Most people who have had their cholesterol checked think they know their cardiovascular risk. The standard panel shows total cholesterol, LDL-C, HDL-C and triglycerides. It is the test almost every physician orders, and it has been used for decades. The problem is that, on its own, it is not the best test available.
Two better markers have existed for years. They are inexpensive, accurate and endorsed by European guidelines: the ESC/EAS recommends ApoB for risk assessment (Class I) and advises considering an Lp(a) measurement at least once in every adult's lifetime (Class IIa). And yet most standard check-ups still do not include them. Here is what they are and why they matter.
Marker 1: ApoB
Atherosclerosis — the underlying cause of heart attacks and strokes — develops when cholesterol-carrying particles become trapped in the walls of the arteries. Every one of these particles carries a single protein on its surface called apolipoprotein B, or ApoB for short. One particle, one ApoB.
This means that measuring ApoB tells you how many atherogenic particles are circulating in the bloodstream. It is a direct count.
LDL-C (traditional)
Measures the cholesterol content inside particles. Often calculated by estimation. Two people can have the same LDL-C but very different particle counts.
ApoB (better)
Directly counts every atherogenic particle. More accurate. More predictive. Recommended by the ESC/EAS for risk assessment (Class I).
Here is why this matters clinically. Imagine two people, each with an LDL-C of 120 mg/dL. Person A has fewer, larger particles, each carrying more cholesterol. Person B has many smaller particles, each carrying less. Their LDL-C is identical. Their risk is not — person B has far more particles that can lodge in arterial walls, and therefore a much higher cardiovascular risk.
ApoB catches this; LDL-C can miss it. In most people the two markers agree, but in a meaningful minority — particularly with high triglycerides, diabetes or obesity — they diverge, and then ApoB tracks risk more closely.
Why isn't this in standard panels?
Inertia, mostly. The LDL-C estimate has been used since the 1970s, and changing the standard of care takes decades. The ESC/EAS guidelines recommend ApoB for risk assessment and accept it as an alternative to LDL-C — particularly for people with metabolic syndrome, diabetes, obesity or elevated triglycerides, where LDL-C is least reliable.
Marker 2: Lipoprotein(a)
Lipoprotein(a) — usually written as Lp(a) — is a special type of LDL particle with an extra protein attached. Unlike regular LDL, the Lp(a) level is almost entirely determined by genetics. It cannot be changed meaningfully with diet, exercise or lifestyle.
And it is common. About 20% of the population — 1 in 5 people — has elevated Lp(a). Risk rises continuously with the level: in people with the highest values (roughly the top 5%), the risk of heart attack and of aortic valve stenosis is about two to three times higher, while the link with stroke is weaker.
The evidence is among the strongest in cardiology. Mendelian randomization studies — in which researchers use genetic variants as natural experiments — have shown that Lp(a) is a direct causal driver of cardiovascular disease, not just an associated marker. It is not a correlation that can be explained away.
The European Atherosclerosis Society's 2022 consensus statement recommends measuring Lp(a) at least once in every adult. The 2025 ESC/EAS focused update advises considering such a measurement in each adult's lifetime and regards levels above 50 mg/dL (105 nmol/L) as clinically significant.
Why does it matter if it can't be changed?
Because although Lp(a) cannot be lowered directly with lifestyle, knowing that it is high changes the strategy for everything else. If Lp(a) is elevated, it can move a person into a higher risk category, and the target for LDL-C (or ApoB) is then usually set lower. Statin therapy tends to be started sooner and pursued more intensively. Blood pressure deserves closer monitoring. A cardiologist may recommend additional imaging, such as a coronary calcium score.
In short: knowing your Lp(a) status is not a diagnosis — it is a change of strategy. And for the 20% of people with elevated levels, it may be the single most important piece of cardiovascular information they ever receive.
Specific Lp(a)-lowering drugs are in development, but none is approved yet, and it has not been shown that lowering Lp(a) prevents heart attacks or strokes. In September 2026 the first large outcome trial, Lp(a)HORIZON with pelacarsen, missed its primary endpoint despite lowering Lp(a); trials of other agents such as olpasiran, lepodisiran and zerlasiran are still running. Knowing your level is useful now, because it changes how the other risk factors are managed.
What this means for your check-up
Standard cardiovascular screening typically includes LDL-C, HDL-C, triglycerides and total cholesterol. It usually does not include ApoB or Lp(a) — even though both are inexpensive, widely available and have been recommended by international cardiology guidelines for years.
A sensible lipid assessment therefore looks at ApoB and Lp(a) alongside triglycerides and HDL-C. Together, these four markers give a far more accurate picture of cardiovascular risk than the traditional cholesterol panel alone. And because Lp(a) is largely genetic, it usually needs to be measured only once — the result stays relevant for life. If a close relative had a heart attack or stroke at a young age, this is all the more reason to ask for it (see why family history matters).
Questions to ask your doctor
- Has my Lp(a) ever been measured? If not, can it be added to my next blood test?
- Would ApoB give a clearer picture of my risk than LDL-C — for example because my triglycerides are high or I have diabetes?
- If my Lp(a) is elevated, how does that change my LDL-C or ApoB target?
The bottom line
If your last cardiovascular work-up did not include ApoB and Lp(a), it was incomplete. Both are inexpensive. Both are backed by ESC/EAS guideline recommendations. And both can change treatment strategy in ways the traditional panel cannot.
References
- Mach F, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111-188.
- Mach F, Koskinas KC, et al. 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J. 2025;46(42):4359-4378. doi:10.1093/eurheartj/ehaf190
- Burgess S, et al. Association of LPA variants with risk of coronary disease and the implications for lipoprotein(a)-lowering therapies. JAMA Cardiol. 2018;3(7):619-627.
- Ference BA, et al. Association of triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants with risk of coronary heart disease. JAMA. 2019;321(4):364-373.
- 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.
- Sniderman AD, et al. Apolipoprotein B particles and cardiovascular disease: a narrative review. JAMA Cardiol. 2019;4(12):1287-1295.
- Novartis. Lp(a)HORIZON Phase III topline results for pelacarsen (press release). 4 September 2026.
This article is general information and not individual medical advice. Decisions about tests and treatment belong in a conversation with your own physician.