Calcified Plaques in Patients With Acute Coronary Syndromes.


Journal

JACC. Cardiovascular interventions
ISSN: 1876-7605
Titre abrégé: JACC Cardiovasc Interv
Pays: United States
ID NLM: 101467004

Informations de publication

Date de publication:
25 03 2019
Historique:
received: 30 09 2018
revised: 26 11 2018
accepted: 12 12 2018
entrez: 23 3 2019
pubmed: 23 3 2019
medline: 19 5 2020
Statut: ppublish

Résumé

This study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS). Calcified plaques as an underlying pathology in patients with ACS have not been systematically studied. From 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque. Three distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032). Three distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723).

Sections du résumé

OBJECTIVES
This study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS).
BACKGROUND
Calcified plaques as an underlying pathology in patients with ACS have not been systematically studied.
METHODS
From 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque.
RESULTS
Three distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032).
CONCLUSIONS
Three distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723).

Identifiants

pubmed: 30898249
pii: S1936-8798(18)32482-8
doi: 10.1016/j.jcin.2018.12.013
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT03479723']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

531-540

Commentaires et corrections

Type : CommentIn

Informations de copyright

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

Auteurs

Tomoyo Sugiyama (T)

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

Erika Yamamoto (E)

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

Francesco Fracassi (F)

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

Hang Lee (H)

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

Taishi Yonetsu (T)

Department of Interventional Cardiology, Tokyo Medical and Dental University, Tokyo, Japan. Electronic address: t-yonetsu.cvm@tmd.ac.jp.

Tsunekazu Kakuta (T)

Department of Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Tsuchiura, Japan.

Tsunenari Soeda (T)

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

Yoshihiko Saito (Y)

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

Bryan P Yan (BP)

Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, China.

Osamu Kurihara (O)

Cardiovascular Center, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Japan.

Masamichi Takano (M)

Cardiovascular Center, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Japan.

Giampaolo Niccoli (G)

Department of Cardiovascular and Thoracic Science, Catholic University of the Sacred Heart, Rome, Italy.

Filippo Crea (F)

Department of Cardiovascular and Thoracic Science, Catholic University of the Sacred Heart, Rome, Italy.

Takumi Higuma (T)

Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Shigeki Kimura (S)

Department of Cardiology, Kameda Medical Center, Kamogawa, Japan.

Yoshiyasu Minami (Y)

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

Junya Ako (J)

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

Tom Adriaenssens (T)

Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.

Niklas F Boeder (NF)

Department of Cardiology, University of Giessen, Giessen, Germany.

Holger M Nef (HM)

Department of Cardiology, University of Giessen, Giessen, Germany.

James G Fujimoto (JG)

Research Laboratory of Electronics, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts.

Valentin Fuster (V)

Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York.

Aloke V Finn (AV)

CVPath Institute, Gaithersburg, Maryland.

Erling Falk (E)

Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.

Ik-Kyung Jang (IK)

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

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