen in the standard Vorsorgeuntersuchung (the Austrian check-up), are not reimbursed.[25]

In Switzerland both tests are on the federal Analysenliste, the list of lab tests that basic insurance (OKP) pays for, with no special limits.[13] Each is tariffed at 17.9 tax points at 1 CHF per point.[13] Both together therefore come to roughly 36 CHF, before order fees, the blood draw and the consultation.[13] If your doctor orders them for a medical reason, OKP pays, and the bill counts toward your Franchise (annual deductible) and Selbstbehalt (your share above it). Pure lifestyle screening you usually pay yourself, and online self-pay services often charge well above the tariff.

Before the blood draw

Wherever you test, you do not need to fast for ApoB or Lp(a).[5, 26] European societies have recommended non-fasting blood for routine lipid tests since 2016.[26] Fast only if your doctor asks, for example because another test needs it or a non-fasting triglyceride value came back very high.[26] The German check-up measures fasting glucose, so fast if it is done at the same draw.[16]

What can distort the result is an illness on the day or the lab's method. Avoid a draw during an acute illness, which can shift lipids.[5] Lp(a) also runs higher in some inflammatory conditions, though the effect in population studies is small.[5] Ask the lab in advance which Lp(a) unit it reports and whether its assay is isoform-insensitive, meaning it reads correctly whatever the size of your Lp(a) particles.[5]

Your ApoB or Lp(a) is high. What now?

If your ApoB or Lp(a) is high, discuss the result with your GP or, better, with a cardiologist or a doctor trained in lipid medicine. There is no single right answer, because what follows depends on your age, other risk factors, family history and any earlier cardiovascular event.

That conversation goes further when you bring your full lipid panel and a documented family history of cardiovascular events, with ages. Add your blood pressure trend, glucose or HbA1c if you have them, your smoking status and a list of medications. If you want to read up beforehand, the Lipid-Liga (the German Society for Lipidology, DGFL) offers patient information on Lp(a).[24] Then ask your questions out loud instead of waiting for them to come up:

  • "Which risk calculator fits me, and where do I land?" SCORE2, the ESC's 10-year calculator, is built for people aged 40 to 69 without heart disease or diabetes.[18] If you are outside that age range or already have one of these, your doctor uses other tools.
  • "Does my Lp(a) push me into a higher risk category that changes how hard we treat my LDL-C and blood pressure?"
  • "Is a coronary calcium score (CAC) reasonable for me as a tiebreaker?"
  • "Do I meet the criteria for lipid-lowering therapy, given my full picture?"

Because Lp(a) is inherited, a high value matters for your family too. The EAS recommends testing relatives when Lp(a) is very high, in familial hypercholesterolaemia, or when heart disease runs in the family.[5] So ask whether your parents, siblings and children should be tested.

Lifestyle belongs in the same conversation, with the right expectations. A Mediterranean-style diet, regular exercise, not smoking and less belly fat all help your heart, and diet changes and weight loss also lower LDL-C a little.[1] None of them normalises a genetically high Lp(a), and exercise in particular has little or no effect on it.[5] These habits are worth keeping for your heart whatever your Lp(a) is, but they are not an Lp(a) treatment.

How much a high value should worry you depends on your history. Knowing early helps most if you have a strong family history of early heart attacks or strokes. For a healthy person with no symptoms and no such history, a single raised number is a poor reason for anxiety. A high ApoB can be a reason for lipid-lowering medication, depending on your overall risk.[1] A high Lp(a) mainly means treating your LDL-C and your other risk factors more strictly.[5] A reasonable aim for the appointment is a clear plan for which of those you will treat, and how hard.

Frequently asked questions

Should I get ApoB tested?

ApoB is most worth measuring if you have high triglycerides, diabetes, obesity, metabolic syndrome or a very low LDL-C, the settings where the 2019 ESC/EAS guidelines recommend it for risk assessment.[1] In those groups LDL particles tend to be small and low in cholesterol, so a "normal" LDL-C can hide a high particle count.[3] A family history of early heart disease or an LDL-C that does not fit your overall risk are further reasons to ask. For a person with low triglycerides and no family history, ApoB usually tracks LDL-C closely enough that it adds little.[3]

What is a "good" Lp(a)?

