04/29/2026
…
The 2026 ACC/AHA Dyslipidemia Guidelines recommend measuring Lp(a) at least once in all adults, ideally with the first lipid profile.
A single measurement is generally sufficient since levels are predominantly genetically determined and remain stable over a lifetime.
Fasting is not required.
Secondary causes of elevated Lp(a) include kidney, liver, or thyroid disease; pregnancy; and menopause.
Testing first-degree relatives is recommended when high Lp(a) is identified, particularly with a personal or family history of premature ASCVD.
- Lifestyle changes (smoking cessation, diet, exercise) do not meaningfully lower Lp(a) itself but are associated with a 67% lower ASCVD risk even among those with elevated Lp(a).
- Statins do not lower Lp(a) (and may modestly increase it by ~1 mg/dL), but remain essential for LDL-C reduction and overall cardiovascular benefit.
In the JUPITER trial, high-intensity statin therapy reduced events by 30–40% in individuals with elevated Lp(a).
- PCSK9 inhibitors (evolocumab, alirocumab, inclisiran) lower Lp(a) by approximately 15–30% in addition to substantial LDL-C lowering. Post hoc analyses from FOURIER and ODYSSEY Outcomes suggest patients with higher Lp(a) may derive greater benefit.
PCSK9 inhibitors should be preferentially considered in high-risk ASCVD patients with elevated Lp(a) who have not reached LDL-C goals.
- Lipoprotein apheresis is FDA-approved for Lp(a) ≥60 mg/dL in patients with FH and CAD or PAD, acutely lowering Lp(a) by 50–85% per session.
#