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After a reperfused myocardial infarction (MI), dynamic tissue changes occur (edema, inflammation, microvascular obstruction, hemorrhage, cardiomyocyte necrosis, and ultimately replacement by fibrosis). The extension and magnitude of these changes contribute to long-term prognosis after MI. Cardiac magnetic resonance (CMR) is the gold-standard technique for noninvasive myocardial tissue characterization. CMR is also the preferred methodology for the identification of potential benefits associated with new cardioprotective strategies both in experimental and clinical trials. However, there is a wide heterogeneity in CMR methodologies used in experimental and clinical trials, including time of post-MI scan, acquisition protocols, and, more importantly, selection of endpoints. There is a need for standardization of these methodologies to improve the translation into a real clinical benefit. The main objective of this scientific expert panel consensus document is to provide recommendations for CMR endpoint selection in experimental and clinical trials based on pathophysiology and its association with hard outcomes. ; The CNIC is supported by the ISCiii, MICINN, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (award SEV-2015-0505). This research was supported (in part) by the Intramural Research Program of the National Institutes of Health, National Heart, Lung, and Blood Institute. BI received funding for work in the topic of this review from the Carlos III Institute of Health–Fondo de Investigacion Sanitaria- and the European Regional Development Fund (ERDF/FEDER) (PI13/01979, DTS17/00136), the Spanish Ministry of Science, Innovation and Universities (MICINN) and ERDF/FEDER SAF2013-49663-EXP, Red Madrileña de nanomedicina en imagen molecular (RENIM-CM Ref# B2017/BMD-3867), H2020 ERA-CVD (JTC2016/APCIN-ISCIII-2016/AC16/00021), and Fundación BBVA 2016. CBD is supported by the NIHR Biomedical Research Centre at University Hospitals Bristol NHS Foundation Trust and the University of Bristol. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health and Social Care. RF-J is a recipient of funding from the European Union Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No. 707642. DGD was supported by the Instituto de Salud Carlos III, CIBERCV-Instituto de Salud Carlos III, Spain (grant CB16/11/00479), co-funded with European Regional Development Fund-FEDER contribution), and grants PIE/ 2013-00047 and PI 17/1397. DJH was supported by the British Heart Foundation (CS/14/3/31002), the National Institute for Health Research University College London Hospitals Biomedical Research Centre, Duke-National University Singapore Medical School, Singapore Ministry of Health's National Medical Research Council under its Clinician Scientist-Senior Investigator scheme (NMRC/CSA-SI/0011/2017) and Collaborative Centre Grant scheme (NMRC/CGAug16C006), and the Singapore Ministry of Education Academic Research Fund Tier 2 (MOE2016-T2-2-021). This article is based upon work from COST Action EU-CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology). CB funding from British Heart Foundation (BHF) (RE/18/6134217) and Institute of Health Efficacy Mechanism and Evaluation Programme (12/170/45). PC was supported by the RHU MARVELOUS (ANR-16-RHUS-0009) of Université Claude Bernard Lyon 1 (UCBL), within the program "Investissements d'Avenir" operated by the French National Research Agency (ANR). RD is funded by NIH (R01 HL136578 and R01 HL133407). MS received research support from Siemens Healthineers, and NIH R01 HL131919-01A1. HA was funded by the Swedish Heart-Lung Foundation, Lund University, Lund Sweden and Region of Scania, Sweden. EDA is funded by the British Heart Foundation (FS/13/71/30378). ; Sí

