The super-tests: ApoB & Lp(a)

Two 'beyond standard cholesterol' tests do more than the whole basic panel for many people — one because it counts particles instead of cholesterol, the other because it catches a common, silent, genetic risk the panel simply can't see.

ApoB — the particle count

The better number: ApoB directly counts the atherogenic particles (one ApoB each), so it beats LDL-C and non-HDL-C as a risk marker — superior in 9 of 9 head-to-head discordance studies, and the metric to which clinical benefit is proportional. It shines exactly where LDL-C misleads: insulin resistance, high triglycerides, small dense LDL, diabetes — where LDL can read 'normal' while particle number (and true risk) is high. Targets: <90 desirable, <80 optimal, <65 for very-high risk (mg/dL). A serious expert case says it should replace LDL-C outright; guidelines currently call it a superior add-on. Evidence ●●●●●

Lp(a) — measure once in a lifetime

The silent genetic one: Lp(a) is an LDL-like particle with an extra prothrombotic tail. It's ~90% genetically fixed, essentially lifelong, and elevated in ~20% of people (~1.4 billion) — an independent, causal risk factor for both heart disease and aortic valve stenosis. Because it's stable, you measure it once: desirable <30 mg/dL (<75 nmol/L), high risk >50 mg/dL (>125 nmol/L). Prefer the nmol/L assay (the two units don't convert cleanly). The catch: statins, diet, and exercise barely move it — so an elevated Lp(a) is a reason to drive everything else (ApoB, blood pressure) harder, and targeted drugs are only now in trials. Evidence ●●●●○

If you add two tests, add these

For most people the highest-value additions to a standard panel are a single ApoB (cheap, standardised, the true particle count) and a one-time Lp(a) (to catch the ~1-in-5 genetic elevation a normal panel hides). Together they cost little and can change the whole risk picture.

The Cholesterol Guide