Transient ST-elevation myocardial infarction versus persistent ST-elevation myocardial infarction. An appraisal of patient characteristics and functional outcome.

Cardiac magnetic resonance imaging Culprit vessel patency Fibrinolysis ST-elevation myocardial infarction Transient ST-elevation myocardial infarction

Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 08 2021
Historique:
received: 16 02 2021
revised: 07 04 2021
accepted: 10 05 2021
pubmed: 19 5 2021
medline: 8 7 2021
entrez: 18 5 2021
Statut: ppublish

Résumé

Up to 24% of patients presenting with ST-elevation myocardial infarction (STEMI) show resolution of ST-elevation and symptoms before revascularization. The mechanisms of spontaneous reperfusion are unclear. Given the more favorable outcome of transient STEMI, it is important to obtain further insights in differential aspects. We compared 251 patients who presented with transient STEMI (n = 141) or persistent STEMI (n = 110). Clinical angiographic and laboratory data were collected at admission and in subset of patients additional index hemostatic data and at steady-state follow-up. Cardiac magnetic resonance imaging (CMR) was performed at 2-8 days to assess myocardial injury. Transient STEMI patients had more cardiovascular risk factors than STEMI patients, including more arterial disease and higher cholesterol values. Transient STEMI patients showed angiographically more often no intracoronary thrombus (41.1% vs. 2.7%, P < 0.001) and less often a high thrombus burden (9.2% vs. 40.0%, P < 0.001). CMR revealed microvascular obstruction less frequently (4.2% vs. 34.6%, P < 0.001) and smaller infarct size [1.4%; interquartile range (IQR), 0.0-3.7% vs. 8.8%; IQR, 3.9-17.1% of the left ventricle, P < 0.001] with a better preserved left ventricular ejection fraction (57.8 ± 6.7% vs. 52.5 ± 7.6%, P < 0.001). At steady state, fibrinolysis was higher in transient STEMI, as demonstrated with a reduced clot lysis time (89 ± 20% vs. 99 ± 25%, P = 0.03). Transient STEMI is a syndrome with less angiographic thrombus burden and spontaneous infarct artery reperfusion, resulting in less myocardial injury than STEMI. The presence of a more effective fibrinolysis in transient STEMI patients may explain these differences and might provide clues for future treatment of STEMI.

Sections du résumé

BACKGROUND
Up to 24% of patients presenting with ST-elevation myocardial infarction (STEMI) show resolution of ST-elevation and symptoms before revascularization. The mechanisms of spontaneous reperfusion are unclear. Given the more favorable outcome of transient STEMI, it is important to obtain further insights in differential aspects.
METHODS
We compared 251 patients who presented with transient STEMI (n = 141) or persistent STEMI (n = 110). Clinical angiographic and laboratory data were collected at admission and in subset of patients additional index hemostatic data and at steady-state follow-up. Cardiac magnetic resonance imaging (CMR) was performed at 2-8 days to assess myocardial injury.
RESULTS
Transient STEMI patients had more cardiovascular risk factors than STEMI patients, including more arterial disease and higher cholesterol values. Transient STEMI patients showed angiographically more often no intracoronary thrombus (41.1% vs. 2.7%, P < 0.001) and less often a high thrombus burden (9.2% vs. 40.0%, P < 0.001). CMR revealed microvascular obstruction less frequently (4.2% vs. 34.6%, P < 0.001) and smaller infarct size [1.4%; interquartile range (IQR), 0.0-3.7% vs. 8.8%; IQR, 3.9-17.1% of the left ventricle, P < 0.001] with a better preserved left ventricular ejection fraction (57.8 ± 6.7% vs. 52.5 ± 7.6%, P < 0.001). At steady state, fibrinolysis was higher in transient STEMI, as demonstrated with a reduced clot lysis time (89 ± 20% vs. 99 ± 25%, P = 0.03).
CONCLUSIONS
Transient STEMI is a syndrome with less angiographic thrombus burden and spontaneous infarct artery reperfusion, resulting in less myocardial injury than STEMI. The presence of a more effective fibrinolysis in transient STEMI patients may explain these differences and might provide clues for future treatment of STEMI.

