Evidence and education for clinicians: curated, dated and linked to the source.
1668 studies (119 landmark), 10 trials tracked, 10 guideline documents, 10 educational videos. Updated 11 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.
Aortic stenosis
This retrospective cohort study of 1,799 patients measured Lp(a) concentrations and assessed polyvascular disease burden using a five-domain score. Patients with polyvascular disease had significantly higher Lp(a) levels than those without (57.9 [24.0-118.3]…
Mechanisms
In a cross-sectional analysis of 854 patients with recent myocardial infarction from the PROSPECT II study, higher non-Lp(a) apoB independently associated with greater plaque percentage volume (β = 0.19, 95% CI 0.05-0.33; P = 0.009), while a lower non-Lp(a)…
Epidemiology
In a single-centre cohort of 4,591 patients undergoing percutaneous coronary intervention or coronary artery bypass surgery, elevated lipoprotein(a) (≥50 mg/dL) was independently associated with a higher incidence of the primary composite endpoint of…
PCSK9 inhibition
This prospective single-centre registry evaluated lipoprotein(a) changes in 1112 patients treated with alirocumab, evolocumab, or inclisiran. Mean reductions were -15.3%, -16.7%, and -19.0% at 3, 9, and 21 months. Unadjusted decreases ranged from -14% to…
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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.
