Lp(a) rises marginally but stays within risk categories after STEMI and does not associate with infarct size in the ASSAIL-MI trial (Atherosclerosis 2026)

Original title: Lipoprotein(a) in acute myocardial infarction - insights from the randomised ASSAIL-MI trial

Atherosclerosis · 15 September 2026 · 7

Broch K, Andreassen AK, Anstensrud AK, Woxholt S, Flø A, Bjørkelund E, Ueland T, Halvorsen B, Lie ØH, Aukrust P, Andersen GØ, Wiseth R et al.

In the randomised ASSAIL-MI trial of 199 patients with ST-elevation myocardial infarction, plasma Lp(a) concentrations were measured serially alongside interleukin-6 receptor inhibition with tocilizumab or placebo. Median baseline Lp(a) was 17 (interquartile range 6 - 86) nmol/L, rising to a peak of 25 (9 - 118) nmol/L at 3-7 days (p < 0.001) before settling at 22 (8 - 110) nmol/L at 6 months. Few patients shifted between low- and high-risk categories, tocilizumab did not alter Lp(a) levels, and baseline concentrations showed no association with myocardial salvage, infarct size, or microvascular obstruction. This trial confirms that acute inflammation and IL-6 blockade do not meaningfully perturb Lp(a) or alter its prognostic value for early post-infarction myocardial damage.

Original abstract

Background And Aims: Elevated circulating levels of lipoprotein(a) [Lp(a)] increase the risk of cardiovascular events. Plasma concentrations of biomarkers and lipoproteins may change substantially in the aftermath of myocardial infarction and may fluctuate with inflammation and lipid-lowering treatment. We aimed to assess the stability of plasma Lp(a) concentrations throughout the course of an ST-elevation myocardial infarction (STEMI) and to determine how Lp(a) levels changed with inflammation and anti-inflammatory treatment.

Methods: In 199 patients with STEMI who were randomized 1:1 to receive the interleukin-6 receptor inhibitor tocilizumab or placebo within 6 h of symptom onset, we measured Lp(a) at baseline, at 24 h, at 3-7 days, and at 3 and 6 months. We measured the myocardial salvage index, infarct size, and microvascular obstruction by magnetic resonance imaging 3-7 days after the STEMI.

Results: The median plasma level of Lp(a) at baseline was 17 (interquartile range 6 - 86) nmol/L. Plasma levels rose slightly over the first days after the infarction to a peak value of 25 (9 - 118) nmol/L at 3-7 days (p < 0.001) and 22 (8 - 110) at 6 months. Few patients moved between low- and high-risk categories during follow-up. Tocilizumab did not affect Lp(a) levels. Baseline Lp(a) was not associated with myocardial salvage, final infarct size, or the extent of microvascular obstruction.

Conclusion: After myocardial infarction, there was a statistically significant, but not clinically relevant increase in Lp(a) levels that was not affected by inhibition of interleukin 6 signalling.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 26 September 2026. Methods.