Evolution of Myocardial Tissue Injury: A CMR Study Over a Decade After STEMI.


Journal

JACC. Cardiovascular imaging
ISSN: 1876-7591
Titre abrégé: JACC Cardiovasc Imaging
Pays: United States
ID NLM: 101467978

Informations de publication

Date de publication:
06 2022
Historique:
received: 16 07 2021
revised: 11 01 2022
accepted: 10 02 2022
entrez: 9 6 2022
pubmed: 10 6 2022
medline: 14 6 2022
Statut: ppublish

Résumé

In patients with a first ST-segment elevation myocardial infarction (STEMI), the multi-annual evolution of myocardial tissue injury parameters, as assessed by cardiac magnetic resonance (CMR), has not yet been described. This study examined myocardial tissue injury dynamics over a decade after STEMI. Sequential CMR examinations (within the first week after STEMI, and at 4, 12, months, and 9 years thereafter) were conducted in 74 patients with STEMI treated with primary percutaneous coronary intervention. Left ventricular function, infarct size (IS), and microvascular obstruction (MVO) were assessed at all time points. T2∗, T2, and T1 mapping (n = 59) were added at 9-year scan to evaluate the presence of iron and edema within the infarct core, respectively. IS decreased progressively and significantly between all CMR time points (all P < 0.001), with an average reduction rate of 5.8% per year (IQR: 3.5%-8.8%) and a relative reduction of 49% (IQR: 39%-76%) over a decade. MVO was present in 61% of patients at baseline, but was not present at the follow-up examinations. At 9-year CMR, 17 of 59 (29%) patients showed iron deposition within the infarct core, whereas 82% had persistent edema. Persistent iron and edema were associated with greater IS on any occasion (all P < 0.001), as well as the presence of MVO (P < 0.001). Patients with persistent iron and edema showed a lower relative regression of IS (P = 0.005 and P = 0.032, respectively) and greater end-systolic volumes over a decade (all P < 0.012 and P > 0.023, respectively). A T1 hypointense infarct core without evidence of T2∗ iron deposition (14 of 59 [24%] patients) was attributed to lipomatous metaplasia of the infarct. The evolution of IS is a dynamic process that extends well beyond the first few months after STEMI. Persistence of iron and edema within the infarct core occurs up to a decade after STEMI and is associated with initial infarct severity and poor infarct healing.

Sections du résumé

BACKGROUND
In patients with a first ST-segment elevation myocardial infarction (STEMI), the multi-annual evolution of myocardial tissue injury parameters, as assessed by cardiac magnetic resonance (CMR), has not yet been described.
OBJECTIVES
This study examined myocardial tissue injury dynamics over a decade after STEMI.
METHODS
Sequential CMR examinations (within the first week after STEMI, and at 4, 12, months, and 9 years thereafter) were conducted in 74 patients with STEMI treated with primary percutaneous coronary intervention. Left ventricular function, infarct size (IS), and microvascular obstruction (MVO) were assessed at all time points. T2∗, T2, and T1 mapping (n = 59) were added at 9-year scan to evaluate the presence of iron and edema within the infarct core, respectively.
RESULTS
IS decreased progressively and significantly between all CMR time points (all P < 0.001), with an average reduction rate of 5.8% per year (IQR: 3.5%-8.8%) and a relative reduction of 49% (IQR: 39%-76%) over a decade. MVO was present in 61% of patients at baseline, but was not present at the follow-up examinations. At 9-year CMR, 17 of 59 (29%) patients showed iron deposition within the infarct core, whereas 82% had persistent edema. Persistent iron and edema were associated with greater IS on any occasion (all P < 0.001), as well as the presence of MVO (P < 0.001). Patients with persistent iron and edema showed a lower relative regression of IS (P = 0.005 and P = 0.032, respectively) and greater end-systolic volumes over a decade (all P < 0.012 and P > 0.023, respectively). A T1 hypointense infarct core without evidence of T2∗ iron deposition (14 of 59 [24%] patients) was attributed to lipomatous metaplasia of the infarct.
CONCLUSIONS
The evolution of IS is a dynamic process that extends well beyond the first few months after STEMI. Persistence of iron and edema within the infarct core occurs up to a decade after STEMI and is associated with initial infarct severity and poor infarct healing.

Identifiants

pubmed: 35680211
pii: S1936-878X(22)00142-5
doi: 10.1016/j.jcmg.2022.02.010
pii:
doi:

Substances chimiques

Iron E1UOL152H7

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1030-1042

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The study was supported by grants from the Austrian Science Fund (FWF): KLI 772-B (BM) and by the Austrian Society of Cardiology. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Agnes Mayr (A)

University Clinic of Radiology, Medical University of Innsbruck, Innsbruck, Austria.

Gert Klug (G)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Martin Reindl (M)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Ivan Lechner (I)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Christina Tiller (C)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Magdalena Holzknecht (M)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Mathias Pamminger (M)

University Clinic of Radiology, Medical University of Innsbruck, Innsbruck, Austria.

Felix Troger (F)

University Clinic of Radiology, Medical University of Innsbruck, Innsbruck, Austria.

Michael Schocke (M)

University Clinic of Radiology, Medical University of Innsbruck, Innsbruck, Austria.

Axel Bauer (A)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Sebastian J Reinstadler (SJ)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Bernhard Metzler (B)

University Clinic of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: Bernhard.Metzler@tirol-kliniken.at.

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Classifications MeSH