Related Experiment Video
Updated: Sep 22, 2026
Murine Left Anterior Descending (LAD) Coronary Artery Ligation: An Improved and Simplified Model for Myocardial Infarction
Published on: April 2, 2017
Lipoprotein(a) in acute myocardial infarction - insights from the randomised ASSAIL-MI trial
Kaspar Broch1, Arne K Andreassen1, Anne K Anstensrud1
1Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
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.
