Lp(a) increases by 16.5% after acute myocardial infarction and misses 17% of relatives with elevated concentrations when measured at admission (J Clin Lipidol 2026)

Background: Lipoprotein(a) [Lp(a)] is a genetically mediated, causal risk factor for atherosclerotic cardiovascular disease.

Objective: We examined Lp(a) changes during and after acute myocardial infarction (AMI), their associations with the LPA genetic risk score (GRS), and within-subject variability in the clinically stable post-AMI period, as well as the efficiency of Lp(a) cascade testing of first-degree relatives.

Method: Plasma concentrations of Lp(a) were re-measured in 173 patients with AMI and elevated Lp(a) (≥75 nmol/L) at outpatient follow-up when clinically stable. Within-subject variability was assessed in 52 patients with ≥2 follow-up Lp(a) measurements. LPA GRS was determined using 41 LPA variants. Forty-four relatives from 23 probands with Lp(a) ≥200 nmol/L at the follow-up visit were tested for Lp(a).

Results: The median plasma concentrations of Lp(a) increased by 16.5% from 214 (166-276) nmol/L at admission for AMI to 249 (185-323) nmol/L (P < .001, follow-up:108 days); the 2 Lp(a) measurements were positively associated (r = 0.794, P < .001); the LPA GRS was only significantly associated with the Lp(a) concentrations at follow-up (P < .05). The within-subject CV of Lp(a) during follow-up was 11.4% ± 10.5%. The yield for detecting new cases among relatives was 0.52 (95%CI 0.37-0.67); 4 relatives (17%) with elevated Lp(a) would have been missed from not undertaking testing if Lp(a) concentration at the time of AMI was used for cascade testing.

Conclusion: Lp(a) levels may be underestimated at the time of AMI. Repeat measurement is required when stable for clinical decision making, including cascade testing of relatives of probands with high Lp(a).