Prognostically relevant periprocedural myocardial injury and infarction associated with percutaneous coronary interventions: A Consensus Document of the ESC Working Group on Cellular Biology of the Heart and European Association of Percutaneous Cardiovascular Interventions (EAPCI)
Bulluck, Heerajnarain; Paradies, Valeria; Barbato, Emanuele; Baumbach, Andreas; Bøtker, Hans Erik; Capodanno, Davide; De Caterina, Raffaele; Cavallini, Claudio; Davidson, Sean M.; Feldman, Dmitriy N.; Ferdinandy, Péter; Gili, Sebastiano; Gyöngyösi, Mariann; Kunadian, Vijay; Ooi, Sze Yuan; Madonna, Rosalinda; Marber, Michael; Mehran, Roxana; Ndrepepa, Gjin; Perrino, Cinzia; Schüpke, Stefanie; Silvain, Johanne; Sluijter, Joost P.G.; Tarantini, Giuseppe; Toth, Gabor G.; Van Laake, Linda W.; Von Birgelen, Clemens; Zeitouni, Michel; Jaffe, Allan S.; Thygesen, Kristian; Hausenloy, Derek J.
(2021) European heart journal, volume 42, issue 27, pp. 2630 - 2642
(Article)
Abstract
A substantial number of chronic coronary syndrome (CCS) patients undergoing percutaneous coronary intervention (PCI) experience periprocedural myocardial injury or infarction. Accurate diagnosis of these PCI-related complications is required to guide further management given that their occurrence may be associated with increased risk of major adverse cardiac events (MACE). Due to
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lack of scientific data, the cut-off thresholds of post-PCI cardiac troponin (cTn) elevation used for defining periprocedural myocardial injury and infarction, have been selected based on expert consensus opinions, and their prognostic relevance remains unclear. In this Consensus Document from the ESC Working Group on Cellular Biology of the Heart and European Association of Percutaneous Cardiovascular Interventions (EAPCI), we recommend, whenever possible, the measurement of baseline (pre-PCI) cTn and post-PCI cTn values in all CCS patients undergoing PCI. We confirm the prognostic relevance of the post-PCI cTn elevation >5× 99th percentile URL threshold used to define type 4a myocardial infarction (MI). In the absence of periprocedural angiographic flow-limiting complications or electrocardiogram (ECG) and imaging evidence of new myocardial ischaemia, we propose the same post-PCI cTn cut-off threshold (>5× 99th percentile URL) be used to define prognostically relevant 'major' periprocedural myocardial injury. As both type 4a MI and major periprocedural myocardial injury are strong independent predictors of all-cause mortality at 1 year post-PCI, they may be used as quality metrics and surrogate endpoints for clinical trials. Further research is needed to evaluate treatment strategies for reducing the risk of major periprocedural myocardial injury, type 4a MI, and MACE in CCS patients undergoing PCI.
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Keywords: Chronic coronary syndrome, Percutaneous coronary intervention, Periprocedural myocardial infarction, Periprocedural myocardial injury, Type 4a myocardial infarction, Percutaneous Coronary Intervention/adverse effects, Humans, Risk Factors, Treatment Outcome, Coronary Artery Disease, Consensus, Myocardial Infarction/etiology, Heart Injuries, Biomarkers, Cardiology and Cardiovascular Medicine, Research Support, Non-U.S. Gov't, Journal Article
ISSN: 0195-668X
Publisher: Oxford University Press
Note: Funding Information: AB is supported by the Barts NIHR Cardiovascular Biomedical Research Centre. HEB was funded by the Novo Nordisk Foundation (grant numbers NNF14OC0013337, NNF15OC0016674), The Danish Council for Strategic Research (11-108354), and Trygfonden (109624). DC was supported by Ministero dell'Università e della Ricerca, Progetti di Rilevante Interesse Nazionale (PRIN 2017 - 2017N8K7S2). SD was supported by the National Institute for Health Research Biomedical Research Centre (NIHR-BRC) (BRC233/CM/SD/101320) and the British Heart Foundation (PG/18/ 44/33790 and PG/16/85/32471). PF was supported by the National Research, Development and Innovation Office of Hungary (Research Excellence Program - TKP/FIKP, National Heart Program NVKP 16- 1-2016-0017). VK is supported by the British Heart Foundation Clinical Study Grant (CS/15/7/316), Newcastle NIHR Biomedical Research Centre, and Institutional Research Grant from Astra Zeneca (ISSBRIL0303). MM is supported by the National Institute for Health Research comprehensive Biomedical Research Centre award to Guy's and St Thomas' NHS Foundation Trust in partnership with King's College London. CP was supported by Ministero dell'Istruzione, Università e Ricerca Scientifica (2015583WMX) and by Programma STAR, Federico II University (Unina) and Compagnia di San Paolo. LL was supported by the Netherlands Heart Foundation (Dekker Senior Clinical Scientist). JPGS is supported by Horizon2020 ERC-2016-COG EVICARE (725229). DJH was supported by the Duke-National University Singapore Medical School, Singapore Ministry of Health's National Medical Research Council under its Clinician Scientist-Senior Investigator scheme (NMRC/CSASI/ 0011/2017) and Collaborative Centre Grant scheme (NMRC/ CGAug16C006). DJH, SD, PF, and MG are members of the COST Action EU-CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology). Publisher Copyright: © 2021 Published on behalf of the European Society of Cardiology. All rights reserved.
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