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Arnold, N.* ; Blaum, C.* ; Goßling, A.* ; Brunner, F.J.* ; Bay, B.* ; Ferrario, M.M.* ; Brambilla, P.* ; Cesana, G.* ; Leoni, V.* ; Palmieri, L.* ; Donfrancesco, C.* ; Padró, T.* ; Andersson, J.* ; Jousilahti, P.* ; Ojeda, F.* ; Zeller, T.* ; Linneberg, A.* ; Söderberg, S.* ; Iacoviello, L.* ; Gianfagna, F.* ; Sans, S.* ; Veronesi, G.* ; Thorand, B. ; Peters, A. ; Tunstall-Pedoe, H.* ; Kee, F.* ; Salomaa, V.* ; Schnabel, R.B.* ; Kuulasmaa, K.* ; Blankenberg, S.* ; Koenig, W.* ; Waldeyer, C.*

C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease: the BiomarCaRE project.

Eur. Heart J. 45, 1043-1054 (2024)
DOI PMC
Free by publisher: Publ. Version/Full Text online available 04/2025
BACKGROUND AND AIMS: Recent investigations have suggested an interdependence of lipoprotein(a) [Lp(a)]-related risk for cardiovascular disease with background inflammatory burden. The aim the present analysis was to investigate whether high-sensitive C-reactive protein (hsCRP) modulates the association between Lp(a) and coronary heart disease (CHD) in the general population. METHODS: Data from 71 678 participants from 8 European prospective population-based cohort studies were used (65 661 without/6017 with established CHD at baseline; median follow-up 9.8/13.8 years, respectively). Fine and Gray competing risk-adjusted models were calculated according to accompanying hsCRP concentration (<2 and ≥2 mg/L). RESULTS: Among CHD-free individuals, increased Lp(a) levels were associated with incident CHD irrespective of hsCRP concentration: fully adjusted sub-distribution hazard ratios [sHRs (95% confidence interval)] for the highest vs. lowest fifth of Lp(a) distribution were 1.45 (1.23-1.72) and 1.48 (1.23-1.78) for a hsCRP group of <2 and ≥2 mg/L, respectively, with no interaction found between these two biomarkers on CHD risk (Pinteraction = 0.82). In those with established CHD, similar associations were seen only among individuals with hsCRP ≥ 2 mg/L [1.34 (1.03-1.76)], whereas among participants with a hsCRP concentration <2 mg/L, there was no clear association between Lp(a) and future CHD events [1.29 (0.98-1.71)] (highest vs. lowest fifth, fully adjusted models; Pinteraction = 0.024). CONCLUSIONS: While among CHD-free individuals Lp(a) was significantly associated with incident CHD regardless of hsCRP, in participants with CHD at baseline, Lp(a) was related to recurrent CHD events only in those with residual inflammatory risk. These findings might guide adequate selection of high-risk patients for forthcoming Lp(a)-targeting compounds.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Coronary Heart Disease ; Epidemiology ; General Population ; High-sensitive C-reactive Protein ; Lipoprotein(a); Cardiovascular Risk; Nlrp3 Inflammasome; Biomarkers; Design
ISSN (print) / ISBN 0195-668X
e-ISSN 1522-9645
Quellenangaben Volume: 45, Issue: 12, Pages: 1043-1054 Article Number: , Supplement: ,
Publisher Oxford University Press
Publishing Place Great Clarendon St, Oxford Ox2 6dp, England
Non-patent literature Publications
Reviewing status Peer reviewed
Grants European Research Council