Neutrophil extracellular traps (NETs) in patients with STEMI. Association with percutaneous coronary intervention and antithrombotic treatments.


Journal

Thrombosis research
ISSN: 1879-2472
Titre abrégé: Thromb Res
Pays: United States
ID NLM: 0326377

Informations de publication

Date de publication:
05 2022
Historique:
received: 26 12 2021
revised: 15 02 2022
accepted: 01 03 2022
pubmed: 21 3 2022
medline: 26 4 2022
entrez: 20 3 2022
Statut: ppublish

Résumé

Neutrophil extracellular traps (NETs) are formed by DNA, histones and proteolytic enzymes, and are produced by activated neutrophils through different mechanisms. In turn, NETs can activate platelets and coagulation cascade favoring thrombotic processes. The aims of this study were to analyze levels and kinetics of NETs in ST-segment elevation myocardial infarction (STEMI) patients and correlate them with antithrombotic therapy and cardiovascular outcomes at follow-up. 150 consecutive STEMI patients referred to primary percutaneous coronary intervention (pPCI) were included. Citrate anticoagulated blood was extracted immediately before pPCI, 30 min and 24 h after the procedure. As markers of NETS cell free DNA (cfDNA), nucleosomes and citrullinated Histone 3 (citH3) were determined. 46 healthy subjects were included as controls. Patients were follow-up for 1.4 ± 0.56 years. Before pPCI, NETs markers were elevated in STEMI patients compared to healthy controls (p < 0.05); these increased significantly 30 min post pPCI (p ≤ 0.001) and decreased at 24 h but remained elevated compared with the control group (p < 0.05). Patients treated with bivalirudin presented a lower increase of NETs 30 min post pPCI compared to patients treated with heparin (p < 0.05). Cardiovascular risk factors or type of stent implanted did not modify NETs levels. Cit3H (HR = 3.74; 95%CI 1.05-13.4; p = 0.042) and left ventricular ejection fraction ≤35% (HR = 6.84; 95%CI 2-23; p = 0.002) were independent predictors of composite endpoint of myocardial infarction, stroke, stent thrombosis and/or cardiovascular-cause death. NETs were elevated in STEMI patients, increased by pPCI and decreased thereafter. One of the most specific NETs markers was associated with cardiovascular outcomes.

Sections du résumé

BACKGROUND
Neutrophil extracellular traps (NETs) are formed by DNA, histones and proteolytic enzymes, and are produced by activated neutrophils through different mechanisms. In turn, NETs can activate platelets and coagulation cascade favoring thrombotic processes. The aims of this study were to analyze levels and kinetics of NETs in ST-segment elevation myocardial infarction (STEMI) patients and correlate them with antithrombotic therapy and cardiovascular outcomes at follow-up.
METHODS
150 consecutive STEMI patients referred to primary percutaneous coronary intervention (pPCI) were included. Citrate anticoagulated blood was extracted immediately before pPCI, 30 min and 24 h after the procedure. As markers of NETS cell free DNA (cfDNA), nucleosomes and citrullinated Histone 3 (citH3) were determined. 46 healthy subjects were included as controls. Patients were follow-up for 1.4 ± 0.56 years.
RESULTS
Before pPCI, NETs markers were elevated in STEMI patients compared to healthy controls (p < 0.05); these increased significantly 30 min post pPCI (p ≤ 0.001) and decreased at 24 h but remained elevated compared with the control group (p < 0.05). Patients treated with bivalirudin presented a lower increase of NETs 30 min post pPCI compared to patients treated with heparin (p < 0.05). Cardiovascular risk factors or type of stent implanted did not modify NETs levels. Cit3H (HR = 3.74; 95%CI 1.05-13.4; p = 0.042) and left ventricular ejection fraction ≤35% (HR = 6.84; 95%CI 2-23; p = 0.002) were independent predictors of composite endpoint of myocardial infarction, stroke, stent thrombosis and/or cardiovascular-cause death.
CONCLUSIONS
NETs were elevated in STEMI patients, increased by pPCI and decreased thereafter. One of the most specific NETs markers was associated with cardiovascular outcomes.

Identifiants

pubmed: 35306431
pii: S0049-3848(22)00071-8
doi: 10.1016/j.thromres.2022.03.002
pii:
doi:

Substances chimiques

Fibrinolytic Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

78-83

Informations de copyright

Copyright © 2022 Elsevier Ltd. All rights reserved.

Auteurs

Maria Ferré-Vallverdú (M)

Cardiology Department, Hospital Universitari i Politècnic La Fe, Valencia, Spain.

Ana María Latorre (AM)

Health Research Institute La Fe, Valencia, Spain.

María Paz Fuset (MP)

Intensive Care Unit Department, Hospital Universitari i Politècnic La Fe, Valencia, Spain; Intensive Care Unit, Hospital Universitari de Bellvitge, Barcelona, Spain.

Elena Sánchez (E)

Cardiology Department, Hospital Universitari i Politècnic La Fe, Valencia, Spain.

Isabel Madrid (I)

Intensive Care Unit Department, Hospital Universitari i Politècnic La Fe, Valencia, Spain.

Francisco Ten (F)

Cardiology Department, Hospital Universitari i Politècnic La Fe, Valencia, Spain.

Juana Vallés (J)

Health Research Institute La Fe, Valencia, Spain.

María Teresa Santos (MT)

Health Research Institute La Fe, Valencia, Spain.

Santiago Bonanad (S)

Health Research Institute La Fe, Valencia, Spain.

Antonio Moscardó (A)

Health Research Institute La Fe, Valencia, Spain. Electronic address: moscardo_ant@gva.es.

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Classifications MeSH