Characteristics of non-culprit plaques in acute coronary syndrome patients with layered culprit plaque.


Journal

European heart journal. Cardiovascular Imaging
ISSN: 2047-2412
Titre abrégé: Eur Heart J Cardiovasc Imaging
Pays: England
ID NLM: 101573788

Informations de publication

Date de publication:
01 12 2020
Historique:
received: 15 07 2019
revised: 25 09 2019
accepted: 30 11 2019
pubmed: 19 12 2019
medline: 29 6 2021
entrez: 19 12 2019
Statut: ppublish

Résumé

Layered plaques represent signs of previous plaque destabilization. A recent study showed that acute coronary syndrome (ACS) patients with layered culprit plaque have more vulnerability at the culprit lesion and systemic inflammation. We aimed to compare the characteristics of non-culprit plaques between patients with or without layered plaque at the culprit lesion. We also evaluated the characteristics of layered non-culprit plaques, irrespective of culprit plaque phenotype. We studied ACS patients who had undergone pre-intervention optical coherence tomography (OCT) imaging. The number of non-culprit lesions was evaluated on coronary angiogram and morphological characteristics of plaques were studied by OCT. In 349 patients, 99 (28.4%) had layered culprit plaque. The number of non-culprit plaques in patients with or without layered culprit plaque was similar (3.2 ± 0.8 and 2.8 ± 0.8, P = 0.23). Among 465 non-culprit plaques, 145 from patients with layered culprit plaque showed a higher prevalence of macrophage infiltration (71.0% vs. 60.9%, P = 0.050). When analysed irrespective of culprit plaque phenotype, layered non-culprit plaques showed higher prevalence of lipid (93.3% vs. 86.0%, P = 0.028), thin cap fibroatheroma (29.7% vs. 13.7%, P < 0.001), and macrophage infiltration (82.4% vs. 54.0%, P < 0.001) than non-layered plaques. Plaques with layered phenotype at both culprit and non-culprit lesions had the highest vulnerability. In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites. Layered plaque at the non-culprit lesions was associated with more features of plaque vulnerability, particularly when the culprit lesion also had a layered pattern.

Identifiants

pubmed: 31848590
pii: 5680023
doi: 10.1093/ehjci/jez308
doi:

Substances chimiques

Lipids 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1421-1430

Informations de copyright

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.

Auteurs

Michele Russo (M)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.

Hyung Oh Kim (HO)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.

Osamu Kurihara (O)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.

Makoto Araki (M)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.

Hiroki Shinohara (H)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.

Vikas Thondapu (V)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.

Taishi Yonetsu (T)

Department of Interventional Cardiology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo Ward, Tokyo 113-8519, Japan.

Tsunenari Soeda (T)

Department of Cardiovascular Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan.

Yoshiyasu Minami (Y)

Department of Cardiovascular Medicine, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa 252-0373, Japan.

Takumi Higuma (T)

Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki, Kanagawa 216-8511, Japan.

Hang Lee (H)

Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, 50 Staniford Street, Boston, MA 02114, USA.

Francesco Fracassi (F)

Department of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Catholic University of the Sacred Heart, L.go F. Vito 1, 00168 Rome, Italy.

Rocco Vergallo (R)

Department of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Catholic University of the Sacred Heart, L.go F. Vito 1, 00168 Rome, Italy.

Giampaolo Niccoli (G)

Department of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Catholic University of the Sacred Heart, L.go F. Vito 1, 00168 Rome, Italy.

Filippo Crea (F)

Department of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Catholic University of the Sacred Heart, L.go F. Vito 1, 00168 Rome, Italy.

Valentin Fuster (V)

Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, 1 Gustave L Levy Place, New York City, NY 10029, USA.

Ik-Kyung Jang (IK)

Cardiology Division, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRB 800, Boston, MA 02114, USA.
Division of Cardiology, Kyung Hee University Hospital, 1 Hoeki-dong, Dongdaemoon-ku, Seoul, 130-701, Korea.

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