Interleukin 6 plasma levels are associated with progression of coronary plaques.


Journal

Open heart
ISSN: 2053-3624
Titre abrégé: Open Heart
Pays: England
ID NLM: 101631219

Informations de publication

Date de publication:
19 Sep 2024
Historique:
received: 05 06 2024
accepted: 19 08 2024
medline: 21 9 2024
pubmed: 21 9 2024
entrez: 20 9 2024
Statut: epublish

Résumé

Inflammation plays a pivotal role in atherogenesis and is a causal risk factor for atherosclerotic cardiovascular disease. Non-invasive coronary CT angiography (CCTA) enables evaluation of coronary plaque phenotype. This study investigates the relationship between a comprehensive panel of inflammatory markers and short-term plaque progression on serial CCTA imaging, hypothesising that inflammation is associated with increased plaque volume. A total of 161 patients aged ≥40 years with stable multivessel coronary artery disease were included, who underwent CCTA at baseline and 12 months follow-up. Baseline plasma levels of interleukin 6 (IL-6), high-sensitivity C-reactive protein and other inflammatory markers were measured. Plaque volumes were assessed using semiautomated software, calculating total, noncalcified, calcified and low-attenuation noncalcified plaque volumes. Linear regression models, adjusted for ASSIGN score, segment involvement score and body mass index, evaluated associations between inflammatory markers and plaque volume changes. The mean±SD age was 65.4±8.4 years, with 129 (80.6%) male participants. Baseline total plaque volume was 1394 (1036, 1993) mm³. After 12 months, total plaque volume changed by 78 (-114, 244) mm³. IL-6 levels were associated with a 4.9% increase in total plaque volume (95% CI: 0.9 to 8.9, p=0.018) and a 4.8% increase in noncalcified plaque volume (95% CI: 0.7 to 8.9, p=0.022). No significant associations were observed for other inflammatory markers. Plasma IL-6 levels are significantly associated with increased total and noncalcified short-term plaque progression in patients with stable coronary artery disease. This supports the potential of IL-6 as a target for reducing plaque progression and cardiovascular risk.

Sections du résumé

BACKGROUND BACKGROUND
Inflammation plays a pivotal role in atherogenesis and is a causal risk factor for atherosclerotic cardiovascular disease. Non-invasive coronary CT angiography (CCTA) enables evaluation of coronary plaque phenotype. This study investigates the relationship between a comprehensive panel of inflammatory markers and short-term plaque progression on serial CCTA imaging, hypothesising that inflammation is associated with increased plaque volume.
METHODS METHODS
A total of 161 patients aged ≥40 years with stable multivessel coronary artery disease were included, who underwent CCTA at baseline and 12 months follow-up. Baseline plasma levels of interleukin 6 (IL-6), high-sensitivity C-reactive protein and other inflammatory markers were measured. Plaque volumes were assessed using semiautomated software, calculating total, noncalcified, calcified and low-attenuation noncalcified plaque volumes. Linear regression models, adjusted for ASSIGN score, segment involvement score and body mass index, evaluated associations between inflammatory markers and plaque volume changes.
RESULTS RESULTS
The mean±SD age was 65.4±8.4 years, with 129 (80.6%) male participants. Baseline total plaque volume was 1394 (1036, 1993) mm³. After 12 months, total plaque volume changed by 78 (-114, 244) mm³. IL-6 levels were associated with a 4.9% increase in total plaque volume (95% CI: 0.9 to 8.9, p=0.018) and a 4.8% increase in noncalcified plaque volume (95% CI: 0.7 to 8.9, p=0.022). No significant associations were observed for other inflammatory markers.
CONCLUSIONS CONCLUSIONS
Plasma IL-6 levels are significantly associated with increased total and noncalcified short-term plaque progression in patients with stable coronary artery disease. This supports the potential of IL-6 as a target for reducing plaque progression and cardiovascular risk.

Identifiants

pubmed: 39304297
pii: openhrt-2024-002773
doi: 10.1136/openhrt-2024-002773
pii:
doi:

Substances chimiques

Interleukin-6 0
Biomarkers 0
IL6 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY. Published by BMJ.

Déclaration de conflit d'intérêts

Competing interests: JMK, ET, MM, JG, YK, JK and MRD have no conflicts of interest. NSN reports grants from the Dutch Heart Foundation (Dekker 03-007-2023-0068), European Atherosclerosis Society (2023), research funding/speaker fees from Cleerly, Daiichi Sankyo and Novartis and is cofounder of Lipid Tools. GKH is part-time employed by Novo Nordisk and holds shares in Novo Nordisk. ESGS has received fees paid to his institution from Amgen, Akcea, Athera, Sanofi-Regeneron, Esperion, Novo Nordisk, Lily and Novartis.

Auteurs

Jordan M Kraaijenhof (JM)

Department of Vascular Medicine, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands.

Nick S Nurmohamed (NS)

Department of Vascular Medicine, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands.
Department of Cardiology, Amsterdam University Medical Centers, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.

Evangelos Tzolos (E)

British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.

Mo Meah (M)

British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.

Jolien Geers (J)

British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
Department of Cardiology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium.

Yannick Kaiser (Y)

Department of Vascular Medicine, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands.

Jeffrey Kroon (J)

Department of Experimental Vascular Medicine, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.
Atherosclerosis and Ischemic Syndromes, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands.
Laboratory of Angiogenesis and Vascular Metabolism, VIB-KU Leuven Center for Cancer Biology, VIB, Leuven, Belgium.
Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven and Leuven Cancer Institute (LKI), Leuven, Belgium.

G Kees Hovingh (GK)

Department of Vascular Medicine, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands.

Erik S G Stroes (ESG)

Department of Vascular Medicine, Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands.

Marc R Dweck (MR)

British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK marc.dweck@ed.ac.uk.

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Classifications MeSH