Discovery of plasma proteins associated with ventricular fibrillation during first ST-elevation myocardial infarction via proteomics.
Mass spectrometry (MS)
Myocardial infarction
Proteomics
ST-elevation myocardial infarction (STEMI)
Ventricular fibrillation (VF)
Journal
European heart journal. Acute cardiovascular care
ISSN: 2048-8734
Titre abrégé: Eur Heart J Acute Cardiovasc Care
Pays: England
ID NLM: 101591369
Informations de publication
Date de publication:
09 Oct 2023
09 Oct 2023
Historique:
received:
03
08
2023
revised:
26
08
2023
accepted:
06
10
2023
medline:
9
10
2023
pubmed:
9
10
2023
entrez:
9
10
2023
Statut:
aheadofprint
Résumé
The underlying biological mechanisms of ventricular fibrillation (VF) during acute myocardial infarction are largely unknown. To our knowledge, this is the first proteomic study for this trait, with the aim to identify and characterize proteins that are associated with VF during first ST-elevation myocardial infarction (STEMI). We included 230 participants from a Danish ongoing case-control study on patients with first STEMI with VF (case, n = 110) and without VF (control, n = 120) before guided catheter insertion for primary percutaneous coronary intervention. The plasma proteome was investigated using mass spectrometry-based proteomics on plasma samples collected within 24 hours of symptom onset. In 229 STEMI patients (72% men, median age 62 years (interquartile range (IQR): 54-70)), a median of 257 proteins (IQR: 244-281) were quantified per patient. A total of 26 proteins were associated with VF, these proteins were involved in several biological processes including blood coagulation, hemostasis, and immunity. After correcting for multiple testing, two up-regulated proteins remained significantly associated with VF, actin beta-like 2 (ACTBL2, fold-change (FC) 2.25, p < 0.001, q = 0.023) and coagulation factor XIII-A (F13A1, FC 1.48, p < 0.001, q = 0.023). None of the proteins were correlated with anterior infarct location. VF due to first STEMI was significantly associated with two up-regulated proteins (ACTBL2 and F13A1), suggesting that they may represent novel underlying molecular VF mechanisms. Further research is needed to determine whether these proteins are predictive biomarkers or acute phase response proteins to VF during acute ischemia.
Sections du résumé
BACKGROUND AND AIMS
OBJECTIVE
The underlying biological mechanisms of ventricular fibrillation (VF) during acute myocardial infarction are largely unknown. To our knowledge, this is the first proteomic study for this trait, with the aim to identify and characterize proteins that are associated with VF during first ST-elevation myocardial infarction (STEMI).
METHODS
METHODS
We included 230 participants from a Danish ongoing case-control study on patients with first STEMI with VF (case, n = 110) and without VF (control, n = 120) before guided catheter insertion for primary percutaneous coronary intervention. The plasma proteome was investigated using mass spectrometry-based proteomics on plasma samples collected within 24 hours of symptom onset.
RESULTS
RESULTS
In 229 STEMI patients (72% men, median age 62 years (interquartile range (IQR): 54-70)), a median of 257 proteins (IQR: 244-281) were quantified per patient. A total of 26 proteins were associated with VF, these proteins were involved in several biological processes including blood coagulation, hemostasis, and immunity. After correcting for multiple testing, two up-regulated proteins remained significantly associated with VF, actin beta-like 2 (ACTBL2, fold-change (FC) 2.25, p < 0.001, q = 0.023) and coagulation factor XIII-A (F13A1, FC 1.48, p < 0.001, q = 0.023). None of the proteins were correlated with anterior infarct location.
CONCLUSION
CONCLUSIONS
VF due to first STEMI was significantly associated with two up-regulated proteins (ACTBL2 and F13A1), suggesting that they may represent novel underlying molecular VF mechanisms. Further research is needed to determine whether these proteins are predictive biomarkers or acute phase response proteins to VF during acute ischemia.
Identifiants
pubmed: 37811694
pii: 7301242
doi: 10.1093/ehjacc/zuad125
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Commentaires et corrections
Type : CommentIn
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.