Pablo Corral: The Interplay Between Lipoprotein(a) and Interleukin-6 in Determining Primary Cardiovascular Risk
Pablo Corral, Pharmacology Professor at FASTA University, Past President of Argentine Lipid Society, shared a post on LinkedIn about a recent article by Johan Skov Bundgaard et al. published in Atherosclerosis, adding:
“Lipoprotein(a), interleukin-6 and cardiovascular risk in a primary prevention setting.
New data from UK Biobank (n=34,092): In primary prevention, the cardiovascular risk associated with elevated Lp(a) was significantly influenced by IL-6, a key upstream inflammatory cytokine.
- Higher Lp(a) increased MACE risk only when IL-6 was elevated (HR 1.17; 95% CI 1.07–1.28), while no significant association was seen when IL-6 was below median levels.
- Inflammation appears to amplify Lp(a) pathogenicity, supporting the concept that not all elevated Lp(a) carries the same biological risk burden.
- Hs-CRP did not show the same modifying effect, suggesting IL-6 may be a more informative biomarker than conventional inflammatory markers for Lp(a)-related risk stratification.
- Clinical implication: Future Lp(a)-lowering therapies may yield greatest benefit in individuals with concomitant elevated IL-6, enabling more precise preventive targeting.
Elevated Lp(a) appears to confer its greatest cardiovascular hazard in the presence of heightened IL-6–mediated inflammation, supporting a biologically integrated model in which inherited atherothrombotic burden and residual inflammatory risk act synergistically.”
Title: Lipoprotein(a), interleukin-6 and cardiovascular risk in a primary prevention setting
Authors: Johan Skov Bundgaard, Søren Albertsen Rand, Stefan Stender, Jesper Hastrup Svendsen, Pia Rengtved Lundegaard, Christian Erikstrup, Gustav Ahlberg, Ruth Frikke-Schmidt, Lars Dyrskjøt, Ole Halfdan Larsen, Henning Bundgaard, Jonas Ghouse
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