Lower is better, because the EAS 2022 consensus treats Lp(a) risk as continuous rather than starting at one cut-off.[5] Below 30 mg/dL (75 nmol/L) Lp(a) is unlikely to add risk, 30 to 50 mg/dL is a grey zone, and above about 50 mg/dL (125 nmol/L in EAS 2022, 105 nmol/L in the 2025 ESC/EAS update) it counts as elevated.[2, 5] Values above 180 mg/dL (430 nmol/L) carry a lifetime risk similar to untreated heterozygous familial hypercholesterolaemia, a high-cholesterol condition inherited from one parent.[5] What any single value means for you still depends on the rest of your risk profile.[5]

Is Lp(a) dangerous?

High Lp(a) is a causal, independent risk factor for atherosclerotic cardiovascular disease and aortic valve stenosis (a narrowing of the heart's main outflow valve).[5, 6] What has not been shown is that lowering it with a drug prevents heart attacks: the first outcome trial, Lp(a)HORIZON, missed its main endpoint in 2026.[10] How much a high value matters depends on the number, your age and the rest of your risk picture, which is why the EAS recommends managing your other risk factors early and intensively.[5]

Why doesn't my doctor order this?

Because the German statutory check-up, open once between 18 and 34 and every three years from 35, includes a standard lipid panel but not ApoB or Lp(a).[16] Most treatment trials were built on lowering LDL-C, and the European risk calculator SCORE2 uses total and HDL cholesterol rather than ApoB or Lp(a).[18] Your doctor can still bill either test to your statutory insurer (Kasse) when it is medically necessary, and without such a reason you can order it as a self-pay IGeL test.[11]

Is the ApoB test covered by insurance, and what does it cost?

In Germany statutory insurance (the Kasse) pays when your doctor finds ApoB medically necessary, for example with high triglycerides, diabetes, obesity or a very low LDL-C,[1] and bills it under EBM 32452.[11] As pure screening it is self-pay, with a GOÄ lab fee of about 13 to 15 EUR plus the blood draw and any consultation (as of October 2026).[12] In Austria a medical reason means a contract lab at little or no cost, while a Wahlarzt refunds 80% of the Kassen tariff rather than of your invoice.[19, 25] In Switzerland basic insurance pays with a medical reason at a tariff of 17.9 CHF per test, with your Franchise and Selbstbehalt applying.[13]

Does German statutory insurance pay for an Lp(a) test?

Yes, when your doctor finds it medically necessary, because Lp(a) has its own code in the statutory fee catalogue (EBM 32456) and the EBM ties it to no fixed list of indications.[11] Typical reasons are known cardiovascular disease, heart disease at a young age in the family or suspected familial hypercholesterolaemia.[1, 5] As pure screening it is IGeL, with a GOÄ lab fee of about 20 to 23 EUR plus the blood draw (as of October 2026),[12] even though the EAS recommends one measurement for every adult.[5] For a small group with very high Lp(a) and progressing disease, the Kasse can also cover lipoprotein apheresis after case-by-case approval.[23]

Can I do anything about a high Lp(a)?

Directly, very little, because diet, exercise and statins barely move a genetically set Lp(a).[5] PCSK9 inhibitors (injectable LDL-lowering drugs) lower it by about a quarter on average across trials but are not licensed for Lp(a) itself,[5, 9] and as of October 2026 no drug specifically for Lp(a) is approved.[5, 10] For a small group with very high Lp(a) and disease that keeps progressing despite optimal treatment, lipoprotein apheresis is an option, which German statutory insurance covers after case-by-case approval, while niacin is not recommended.[5, 23] The practical move is to control what you can change more strictly: blood pressure, ApoB-containing lipoproteins, smoking, glucose and weight.[5]

Is pelacarsen approved, and what does it cost?

No. As of October 2026 pelacarsen is not approved anywhere, so there is no price and you cannot get it on prescription.[10] Its outcome trial, Lp(a)HORIZON, lowered Lp(a) but did not significantly reduce the combined rate of cardiovascular death, heart attack, stroke and urgent procedures to reopen a heart artery compared with placebo.[10] Olpasiran and lepodisiran are still in outcome trials that have not reported,[20, 21] so treat any online offer for these drugs as a red flag.

ApoB or LDL-C: Which actually matters?

If you only have LDL-C, it is still useful and lines up with most of the cardiovascular evidence. If you have both and they disagree, ApoB is the closer count of the particles that drive plaque,[3] and the 2019 ESC/EAS guidelines recommend measuring it for risk assessment, especially with high triglycerides, diabetes, obesity, metabolic syndrome or very low LDL-C.[1] LDL-C stays the main treatment target and ApoB is a secondary target,[1, 15] so the two work as complements, not rivals.

