Predictors of Rapid Plaque Progression: An 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 2021
Historique:
received: 09 07 2020
revised: 21 08 2020
accepted: 27 08 2020
pubmed: 5 10 2020
medline: 26 10 2021
entrez: 4 10 2020
Statut: ppublish

Résumé

This study sought to identify morphological predictors of rapid plaque progression. Two patterns of plaque progression have been described: slow linear progression and rapid step-wise progression. The former pattern will cause stable angina when the narrowing reaches a critical threshold, whereas the latter pattern may lead to acute coronary syndromes or sudden cardiac death. Patients who underwent optical coherence tomography (OCT) imaging during the index procedure and follow-up angiography with a minimum interval of 6 months were selected. Nonculprit lesions with a diameter stenosis of ≥30% on index angiography were assessed. Lesion progression was defined as a decrease of angiographic minimum lumen diameter ≥0.4 mm at follow-up (mean, 7.1 months). Baseline morphological characteristics of plaques with rapid progression were evaluated by OCT. In a subgroup with follow-up OCT imaging for plaques with rapid progression, morphological changes from baseline to follow-up were assessed. Among 517 lesions in 248 patients, 50 lesions showed rapid progression. These lesions had a significantly higher prevalence of lipid-rich plaque (76.0% vs. 50.5%, respectively), thin-cap fibroatheroma (TCFA) (20.0% vs. 5.8%, respectively), layered plaque (60.0% vs. 34.0%, respectively), macrophage accumulation (62.0% vs. 42.4%, respectively), microvessel (46.0% vs. 29.1%, respectively), plaque rupture (12.0% vs. 4.7%, respectively), and thrombus (6.0% vs. 1.1%, respectively) at baseline compared with those without rapid progression. Multivariate analysis identified lipid-rich plaque (odds ratio [OR]: 2.17; 95% confidence interval [CI]: 1.02 to 4.62; p = 0.045]), TCFA (OR: 5.85; 95% CI: 2.01 to 17.03; p = 0.001), and layered plaque (OR: 2.19; 95% CI: 1.03 to 4.17; p = 0.040) as predictors of subsequent rapid lesion progression. In a subgroup analysis for plaques with rapid progression, a new layer was detected in 25 of 41 plaques (61.0%) at follow-up. Lipid-rich plaques, TCFA, and layered plaques were predictors of subsequent rapid plaque progression. A new layer, a signature of previous plaque disruption and healing, was detected in more than half of the lesions with rapid progression at follow-up. (Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).

Sections du résumé

OBJECTIVES
This study sought to identify morphological predictors of rapid plaque progression.
BACKGROUND
Two patterns of plaque progression have been described: slow linear progression and rapid step-wise progression. The former pattern will cause stable angina when the narrowing reaches a critical threshold, whereas the latter pattern may lead to acute coronary syndromes or sudden cardiac death.
METHODS
Patients who underwent optical coherence tomography (OCT) imaging during the index procedure and follow-up angiography with a minimum interval of 6 months were selected. Nonculprit lesions with a diameter stenosis of ≥30% on index angiography were assessed. Lesion progression was defined as a decrease of angiographic minimum lumen diameter ≥0.4 mm at follow-up (mean, 7.1 months). Baseline morphological characteristics of plaques with rapid progression were evaluated by OCT. In a subgroup with follow-up OCT imaging for plaques with rapid progression, morphological changes from baseline to follow-up were assessed.
RESULTS
Among 517 lesions in 248 patients, 50 lesions showed rapid progression. These lesions had a significantly higher prevalence of lipid-rich plaque (76.0% vs. 50.5%, respectively), thin-cap fibroatheroma (TCFA) (20.0% vs. 5.8%, respectively), layered plaque (60.0% vs. 34.0%, respectively), macrophage accumulation (62.0% vs. 42.4%, respectively), microvessel (46.0% vs. 29.1%, respectively), plaque rupture (12.0% vs. 4.7%, respectively), and thrombus (6.0% vs. 1.1%, respectively) at baseline compared with those without rapid progression. Multivariate analysis identified lipid-rich plaque (odds ratio [OR]: 2.17; 95% confidence interval [CI]: 1.02 to 4.62; p = 0.045]), TCFA (OR: 5.85; 95% CI: 2.01 to 17.03; p = 0.001), and layered plaque (OR: 2.19; 95% CI: 1.03 to 4.17; p = 0.040) as predictors of subsequent rapid lesion progression. In a subgroup analysis for plaques with rapid progression, a new layer was detected in 25 of 41 plaques (61.0%) at follow-up.
CONCLUSIONS
Lipid-rich plaques, TCFA, and layered plaques were predictors of subsequent rapid plaque progression. A new layer, a signature of previous plaque disruption and healing, was detected in more than half of the lesions with rapid progression at follow-up. (Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).

Identifiants

pubmed: 33011121
pii: S1936-878X(20)30736-1
doi: 10.1016/j.jcmg.2020.08.014
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT01110538']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1628-1638

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures Dr. Jang has received educational grants from Abbott Vascular; and research was supported by Mr. and Mrs. Michael and Kathryn Park and by Mrs. and Mr. Gill and Allan Gray, who had no role in the design or conduct of this research. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Makoto Araki (M)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Taishi Yonetsu (T)

Department of Interventional Cardiology, Tokyo Medical and Dental University, Tokyo, Japan. Electronic address: yonetsu@gmail.com.

Osamu Kurihara (O)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Akihiro Nakajima (A)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Hang Lee (H)

Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Tsunenari Soeda (T)

Department of Cardiovascular Medicine, Nara Medical University, Kashihara, Nara, Japan.

Yoshiyasu Minami (Y)

Department of Cardiovascular Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Iris McNulty (I)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Shiro Uemura (S)

Department of Cardiology, Kawasaki Medical School, Kurashiki, Japan.

Tsunekazu Kakuta (T)

Department of Cardiology, Tsuchiura Kyodo General Hospital, Tsuchiura, Ibaraki, Japan.

Ik-Kyung Jang (IK)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; Division of Cardiology, Kyung Hee University Hospital, Seoul, South Korea. Electronic address: ijang@mgh.harvard.edu.

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