Effects of early myocardial reperfusion and perfusion on myocardial necrosis/dysfunction and inflammation in patients with ST-segment and non-ST-segment elevation acute coronary syndrome: results from the PLATelet inhibition and patients Outcomes (PLATO) trial.


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:
07 Jun 2022
Historique:
received: 23 09 2021
revised: 10 01 2022
accepted: 09 02 2022
pubmed: 26 2 2022
medline: 10 6 2022
entrez: 25 2 2022
Statut: ppublish

Résumé

Restoration of myocardial blood flow and perfusion during percutaneous coronary intervention (PCI) measured using Thrombolysis in Myocardial Infarction (TIMI) flow grade (TFG) and perfusion grade (TMPG) is associated with improved outcomes in acute coronary syndrome (ACS). Associations between TFG/TMPG and changes in biomarkers reflecting myocardial damage/dysfunction and inflammation is unknown. Among 2606 patients included, TFG was evaluated in 2198 and TMPG in 1874 with ST-segment elevation myocardial infarction (STEMI) or non-ST-segment ACS (NSTE-ACS). Biomarkers reflecting myocardial necrosis [troponin T (TnT)], myocardial dysfunction [N-terminal prohormone brain natriuretic peptide (NT-proBNP)], inflammation [interleukin-6 (IL-6) and C-reactive protein (CRP)], and oxidative stress/ageing/inflammation [growth differentiation factor-15 (GDF-15)] were measured at baseline, discharge, and 1- and 6-month post-randomization. Associations between TFG/TMPG and changes in biomarker levels were evaluated using the Mann-Whitney-Wilcoxon signed test. In total, 1423 (54.6%) patients had STEMI and 1183 (45.4%) NSTE-ACS. Complete reperfusion after PCI with TFG = 3 was achieved in 1110 (85.3%) with STEMI and in 793 (88.5%) with NSTE-ACS. Normal myocardial perfusion with TMPG = 3 was achieved in 475 (41.6%) with STEMI and in 396 (54.0%) with NSTE-ACS. Levels of TnT, NT-proBNP, IL-6, CRP, and GDF-15 were substantially lower at discharge in patients with complete vs. incomplete TFG and STEMI (P < 0.01). This pattern was not observed for patients with NSTE-ACS. Patients with normal vs. abnormal TMPG and NSTE-ACS had lower levels of NT-proBNP at discharge (P = 0.01). Successful restoration of epicardial blood flow in STEMI was associated with less myocardial necrosis/dysfunction and inflammation. Attainment of normal myocardial perfusion was associated with less myocardial dysfunction in NSTE-ACS.

Identifiants

pubmed: 35213721
pii: 6537070
doi: 10.1093/ehjacc/zuac020
pmc: PMC9173680
doi:

Substances chimiques

Biomarkers 0
Growth Differentiation Factor 15 0
Interleukin-6 0
Troponin T 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

336-349

Subventions

Organisme : British Heart Foundation
ID : CS/15/7/31679
Pays : United Kingdom
Organisme : AstraZeneca

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

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Auteurs

Gorav Batra (G)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Uppsala Clinical Research Center, Uppsala University, Uppsala Science Park, Hubben, Dag Hammarskjölds väg 38, 751 85 Uppsala, Sweden.

Henrik Renlund (H)

Uppsala Clinical Research Center, Uppsala University, Uppsala Science Park, Hubben, Dag Hammarskjölds väg 38, 751 85 Uppsala, Sweden.

Vijay Kunadian (V)

Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University and Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK.

Stefan K James (SK)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Uppsala Clinical Research Center, Uppsala University, Uppsala Science Park, Hubben, Dag Hammarskjölds väg 38, 751 85 Uppsala, Sweden.

Robert F Storey (RF)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.

P Gabriel Steg (PG)

Université de Paris, Assistance Publique-Hôpitaux de Paris, Hôpital Bichat, French Alliance for Cardiovascular Trials, and INSERM U1148, Paris, France.

Hugo A Katus (HA)

Medizinishe Klinik, Universitätsklinikum Heidelberg, Heidelberg, Germany.

Robert A Harrington (RA)

Department of Medicine, Stanford University, Stanford, CA, USA.
Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

C Michael Gibson (CM)

Department of Cardiology, Centre of Postgraduate Medical Education, Grochowski Hospital, Warsaw, Poland.
Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.

Agneta Siegbahn (A)

Uppsala Clinical Research Center, Uppsala University, Uppsala Science Park, Hubben, Dag Hammarskjölds väg 38, 751 85 Uppsala, Sweden.

Lars Wallentin (L)

Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden.
Uppsala Clinical Research Center, Uppsala University, Uppsala Science Park, Hubben, Dag Hammarskjölds väg 38, 751 85 Uppsala, Sweden.

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