Lipoprotein(a) in acute myocardial infarction - insights from the randomised ASSAIL-MI trial.
Kaspar Broch, Arne K Andreassen, Anne K Anstensrud et al.
✦ AI-curated · Sources linked
In 30 seconds
This analysis of the randomised ASSAIL-MI trial assessed serial lipoprotein(a) [Lp(a)] levels in 199 patients with ST-elevation myocardial infarction (STEMI), randomised to tocilizumab or placebo. Median Lp(a) rose from 17 (interquartile range 6 - 86) nmol/L at baseline to a peak of 25 (9 - 118) nmol/L at 3-7 days (p < 0.001), a statistically significant but clinically irrelevant increase. Tocilizumab did not alter Lp(a) levels, and baseline Lp(a) was not associated with myocardial salvage, infarct size, or microvascular obstruction.
Key findings
- Median Lp(a) increased from 17 (interquartile range 6 - 86) nmol/L at baseline to 25 (9 - 118) nmol/L at 3-7 days (p < 0.001).
- Few patients changed between low- and high-risk Lp(a) categories during follow-up.
- Tocilizumab did not affect Lp(a) levels.
- Baseline Lp(a) was not associated with myocardial salvage, final infarct size, or microvascular obstruction.
Why it matters
Lp(a) is a cardiovascular risk marker, but its measurement soon after STEMI may be influenced by the acute event. These findings suggest that levels change modestly in the days after infarction, while risk-category shifts are uncommon. The absence of an association with the measured imaging outcomes also helps define what this study does—and does not—show about Lp(a) in acute myocardial infarction.
What to keep in mind
The study included patients with STEMI and assessed imaging outcomes 3-7 days after infarction; its findings may not apply to other populations or establish associations with longer-term clinical events.