Temporal aspects and implications of the measurement of lipoprotein(a) in patients with acute myocardial infarction

Background Lipoprotein(a) [Lp(a)] is a genetically mediated, causal risk factor for atherosclerotic cardiovascular disease. 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) (≥75nmol/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<0.001, follow-up:108 days); the two Lp(a) measurements were positively associated (r=0.794, P<0.001); the LPA GRS was only significantly associated with the Lp(a) concentrations at follow-up (P<0.05). 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).