Evidence and education for clinicians: curated, dated and linked to the source.
1683 studies (119 landmark), 10 trials tracked, 10 guideline documents, 10 educational videos. Updated 26 October 2026.
Lipoprotein(a), or Lp(a), is a genetically determined and independent risk factor for atherosclerotic cardiovascular disease. As emerging therapies make Lp(a) an increasingly actionable target, understanding its role in residual cardiovascular risk is becoming more important for clinical practice.
Testing
This UK Biobank cohort study examined whether elevated Lp(a) (≥125 nmol/L) provides complementary risk stratification across cardiovascular-kidney-metabolic stages. During 15.3 years of follow-up, elevated Lp(a) was associated with a hazard ratio of 1.31 for…
Testing
Following 6676 participants in the MESA cohort, high glycoprotein acetylation (400 μmol/L) combined with high Lp(a) (50 mg/dL) raised cardiovascular disease risk (HR=1.55) and coronary heart disease risk (HR=1.92) compared with low levels of both. Adding…
Epidemiology
This meta-analysis of seven observational studies comprising 1,008 patients found that elevated lipoprotein(a) was associated with greater odds of thin-cap fibroatheroma (OR 2.90, 95% CI 1.63 to 5.18; I²=51.0%) and lipid-rich plaques (OR 3.03, 95% CI 1.53 to…
Testing
In a cohort of 1,235 patients with acute myocardial infarction from the NARA-MI registry, admission Lp(a) ≥24 mg/dL independently predicted major adverse cardiovascular events and heart failure hospitalization during 3.6 years of follow-up. MACE occurred in…
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| Trial | Agent | N | Status | Registry |
|---|---|---|---|---|
| Lp(a)HORIZON | Pelacarsen | 8,323 | Completed, results awaited | |
| OCEAN(a)-Outcomes | Olpasiran | 7,297 | Ongoing, primary completion March 2028 | |
| ACCLAIM-Lp(a) | Lepodisiran | 17,300 | Ongoing, enrolment complete, primary completion March 2029 | |
| MOVE-Lp(a) (muvalaplin outcomes) | Muvalaplin | 10,450 | Recruiting, primary completion March 2031 |
All 10 trials in the tracker · The agents
Accredited education on Lp(a) is scattered across societies, publishers and specialist providers, and much of it expires. Our Education shelf shows what a curated, permanently maintained collection could look like next to the evidence itself.
Every adult, at least once in a lifetime: that is the recommendation of the 2019 ESC/EAS guidelines, the 2022 EAS consensus statement, the 2021 Canadian guidelines, the 2024 NLA update and the 2026 ACC/AHA multisociety guideline. Because plasma Lp(a) is more than 90 percent genetically determined and stable over decades, one measurement usually settles it; repeat only when a value sits close to a decision threshold, after menopause, in kidney disease, or when a new therapy is started. Cascade testing of first-degree relatives is recommended when the index value is high.
Prefer nmol/L on an isoform-insensitive assay: it counts particles, and apo(a) size varies so much between people that mass units mislead. Conversion is only approximate; a flat factor of 2.0 to 2.5 misclassifies about one in ten patients around trial thresholds, and the Copenhagen conversion formula does better (Lp(a)HORIZON screening data, 2026). Quote whatever unit the laboratory reported and do not convert for a decision if you can re-measure instead.
Risk is continuous. Common markers: below 30 mg/dL (75 nmol/L) low; 50 mg/dL (125 nmol/L) the traditional risk-enhancer threshold used by most guidelines; 70 mg/dL (about 150 nmol/L) the Lp(a)HORIZON entry level; 90 mg/dL and 175 to 200 nmol/L the entry levels of the other outcomes trials; above 180 mg/dL (about 430 nmol/L) a lifetime risk equivalent to heterozygous FH. About one in five adults is above 50 mg/dL; distributions differ by ancestry, the risk per nmol/L largely does not.
Statins do not (they raise it 8 to 20 percent), nor do ezetimibe, bempedoic acid, fibrates or omega-3 fatty acids. PCSK9 monoclonal antibodies lower it 20 to 30 percent and inclisiran about 22 percent; CETP inhibition (obicetrapib) about 37 percent; niacin about 37 percent but without outcome benefit; lipoprotein apheresis 60 to 70 percent per session. None of these is an Lp(a) therapy. What works today is intensive control of everything else, LDL-C first, because Lp(a) and LDL-C risk are independent and additive.