Altres ajuts: The CNIC is supported by the ISCiii, MICINN, and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (award SEV-2015-0505). This research was supported (in part) by the Intramural Research Program of the National Institutes of Health, National Heart, Lung, and Blood Institute. Agencies supporting the research of coauthors are acknowledged in the Online Appendix. The authors appreciate the scientific commitment of the sponsor unrelated to industrial interests. Dr. Arai has a U.S. Government Cooperative Research and Development Agreement with Siements; has a U.S. Government Cooperative Research and Development Agreement (Clinical Trial Agreement) with Bayer; and has a U.S. Government official duty (unpaid consultant) with Circle CVI (licensed software developed at the National Institutes of Health). Dr. Arheden is a shareholder in Imacor AB. Dr. Bax has received speaker fees from Abbott Vascular and Boehringer Ingelheim; and his institution has received unrestricted research grants from Medtronic, Boston Scientific, Biotronik, Edwards Lifesciences, and GE Healthcare. Dr. Berry has institutional agreements between the University of Glasgow (employer) and Abbott Vascular, AstraZeneca, Coroventis, DalCor, GlaxoSmithKline, HeartFlow, Novartis, Philips, and Siemens Healthcare. Dr. Bucciarelli-Ducci has served as a consultant for Circle Cardiovascular Imaging. Dr. Dharmakumar has a research agreement with Siemens Healthcare. Dr. Friedrich has served as a board member and advisor for Circle Cardiovascular Imaging. Dr. Kim has received an educational grant from Siemens Healthineers; and is cofounder of HeartIT LLC. Dr. Salerno has received research support from Siemens Healthineers. Dr Croisille's institution holds a research agreement with Siemens Healthcare, Circle Cardiovascular Imaging, and Olea Medical. Dr. Sánchez-González is an employee of Philips. ; After a reperfused myocardial infarction (MI), dynamic tissue changes occur (edema, inflammation, microvascular obstruction, hemorrhage, ...

BACKGROUND Among patients with acute myocardial infarction, cardiogenic shock, and multivessel coronary artery disease, the risk of a composite of death from any cause or severe renal failure leading to renal-replacement therapy at 30 days was found to be lower with percutaneous coronary intervention (PCI) of the culprit lesion only than with immediate multivessel PCI. We evaluated clinical outcomes at 1 year. METHODS We randomly assigned 706 patients to either culprit-lesion-only PCI or immediate multivessel PCI. The results for the primary end point of death or renal-replacement therapy at 30 days have been reported previously. Prespecified secondary end points at 1 year included death from any cause, recurrent myocardial infarction, repeat revascularization, rehospitalization for congestive heart failure, the composite of death or recurrent infarction, and the composite of death, recurrent infarction, or rehospitalization for heart failure. RESULTS As reported previously, at 30 days, the primary end point had occurred in 45.9% of the patients in the culprit-lesion-only PCI group and in 55.4% in the multivessel PCI group (P=0.01). At 1 year, death had occurred in 172 of 344 patients (50.0%) in the culprit-lesion-only PCI group and in 194 of 341 patients (56.9%) in the multivessel PCI group (relative risk, 0.88; 95% confidence interval [CI], 0.76 to 1.01). The rate of recurrent infarction was 1.7% with culprit-lesion-only PCI and 2.1% with multivessel PCI (relative risk, 0.85; 95% CI, 0.29 to 2.50), and the rate of a composite of death or recurrent infarction was 50.9% and 58.4%, respectively (relative risk, 0.87; 95% CI, 0.76 to 1.00). Repeat revascularization occurred more frequently with culprit-lesion-only PCI than with multivessel PCI (in 32.3% of the patients vs. 9.4%; relative risk, 3.44; 95% CI, 2.39 to 4.95), as did rehospitalization for heart failure (5.2% vs. 1.2%; relative risk, 4.46; 95% CI, 1.53 to 13.04). CONCLUSIONS Among patients with acute myocardial infarction and cardiogenic shock, the risk of death or renal-replacement therapy at 30 days was lower with culprit-lesion-only PCI than with immediate multivessel PCI, and mortality did not differ significantly between the two groups at 1 year of follow-up. (Funded by the European Union Seventh Framework Program and others; CULPRIT-SHOCK ClinicalTrials.gov number, NCT01927549 .).