The novel adipokine CTRP1 is significantly associated with the incidence of major adverse cardiovascular events.


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
07 2019
Historique:
received: 14 01 2019
revised: 12 04 2019
accepted: 16 04 2019
pubmed: 6 5 2019
medline: 10 7 2020
entrez: 4 5 2019
Statut: ppublish

Résumé

The recently identified adiponectin paralogue C1q and tumor necrosis factor-related protein 1 (CTRP1) has been associated with obesity-linked disorders and coronary atherosclerosis. So far, the impact of circulating CTRP1 on the incidence of future cardiovascular events is unclear. Therefore, we aimed at investigating the association between CTRP1 and future cardiovascular risk. We measured CTRP1 serum levels in 539 patients undergoing coronary angiography for the evaluation of established or suspected stable coronary artery disease (CAD). Prospectively, we recorded major adverse cardiovascular events (MACE), defined as the incidence of cardiovascular death, non-fatal myocardial infarction and non-fatal stroke over a follow-up period of 8 years. At baseline, obesity, the metabolic syndrome, type 2 diabetes, and non-alcoholic fatty liver disease were significantly associated with increased CTRP1 (all p-values ≤0.001). Prospectively, MACE rates were lowest in the first quartile (15.3%) and increased over the second (23.7%) to the third and fourth quartile (each 29.0%; p We conclude that high serum levels of CTRP1 are significantly associated with future MACE.

Sections du résumé

BACKGROUND AND AIMS
The recently identified adiponectin paralogue C1q and tumor necrosis factor-related protein 1 (CTRP1) has been associated with obesity-linked disorders and coronary atherosclerosis. So far, the impact of circulating CTRP1 on the incidence of future cardiovascular events is unclear. Therefore, we aimed at investigating the association between CTRP1 and future cardiovascular risk.
METHODS
We measured CTRP1 serum levels in 539 patients undergoing coronary angiography for the evaluation of established or suspected stable coronary artery disease (CAD). Prospectively, we recorded major adverse cardiovascular events (MACE), defined as the incidence of cardiovascular death, non-fatal myocardial infarction and non-fatal stroke over a follow-up period of 8 years.
RESULTS
At baseline, obesity, the metabolic syndrome, type 2 diabetes, and non-alcoholic fatty liver disease were significantly associated with increased CTRP1 (all p-values ≤0.001). Prospectively, MACE rates were lowest in the first quartile (15.3%) and increased over the second (23.7%) to the third and fourth quartile (each 29.0%; p
CONCLUSIONS
We conclude that high serum levels of CTRP1 are significantly associated with future MACE.

Identifiants

pubmed: 31051410
pii: S0021-9150(19)30390-9
doi: 10.1016/j.atherosclerosis.2019.04.222
pii:
doi:

Substances chimiques

C1QTNF1 protein, human 0
Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-6

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Axel Muendlein (A)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.

Andreas Leiherer (A)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Medical Central Laboratories, Feldkirch, Austria; Private University of the Principality of Liechtenstein, Triesen, Liechtenstein.

Christoph Saely (C)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Private University of the Principality of Liechtenstein, Triesen, Liechtenstein; Department of Medicine and Cardiology, Academic Teaching Hospital Feldkirch, Feldkirch, Austria; Division of Angiology, Swiss Cardiovascular Center, University Hospital of Bern, Bern, Switzerland.

Janine Ebner (J)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Medical Central Laboratories, Feldkirch, Austria.

Kathrin Geiger (K)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.

Eva Maria Brandtner (EM)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria.

Alexander Vonbank (A)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Department of Medicine and Cardiology, Academic Teaching Hospital Feldkirch, Feldkirch, Austria.

Peter Fraunberger (P)

Medical Central Laboratories, Feldkirch, Austria.

Heinz Drexel (H)

Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria; Private University of the Principality of Liechtenstein, Triesen, Liechtenstein; Division of Angiology, Swiss Cardiovascular Center, University Hospital of Bern, Bern, Switzerland; Drexel University College of Medicine, Philadelphia, PA, USA. Electronic address: heinz.drexel@extern.insel.ch.

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Classifications MeSH