Circulating levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) are associated with monocyte subsets in patients with stable coronary artery disease.


Journal

Journal of clinical lipidology
ISSN: 1933-2874
Titre abrégé: J Clin Lipidol
Pays: United States
ID NLM: 101300157

Informations de publication

Date de publication:
Historique:
received: 01 11 2020
revised: 23 02 2021
accepted: 24 02 2021
pubmed: 2 4 2021
medline: 31 12 2021
entrez: 1 4 2021
Statut: ppublish

Résumé

Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14+CD16++; NCM). Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R = -0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK9 levels. We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.

Sections du résumé

BACKGROUND
Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets.
OBJECTIVE
The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets.
METHODS
We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14+CD16++; NCM).
RESULTS
Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R = -0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK9 levels.
CONCLUSIONS
We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.

Identifiants

pubmed: 33789832
pii: S1933-2874(21)00034-9
doi: 10.1016/j.jacl.2021.02.005
pii:
doi:

Substances chimiques

Cholesterol, LDL 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
PCSK9 protein, human EC 3.4.21.-
Proprotein Convertase 9 EC 3.4.21.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

512-521

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

Auteurs

Konstantin A Krychtiuk (KA)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria.

Max Lenz (M)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria.

Philipp Hohensinner (P)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Institute for Cardiovascular Research, Vienna, Austria.

Klaus Distelmaier (K)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria.

Lore Schrutka (L)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria.

Stefan P Kastl (SP)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria.

Kurt Huber (K)

Ludwig Boltzmann Institute for Cardiovascular Research, Vienna, Austria; 3rd Medical Department, Wilhelminenhospital, Vienna, Austria.

Elisabeth Dostal (E)

Krankenanstalten Dr. Dostal, Saarplatz 9, 1190 Vienna, Austria.

Stanislav Oravec (S)

1st Medical Clinic; Medical Faculty of Comenius University Bratislava, Bratislava, Slovakia.

Christian Hengstenberg (C)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria.

Johann Wojta (J)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Institute for Cardiovascular Research, Vienna, Austria; Core Facilities, Medical University of Vienna, Vienna, Austria.

Walter S Speidl (WS)

Department of Internal Medicine II - Division of Cardiology, Medical University of Vienna, Vienna, Austria. Electronic address: walter.speidl@meduniwien.ac.at.

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Classifications MeSH