ApoB or Lp(a): What is the difference?

ApoB counts all artery-clogging particles in your blood, from LDL and VLDL to Lp(a) itself, and it responds to diet, weight and drugs such as statins.[1, 3] Lp(a) is one particle type, more than 90% genetic and barely movable, so one measurement in life is usually enough.[5] ApoB shows the part of your risk you can change and Lp(a) your inherited baseline. Lp(a) is worth measuring once in every adult, ApoB mainly when your other values or your family history do not fit together.[1, 5]

How can I lower my ApoB?

The same levers that lower LDL-C lower ApoB, because most ApoB particles are LDL.[3] Statins are the first-line drug, with ezetimibe and PCSK9 inhibitors added when needed.[1] Less saturated fat, more fibre and losing weight help too, though modestly.[1] Whether you need a drug depends on your overall risk category, not on ApoB alone,[1] so decide it with your doctor.

Do I need to fast for an ApoB or Lp(a) test?

No, you do not need to fast for ApoB or Lp(a),[5, 26] and European societies have recommended non-fasting blood for routine lipid tests since 2016.[26] Fast only if your doctor asks, for example because the German check-up's fasting glucose is drawn at the same time or a non-fasting triglyceride value came back very high.[16, 26] Skip the draw during an acute illness, and if your Lp(a) is normal, one test in life is usually enough.[5]

Should my family get Lp(a) tested?

If your Lp(a) is high, quite possibly, because the level is inherited and more than 90% set by your genes.[5] The EAS recommends testing relatives when Lp(a) is very high, in familial hypercholesterolaemia, or when heart disease runs in the family.[5] Ask your doctor whether your parents, siblings and children should have the test.

Does the US guideline now recommend Lp(a) testing too?

Yes. The 2026 ACC/AHA dyslipidaemia guideline, which replaced the 2018 cholesterol guideline, recommends measuring Lp(a) at least once in every adult.[14, 15] It counts an Lp(a) of 50 mg/dL (125 nmol/L) or more and an ApoB of 120 mg/dL or more as risk-enhancing factors, while ApoB stays a selective test rather than one for everyone.[14, 15] That puts the US in line with the EAS, which has recommended a once-in-a-lifetime Lp(a) test since its 2022 consensus.[5]

Sources26

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  2. Mach F, Koskinas KC, Roeters van Lennep JE, Tokgozoglu L, Badimon L, Baigent C, Benn M, Binder CJ, Catapano AL, De Backer G, Delgado V, Fabin N, Ference BA, Graham IM, Landmesser U, Laufs U, Mihaylova B, Nordestgaard BG, Richter DJ, Sabatine MS, et al. (2025). 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. European Heart Journaldoi:10.1093/eurheartj/ehaf190
  3. Sniderman AD, Thanassoulis G, Glavinovic T, Navar AM, Pencina M, Catapano A, Ference BA. (2019). Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review. JAMA Cardiologydoi:10.1001/jamacardio.2019.3780
  4. Marston NA, Giugliano RP, Melloni GEM, Park JG, Morrill V, Blazing MA, Ference B, Stein E, Stroes ES, Braunwald E, Ellinor PT, Lubitz SA, Ruff CT, Sabatine MS. (2022). Association of Apolipoprotein B-Containing Lipoproteins and Risk of Myocardial Infarction in Individuals With and Without Atherosclerosis: Distinguishing Between Particle Concentration, Type, and Content. JAMA Cardiologydoi:10.1001/jamacardio.2021.5083
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  6. Tsimikas S. (2017). A Test in Context: Lipoprotein(a) - Diagnosis, Prognosis, Controversies, and Emerging Therapies. Journal of the American College of Cardiologydoi:10.1016/j.jacc.2016.11.042
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  12. Bundesministerium der Justiz. (2026). Gebührenordnung für Ärzte (GOÄ): § 2 Abs. 3, § 5 Abs. 4 and Gebührenverzeichnis Nr. 250, 3725, 3730gesetze-im-internet.de
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  25. Gesundheitsportal (gesundheit.gv.at). (2026). Was zahlt die Krankenkasse? gesundheit.gv.atgesundheit.gv.at
  26. Nordestgaard BG, Langsted A, Mora S, et al. (2016). 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 Journaldoi:10.1093/eurheartj/ehw152

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