دورية أكاديمية
أعرض في EDS

Remote myocardial fibrosis predicts adverse outcome in patients with myocardial infarction on clinical cardiovascular magnetic resonance imaging.

التفاصيل البيبلوغرافية
العنوان: Remote myocardial fibrosis predicts adverse outcome in patients with myocardial infarction on clinical cardiovascular magnetic resonance imaging.
المؤلفون: Black N; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., Bradley J; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., Schelbert EB; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; UPMC Cardiovascular Magnetic Resonance Center, Heart and Vascular Institute, Pittsburgh, Pennsylvania, USA; Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, Pennsylvania, USA., Bonnett LJ; Department of Health Data Science, University of Liverpool, Liverpool, UK., Lewis GA; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK; Royal Liverpool and Broadgreen University Hospitals NHS Trust, Liverpool, UK., Lagan J; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK; Royal Liverpool and Broadgreen University Hospitals NHS Trust, Liverpool, UK., Orsborne C; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., Brown PF; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK; South Tees NHS Foundation Trust, Middlesbrough, UK., Soltani F; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., Fröjdh F; Department of Clinical Physiology, Karolinska University Hospital, and Karolinska Institutet, Stockholm, Sweden., Ugander M; Department of Clinical Physiology, Karolinska University Hospital, and Karolinska Institutet, Stockholm, Sweden; Kolling Institute, Royal North Shore Hospital, and University of Sydney, Sydney, Australia., Wong TC; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; UPMC Cardiovascular Magnetic Resonance Center, Heart and Vascular Institute, Pittsburgh, Pennsylvania, USA., Fukui M; Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, Minneapolis, Minnesota, USA., Cavalcante JL; Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, Minneapolis, Minnesota, USA., Naish JH; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., Williams SG; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., McDonagh T; King's College Hospital, London, UK., Schmitt M; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK., Miller CA; Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK; Manchester University NHS Foundation Trust, Manchester, UK; Wellcome Centre for Cell-Matrix Research, Division of Cell-Matrix Biology & Regenerative Medicine, School of Biology, Faculty of Biology, Medicine & Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK. Electronic address: Christopher.Miller@manchester.ac.uk.
المصدر: Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance [J Cardiovasc Magn Reson] 2024 Jul 23; Vol. 26 (2), pp. 101064. Date of Electronic Publication: 2024 Jul 23.
Publication Model: Ahead of Print
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 9815616 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-429X (Electronic) Linking ISSN: 10976647 NLM ISO Abbreviation: J Cardiovasc Magn Reson Subsets: MEDLINE
أسماء مطبوعة: Publication: London : BioMed Central
Original Publication: New York : M. Dekker, Inc., c1998-
مستخلص: Background: Heart failure (HF) most commonly occurs in patients who have had a myocardial infarction (MI), but factors other than MI size may be deterministic. Fibrosis of myocardium remote from the MI is associated with adverse remodeling. We aimed to 1) investigate the association between remote myocardial fibrosis, measured using cardiovascular magnetic resonance (CMR) extracellular volume fraction (ECV), and HF and death following MI, 2) identify predictors of remote myocardial fibrosis in patients with evidence of MI and determine the relationship with infarct size.
Methods: Multicenter prospective cohort study of 1199 consecutive patients undergoing CMR with evidence of MI on late gadolinium enhancement. Median follow-up was 1133 (895-1442) days. Cox proportional hazards modeling was used to identify factors predictive of the primary outcome, a composite of first hospitalization for HF (HHF) or all-cause mortality, post-CMR. Linear regression modeling was used to identify determinants of remote ECV.
Results: Remote myocardial fibrosis was a strong predictor of primary outcome (χ 2 : 15.6, hazard ratio [HR]: 1.07 per 1% increase in ECV, 95% confidence interval [CI]: 1.04-1.11, p < 0.001) and was separately predictive of both HHF and death. The strongest predictors of remote ECV were diabetes, sex, natriuretic peptides, and body mass index, but, despite extensive phenotyping, the adjusted model R 2 was only 0.283. The relationship between infarct size and remote fibrosis was very weak.
Conclusion: Myocardial fibrosis, measured using CMR ECV, is a strong predictor of HHF and death in patients with evidence of MI. The mechanisms underlying remote myocardial fibrosis formation post-MI remain poorly understood, but factors other than infarct size appear to be important.
Competing Interests: Declaration of competing interests The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Christopher Miller reports financial support was provided by National Institute for Health and Care Research. Christopher Miller reports financial support was provided by Guerbet. Christopher Miller reports equipment, drugs, or supplies were provided by Roche. Christopher Miller reports financial support was provided by British Heart Foundation. Christopher Miller reports a relationship with HAYA therapeutics that includes consulting or advisory, PureTech Health that includes consulting or advisory, Amicus Therapeutics Inc that includes funding grants, Roche that includes funding grants, Univar Solutions that includes funding grants, Novartis that includes consulting or advisory, Boehringer Ingelheim Ltd that includes consulting or advisory, Lilly Alliance that includes consulting or advisory, and AstraZeneca PLC that includes consulting or advisory. Erik Schelbert reports a relationship with HAYA therapeutics that includes consulting or advisory, PureTech Health that includes consulting or advisory, and Amicus Therapeutics Inc that includes funding grants and travel reimbursement. Joao L. Cavalcante reports a relationship with Abbott Vascular Inc that includes consulting or advisory and funding grants, Boston Scientific Corp that includes consulting or advisory and funding grants, Edwards Lifesciences Corporation that includes consulting or advisory and funding grants, Medtronic that includes consulting or advisory and funding grants, WL Gore and Associates that includes consulting or advisory and funding grants, Circle Cardiovascular Imaging Inc that includes funding grants, Siemens Healthineers that includes funding grants, 3Mension that includes funding grants, Medis that includes funding grants, and Ziosoft that includes funding grants. Theresa McDonagh reports a relationship with Novartis that includes speaking and lecture fees, AstraZeneca Pharmaceuticals LP that includes speaking and lecture fees, and Vifor Pharma Ltd that includes speaking and lecture fees. Fredrika Fröjdh and Martin Ugander were supported in part by grants from the Swedish Research Council, Swedish Heart and Lung Foundation, Stockholm County Council, and Karolinska Institutet. Martin Ugander is the principal investigator on a research and development agreement regarding cardiovascular magnetic resonance between Siemens and Karolinska University Hospital. Timothy C. Wong was supported by an American Heart Association Scientist Development grant and a Children’s Cardiomyopathy Foundation grant. Josephine Naish has a part-time appointment at Bioxydyn Ltd. The remaining authors have nothing to disclose. The other authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
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فهرسة مساهمة: Keywords: Deep phenotyping; Extracellular matrix volume; Myocardial fibrosis; Myocardial infarction
تواريخ الأحداث: Date Created: 20240725 Latest Revision: 20240829
رمز التحديث: 20240830
مُعرف محوري في PubMed: PMC11347049
DOI: 10.1016/j.jocmr.2024.101064
PMID: 39053856
قاعدة البيانات: MEDLINE
الوصف
تدمد:1532-429X
DOI:10.1016/j.jocmr.2024.101064