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

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C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease : the BiomarCaRE project. / Arnold, Natalie; Blaum, Christopher; Goßling, Alina; Brunner, Fabian J.; Bay, Benjamin; Ferrario, Marco M.; Brambilla, Paolo; Cesana, Giancarlo; Leoni, Valerio; Palmieri, Luigi; Donfrancesco, Chiara; Padró, Teresa; Andersson, Jonas; Jousilahti, Pekka; Ojeda, Francisco; Zeller, Tanja; Linneberg, Allan; Söderberg, Stefan; Iacoviello, Licia; Gianfagna, Francesco; Sans, Susana; Veronesi, Giovanni; Thorand, Barbara; Peters, Annette; Tunstall-Pedoe, Hugh; Kee, Frank; Salomaa, Veikko; Schnabel, Renate B.; Kuulasmaa, Kari; Blankenberg, Stefan; Koenig, Wolfgang; Waldeyer, Christoph; the BiomarCaRE investigators.

I: European Heart Journal, Bind 45, Nr. 12, 2024, s. 1043-1054.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Arnold, N, Blaum, C, Goßling, A, Brunner, FJ, Bay, B, Ferrario, MM, 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, RB, Kuulasmaa, K, Blankenberg, S, Koenig, W, Waldeyer, C & the BiomarCaRE investigators 2024, 'C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease: the BiomarCaRE project', European Heart Journal, bind 45, nr. 12, s. 1043-1054. https://doi.org/10.1093/eurheartj/ehad867

APA

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., ... the BiomarCaRE investigators (2024). C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease: the BiomarCaRE project. European Heart Journal, 45(12), 1043-1054. https://doi.org/10.1093/eurheartj/ehad867

Vancouver

Arnold N, Blaum C, Goßling A, Brunner FJ, Bay B, Ferrario MM o.a. C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease: the BiomarCaRE project. European Heart Journal. 2024;45(12):1043-1054. https://doi.org/10.1093/eurheartj/ehad867

Author

Arnold, Natalie ; Blaum, Christopher ; Goßling, Alina ; Brunner, Fabian J. ; Bay, Benjamin ; Ferrario, Marco M. ; Brambilla, Paolo ; Cesana, Giancarlo ; Leoni, Valerio ; Palmieri, Luigi ; Donfrancesco, Chiara ; Padró, Teresa ; Andersson, Jonas ; Jousilahti, Pekka ; Ojeda, Francisco ; Zeller, Tanja ; Linneberg, Allan ; Söderberg, Stefan ; Iacoviello, Licia ; Gianfagna, Francesco ; Sans, Susana ; Veronesi, Giovanni ; Thorand, Barbara ; Peters, Annette ; Tunstall-Pedoe, Hugh ; Kee, Frank ; Salomaa, Veikko ; Schnabel, Renate B. ; Kuulasmaa, Kari ; Blankenberg, Stefan ; Koenig, Wolfgang ; Waldeyer, Christoph ; the BiomarCaRE investigators. / C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease : the BiomarCaRE project. I: European Heart Journal. 2024 ; Bind 45, Nr. 12. s. 1043-1054.

Bibtex

@article{ab8f6db7f04d426d86fd86aa279b079e,
title = "C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease: the BiomarCaRE project",
abstract = "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.",
keywords = "Coronary heart disease, Epidemiology, General population, High-sensitive C-reactive protein, Lipoprotein(a)",
author = "Natalie Arnold and Christopher Blaum and Alina Go{\ss}ling and Brunner, {Fabian J.} and Benjamin Bay and Ferrario, {Marco M.} and Paolo Brambilla and Giancarlo Cesana and Valerio Leoni and Luigi Palmieri and Chiara Donfrancesco and Teresa Padr{\'o} and Jonas Andersson and Pekka Jousilahti and Francisco Ojeda and Tanja Zeller and Allan Linneberg and Stefan S{\"o}derberg and Licia Iacoviello and Francesco Gianfagna and Susana Sans and Giovanni Veronesi and Barbara Thorand and Annette Peters and Hugh Tunstall-Pedoe and Frank Kee and Veikko Salomaa and Schnabel, {Renate B.} and Kari Kuulasmaa and Stefan Blankenberg and Wolfgang Koenig and Christoph Waldeyer and {the BiomarCaRE investigators}",
note = "Publisher Copyright: {\textcopyright} The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved.",
year = "2024",
doi = "10.1093/eurheartj/ehad867",
language = "English",
volume = "45",
pages = "1043--1054",
journal = "European Heart Journal",
issn = "0195-668X",
publisher = "Oxford University Press",
number = "12",

}

RIS

TY - JOUR

T1 - C-reactive protein modifies lipoprotein(a)-related risk for coronary heart disease

T2 - the BiomarCaRE project

AU - Arnold, Natalie

AU - Blaum, Christopher

AU - Goßling, Alina

AU - Brunner, Fabian J.

AU - Bay, Benjamin

AU - Ferrario, Marco M.

AU - Brambilla, Paolo

AU - Cesana, Giancarlo

AU - Leoni, Valerio

AU - Palmieri, Luigi

AU - Donfrancesco, Chiara

AU - Padró, Teresa

AU - Andersson, Jonas

AU - Jousilahti, Pekka

AU - Ojeda, Francisco

AU - Zeller, Tanja

AU - Linneberg, Allan

AU - Söderberg, Stefan

AU - Iacoviello, Licia

AU - Gianfagna, Francesco

AU - Sans, Susana

AU - Veronesi, Giovanni

AU - Thorand, Barbara

AU - Peters, Annette

AU - Tunstall-Pedoe, Hugh

AU - Kee, Frank

AU - Salomaa, Veikko

AU - Schnabel, Renate B.

AU - Kuulasmaa, Kari

AU - Blankenberg, Stefan

AU - Koenig, Wolfgang

AU - Waldeyer, Christoph

AU - the BiomarCaRE investigators

N1 - Publisher Copyright: © The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved.

PY - 2024

Y1 - 2024

N2 - 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.

AB - 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.

KW - Coronary heart disease

KW - Epidemiology

KW - General population

KW - High-sensitive C-reactive protein

KW - Lipoprotein(a)

U2 - 10.1093/eurheartj/ehad867

DO - 10.1093/eurheartj/ehad867

M3 - Journal article

C2 - 38240386

AN - SCOPUS:85189079840

VL - 45

SP - 1043

EP - 1054

JO - European Heart Journal

JF - European Heart Journal

SN - 0195-668X

IS - 12

ER -

ID: 388021700