Differences in Progression to Obstructive Lesions per High-Risk Plaque Features and Plaque Volumes With CCTA.


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 2020
Historique:
received: 01 07 2019
revised: 21 08 2019
accepted: 13 09 2019
pubmed: 18 11 2019
medline: 14 1 2021
entrez: 18 11 2019
Statut: ppublish

Résumé

This study explored whether the pattern of nonobstructive lesion progression into obstructive lesions would differ according to the presence of high-risk plaque (HRP). It is still debatable whether HRP simply represents a certain phase during the natural history of coronary atherosclerotic plaques or if disease progression would differ according to the presence of HRP. Patients with nonobstructive coronary artery disease, defined as percent diameter stenosis (%DS) <50%, were enrolled from a prospective, multinational registry of consecutive patients who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. HRP was defined as lesions with ≥2 features of positive remodeling, spotty calcification, or low-attenuation plaque. Quantitative total and compositional percent atheroma volume (PAV) at baseline and annualized PAV change were compared between non-HRP and HRP lesions. A total of 3,049 nonobstructive lesions were identified from 1,297 patients (mean age 60.3 ± 9.3 years; 56.8% men). There were 2,624 non-HRP and 425 HRP lesions. HRP lesions had a greater total PAV and all noncalcified components of PAV and %DS at baseline compared with non-HRP lesions. However, the annualized total PAV changes were greater in non-HRP lesions than in HRP lesions. On multivariate analysis adjusted for clinical risk factors, drug use, change in lipid level, total PAV, %DS, and HRP, only the baseline total PAV and %DS independently predicted the development of obstructive lesions (hazard ratio [HR]: 1.04; 95% confidence interval [CI]: 1.02 to 1.07, and HR: 1.07; 95% CI: 1.04 to 1.10, respectively, all p < 0.05), whereas the presence of HRP did not (p > 0.05). The pattern of individual coronary atherosclerotic plaque progression differed according to the presence of HRP. Baseline PAV, not the presence of HRP features, was the most important predictor of lesions developing into obstructive lesions. (Progression of Atherosclerotic Plaque Determined By Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411).

Sections du résumé

OBJECTIVES
This study explored whether the pattern of nonobstructive lesion progression into obstructive lesions would differ according to the presence of high-risk plaque (HRP).
BACKGROUND
It is still debatable whether HRP simply represents a certain phase during the natural history of coronary atherosclerotic plaques or if disease progression would differ according to the presence of HRP.
METHODS
Patients with nonobstructive coronary artery disease, defined as percent diameter stenosis (%DS) <50%, were enrolled from a prospective, multinational registry of consecutive patients who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. HRP was defined as lesions with ≥2 features of positive remodeling, spotty calcification, or low-attenuation plaque. Quantitative total and compositional percent atheroma volume (PAV) at baseline and annualized PAV change were compared between non-HRP and HRP lesions.
RESULTS
A total of 3,049 nonobstructive lesions were identified from 1,297 patients (mean age 60.3 ± 9.3 years; 56.8% men). There were 2,624 non-HRP and 425 HRP lesions. HRP lesions had a greater total PAV and all noncalcified components of PAV and %DS at baseline compared with non-HRP lesions. However, the annualized total PAV changes were greater in non-HRP lesions than in HRP lesions. On multivariate analysis adjusted for clinical risk factors, drug use, change in lipid level, total PAV, %DS, and HRP, only the baseline total PAV and %DS independently predicted the development of obstructive lesions (hazard ratio [HR]: 1.04; 95% confidence interval [CI]: 1.02 to 1.07, and HR: 1.07; 95% CI: 1.04 to 1.10, respectively, all p < 0.05), whereas the presence of HRP did not (p > 0.05).
CONCLUSIONS
The pattern of individual coronary atherosclerotic plaque progression differed according to the presence of HRP. Baseline PAV, not the presence of HRP features, was the most important predictor of lesions developing into obstructive lesions. (Progression of Atherosclerotic Plaque Determined By Computed Tomographic Angiography Imaging [PARADIGM]; NCT02803411).

Identifiants

pubmed: 31734214
pii: S1936-878X(19)30934-9
doi: 10.1016/j.jcmg.2019.09.011
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT02803411']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1409-1417

Commentaires et corrections

Type : CommentIn
Type : ErratumIn

Informations de copyright

Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Auteurs

Sang-Eun Lee (SE)

Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, Seoul, South Korea.

Ji Min Sung (JM)

Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea.

Daniele Andreini (D)

Centro Cardiologico Monzino, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy.

Mouaz H Al-Mallah (MH)

Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Houston, Texas.

Matthew J Budoff (MJ)

Department of Medicine, Los Angeles Biomedical Research Institute, Torrance, California.

Filippo Cademartiri (F)

Cardiovascular Imaging Unit, SDN IRCCS, Naples, Italy.

Kavitha Chinnaiyan (K)

Department of Cardiology, William Beaumont Hospital, Royal Oak, Minnesota.

Jung Hyun Choi (JH)

Pusan University Hospital, Busan, South Korea.

Eun Ju Chun (EJ)

Seoul National University Bundang Hospital, Seongnam, South Korea.

Edoardo Conte (E)

Centro Cardiologico Monzino, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy.

Ilan Gottlieb (I)

Department of Radiology, Casa de Saude São Jose, Rio de Janeiro, Brazil.

Martin Hadamitzky (M)

Department of Radiology and Nuclear Medicine, German Heart Center Munich, Munich, Germany.

Yong Jin Kim (YJ)

Department of Internal Medicine, Seoul National University College of Medicine, Cardiovascular Center, Seoul National University Hospital, Seoul, South Korea.

Byoung Kwon Lee (BK)

Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.

Jonathon A Leipsic (JA)

Department of Medicine and Radiology, University of British Columbia, Vancouver, British Columbia, Canada.

Erica Maffei (E)

Department of Radiology, Area Vasta 1/ Azienda Sanitaria Unica Regionale (ASUR) Marche, Urbino, Italy.

Hugo Marques (H)

UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal.

Pedro de Araújo Gonçalves (P)

UNICA, Unit of Cardiovascular Imaging, Hospital da Luz, Lisbon, Portugal.

Gianluca Pontone (G)

Centro Cardiologico Monzino, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy.

Gilbert L Raff (GL)

Department of Cardiology, William Beaumont Hospital, Royal Oak, Minnesota.

Sanghoon Shin (S)

Division of Cardiology, Department of Internal Medicine, Ewha Womans University Seoul Hospital, Seoul, South Korea.

Peter H Stone (PH)

Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Massachusetts.

Habib Samady (H)

Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia.

Renu Virmani (R)

Department of Pathology, CVPath Institute, Gaithersburg, Maryland.

Jagat Narula (J)

Icahn School of Medicine at Mount Sinai, New York, New York.

Daniel S Berman (DS)

Department of Imaging and Medicine, Cedars-Sinai Medical Center, Los Angeles, California.

Leslee J Shaw (LJ)

Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, New York.

Jeroen J Bax (JJ)

Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

Fay Y Lin (FY)

Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, New York.

James K Min (JK)

Department of Radiology, New York-Presbyterian Hospital and Weill Cornell Medicine, New York, New York.

Hyuk-Jae Chang (HJ)

Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea; Yonsei-Cedars-Sinai Integrative Cardiovascular Imaging Research Center, Yonsei University College of Medicine, Yonsei University Health System, Seoul, South Korea. Electronic address: hjchang@yuhs.ac.

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