Changes in Coronary Plaque Composition in Patients With Acute Myocardial Infarction Treated With High-Intensity Statin Therapy (IBIS-4): A Serial Optical Coherence Tomography Study.


Journal

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

Informations de publication

Date de publication:
08 2019
Historique:
received: 05 04 2018
revised: 06 08 2018
accepted: 07 08 2018
pubmed: 17 12 2018
medline: 25 3 2020
entrez: 17 12 2018
Statut: ppublish

Résumé

This study assessed changes in optical coherence tomography (OCT)-defined plaque composition in patients with ST-elevation myocardial infarction (STEMI) receiving high-intensity statin treatment. OCT is a high-resolution modality capable of measuring plaque characteristics including fibrous cap thickness (FCT) and macrophage infiltration. There is limited in vivo evidence regarding the effects of statins on OCT-defined coronary atheroma composition and no evidence in the context of STEMI. In the IBIS-4 (Integrated Biomarker Imaging Study-4), 103 patients underwent intravascular ultrasonography and OCT of 2 noninfarct-related coronary arteries in the acute phase of STEMI. Patients were treated with high-dose rosuvastatin for 13 months. Serial OCT imaging was available in 153 arteries from 83 patients. We measured FCT by using a semi-automated method. Co-primary endpoints consisted of the change in minimum FCT (measured in fibroatheromas) and change in macrophage line arc. At 13 months, median low-density lipoprotein cholesterol had decreased from 128 mg/dl to 73.6 mg/dl. Minimum FCT, measured in 31 lesions from 27 patients, increased from 64.9 ± 19.9 μm to 87.9 ± 38.1 μm (p = 0.008). Macrophage line arc decreased from 9.6° ± 12.8° to 6.4° ± 9.6° (p < 0.0001). The secondary endpoint, mean lipid arc, decreased from 55.9° ± 37° to 43.5° ± 33.5°. In lesion-level analyses (n = 191), 9 of 13 thin-cap fibroatheromata (TCFAs) at baseline (69.2%) regressed to non-TCFA morphology, whereas 2 of 178 non-TCFA lesions (1.1%) progressed to TCFAs. In this observational study, we found significant increase in minimum FCT, reduction in macrophage accumulation, and frequent regression of TCFAs to other plaque phenotypes in nonculprit lesions of patients with STEMI treated with high-intensity statin therapy.

Sections du résumé

OBJECTIVES
This study assessed changes in optical coherence tomography (OCT)-defined plaque composition in patients with ST-elevation myocardial infarction (STEMI) receiving high-intensity statin treatment.
BACKGROUND
OCT is a high-resolution modality capable of measuring plaque characteristics including fibrous cap thickness (FCT) and macrophage infiltration. There is limited in vivo evidence regarding the effects of statins on OCT-defined coronary atheroma composition and no evidence in the context of STEMI.
METHODS
In the IBIS-4 (Integrated Biomarker Imaging Study-4), 103 patients underwent intravascular ultrasonography and OCT of 2 noninfarct-related coronary arteries in the acute phase of STEMI. Patients were treated with high-dose rosuvastatin for 13 months. Serial OCT imaging was available in 153 arteries from 83 patients. We measured FCT by using a semi-automated method. Co-primary endpoints consisted of the change in minimum FCT (measured in fibroatheromas) and change in macrophage line arc.
RESULTS
At 13 months, median low-density lipoprotein cholesterol had decreased from 128 mg/dl to 73.6 mg/dl. Minimum FCT, measured in 31 lesions from 27 patients, increased from 64.9 ± 19.9 μm to 87.9 ± 38.1 μm (p = 0.008). Macrophage line arc decreased from 9.6° ± 12.8° to 6.4° ± 9.6° (p < 0.0001). The secondary endpoint, mean lipid arc, decreased from 55.9° ± 37° to 43.5° ± 33.5°. In lesion-level analyses (n = 191), 9 of 13 thin-cap fibroatheromata (TCFAs) at baseline (69.2%) regressed to non-TCFA morphology, whereas 2 of 178 non-TCFA lesions (1.1%) progressed to TCFAs.
CONCLUSIONS
In this observational study, we found significant increase in minimum FCT, reduction in macrophage accumulation, and frequent regression of TCFAs to other plaque phenotypes in nonculprit lesions of patients with STEMI treated with high-intensity statin therapy.

Identifiants

pubmed: 30553686
pii: S1936-878X(18)30752-6
doi: 10.1016/j.jcmg.2018.08.024
pii:
doi:

Substances chimiques

Biomarkers 0
Cholesterol, LDL 0
Hydroxymethylglutaryl-CoA Reductase Inhibitors 0
Rosuvastatin Calcium 83MVU38M7Q

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1518-1528

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Auteurs

Lorenz Räber (L)

Department of Cardiology, Bern University Hospital, Bern, Switzerland. Electronic address: lorenz.raeber@insel.ch.

Konstantinos C Koskinas (KC)

Department of Cardiology, Bern University Hospital, Bern, Switzerland.

Kyohei Yamaji (K)

Department of Cardiology, Bern University Hospital, Bern, Switzerland; Department of Cardiology, Kokura Memorial Hospital, Kitakyushu, Japan.

Masanori Taniwaki (M)

Department of Cardiology, Bern University Hospital, Bern, Switzerland; Tokorozawa Heart Center, Saitama, Japan.

Marco Roffi (M)

Division of Cardiology, University Hospital Geneva, Geneva, Switzerland.

Lene Holmvang (L)

Heart Center, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.

Hector M Garcia Garcia (HM)

MedStar Cardiovacular Research Network, MedStar Washington Hospital Center, Washington.

Thomas Zanchin (T)

Department of Cardiology, Bern University Hospital, Bern, Switzerland.

Rafaela Maldonado (R)

Department of Cardiology, Bern University Hospital, Bern, Switzerland.

Aris Moschovitis (A)

Department of Cardiology, Bern University Hospital, Bern, Switzerland.

Giovanni Pedrazzini (G)

Cardiocentro, Lugano, Switzerland.

Serge Zaugg (S)

Clinical Trials Unit (CTU), Bern, and Institute of Social and Preventive Medicine, University of Bern, Bern Switzerland.

Jouke Dijkstra (J)

Leiden University Medical Center, Leiden, the Netherlands.

Christian M Matter (CM)

Department of Cardiology, Zurich University Hospital, Zurich, Switzerland.

Patrick W Serruys (PW)

International Centre for Circulatory Health, National Heart and Lung Institute, Imperial College, London, London, United Kingdom.

Thomas F Lüscher (TF)

Royal Brompton and Harefield Hospital Trust and Imperial College, London, United Kingdom.

Henning Kelbaek (H)

Department of Cardiology, Zealand University Hospital, Roskilde, Denmark.

Alexios Karagiannis (A)

Clinical Trials Unit (CTU), Bern, and Institute of Social and Preventive Medicine, University of Bern, Bern Switzerland.

Maria D Radu (MD)

Heart Center, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.

Stephan Windecker (S)

Department of Cardiology, Bern University Hospital, Bern, Switzerland.

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