Identifiants

pubmed: 34004231
pii: S0167-5273(21)00830-5
doi: 10.1016/j.ijcard.2021.05.018
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

22-28

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest Prof. dr. van Royen reports research grants from AstraZeneca, Abbott, Philips, Biotronik and a honorarium from Medtronic. Dr. Lemkes reports grants from Biotronik and Astrazeneca, during the conduct of the study. Prof. dr. Piek reports non-financial support from Abbott Vascular as member medical advisory board, personal fees and non-financial support from Philips/Volcano as Consultant, outside the submitted work. Prof. dr. von Birgelen reports institutional research grants from Abbott Vascular, Biotronik, Boston Scientific and Medtronic, outside the submitted work. Dr. van Leeuwen reports grants from AstraZeneca, grants from Top Sector Life Sciences & Health, during the conduct of the study. Dr. Escaned reports consultancies work for Philips, outside of the submitted work. All other authors declare no competing interests with regards to the study.

Auteurs

Gladys N Janssens (GN)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands.

Jorrit S Lemkes (JS)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands.

Nina W van der Hoeven (NW)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands.

Maarten A H van Leeuwen (MAH)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands; Department of Cardiology, Isala Heart Center, Dokter van Heesweg 2, 8025AB Zwolle, the Netherlands.

Henk Everaars (H)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands.

Peter M van de Ven (PM)

Department of Epidemiology and Biostatistics, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1089a, 1081HV Amsterdam, the Netherlands.

Stijn L Brinckman (SL)

Department of Cardiology, Tergooi Hospital, Rijksstraatweg 1, 1261AN Blaricum, the Netherlands.

Jorik R Timmer (JR)

Department of Cardiology, Isala Heart Center, Dokter van Heesweg 2, 8025AB Zwolle, the Netherlands.

Martijn Meuwissen (M)

Department of Cardiology, Amphia Hospital, Molengracht 21, 4818CK Breda, the Netherlands.

Joost C M Meijers (JCM)

Department of Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105AZ Amsterdam, the Netherlands; Department of Molecular and Cellular Hemostasis, Sanquin Research, Plesmanlaan 125, 1066CX Amsterdam, the Netherlands.

Arno P van der Weerdt (AP)

Department of Cardiology, Medical Center Leeuwarden, Henri Dunantweg 2, 8934AD Leeuwarden, the Netherlands.

Tim J F Ten Cate (TJF)

Department of Cardiology, Radboud University Medical Center, Geert Grooteplein Zuid 10, 6525GA Nijmegen, the Netherlands.

Jan J Piek (JJ)

Department of Cardiology, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105AZ Amsterdam, the Netherlands.

Clemens von Birgelen (C)

Department of Cardiology, Medisch Spectrum Twente, Koningsplein 1, 7512KZ Enschede, the Netherlands.

Roberto Diletti (R)

Department of Cardiology, Erasmus MC, 's Gravendijkwal 230, 3015CE Rotterdam, the Netherlands.

Javier Escaned (J)

Cardiovascular Institute, Hospital Clínico San Carlos IDISSC, Calle del Profesor Martín Lagos, S/N, 28040 Madrid, Spain.

Albert C van Rossum (AC)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands.

Robin Nijveldt (R)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands; Department of Cardiology, Radboud University Medical Center, Geert Grooteplein Zuid 10, 6525GA Nijmegen, the Netherlands.

Niels van Royen (N)

Department of Cardiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, 1081HV Amsterdam, the Netherlands; Department of Cardiology, Radboud University Medical Center, Geert Grooteplein Zuid 10, 6525GA Nijmegen, the Netherlands. Electronic address: niels.vanroyen@radboudumc.nl.

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