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Layered plaque is associated with high levels of vascular inflammation and vulnerability in patients with stable angina pectoris

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Abstract

Layered plaque, a signature of previous plaque destabilization and healing, is a known predictor for rapid plaque progression; however, the mechanism of which is unknown. The aim of the current study was to compare the level of vascular inflammation and plaque vulnerability in layered plaques to investigate possible mechanisms of rapid plaque progression. This is a retrospective, observational, single-center cohort study. Patients who underwent both coronary computed tomography angiography (CTA) and optical coherence tomography (OCT) for stable angina pectoris (SAP) were selected. Plaques were defined as any tissue (noncalcified, calcified, or mixed) within or adjacent to the lumen. Perivascular inflammation was measured by pericoronary adipose tissue (PCAT) attenuation at the plaque levels on CTA. Features of plaque vulnerability were assessed by OCT. Layered plaques were defined as plaques presenting one or more layers of different optical densities and a clear demarcation from underlying components on OCT. A total of 475 plaques from 195 patients who presented with SAP were included. Layered plaques (n = 241), compared with non-layered plaques (n = 234), had a higher level of vascular inflammation (-71.47 ± 10.74 HU vs. -73.69 ± 10.91 HU, P = 0.026) as well as a higher prevalence of the OCT features of plaque vulnerability, including lipid-rich plaque (83.8% vs. 66.7%, P < 0.001), thin-cap fibroatheroma (26.1% vs. 17.5%, P = 0.026), microvessels (61.8% vs. 34.6%, P < 0.001), and cholesterol crystals (38.6% vs. 25.6%, P = 0.003). Layered plaque was associated with a higher level of vascular inflammation and a higher prevalence of plaque vulnerability, which might play an important role in rapid plaque progression.

Clinical trial registration: https://classic.clinicaltrials.gov/ct2/show/NCT04523194.

Graphical abstract

Level of vascular inflammation and plaque vulnerability in patients with versus without layered plaque phenotype. In patients with stable angina pectoris, layered plaques had a higher level of pericoronary adipose tissue attenuation indicating a higher level of perivascular inflammation and a higher prevalence of optical coherence tomography features of plaque vulnerability

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Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Abbreviations

CAD:

Coronary artery disease

CT:

Computed tomography

CTA:

Coronary computed tomography angiography

DS:

Diameter stenosis

ECG:

Electrocardiography

FCT:

Fibrous cap thickness

HU:

Hounsfield unit

LL:

Lesion length

MLD:

Minimal lumen diameter

OCT:

Optical coherence tomography

PCAT:

Pericoronary adipose tissue

RD:

Reference vessel diameter

SAP:

Stable angina pectoris

TCFA:

Thin-cap fibroatheroma

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Funding

Dr. Ik-Kyung Jang’s research has been supported by Mrs. Gillian Gray through the Allan Gray Fellowship Fund in Cardiology and Mukesh and Priti Chatter through the Chatter Foundation.

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Authors and Affiliations

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

    Takayuki Niida, Daisuke Kinoshita, Keishi Suzuki, Haruhito Yuki, Daichi Fujimoto, Iris McNulty & Ik-Kyung Jang

  2. Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA

    Damini Dey

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

    Hang Lee

  4. Knight Cardiovascular Institute, Oregon Health and Science University, Portland, OR, USA

    Maros Ferencik

  5. Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan

    Taishi Yonetsu

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

    Tsunekazu Kakuta

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  1. Takayuki Niida
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Correspondence to Ik-Kyung Jang.

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Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

Informed consent

Informed consent was obtained from all individual participants included in the study.

Conflict of interest

Dr. Niida received a grant from the Japan Heart Foundation/Bayer Yakuhin Research Grant Abroad. Outside the present study, Dr. Dey has received software royalties from Cedars-Sinai Medical Center and has a patent. Dr. Ferencik has received consulting fees from Siemens Healthineers, HeartFlow, and Elucid and stock options from Elucid. The remaining authors have nothing to disclose. Dr. Jang has received educational grants from Abbott Vascular and a consulting fee from Svelte Medical Systems.

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Highlights

• Layered plaque is a predictor for rapid plaque progression, the mechanism of which is unknown.

• The level of vascular inflammation and plaque vulnerability can be assessed by coronary computed tomography and optical coherence tomography, respectively.

• A level of vascular inflammation and a prevalence of the OCT features of plaque vulnerability were higher in layered plaques, compared with non-layered plaques.

• High levels of vascular inflammation and plaque vulnerability in layered plaque may explain the mechanism of rapid plaque progression.

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Niida, T., Kinoshita, D., Suzuki, K. et al. Layered plaque is associated with high levels of vascular inflammation and vulnerability in patients with stable angina pectoris. J Thromb Thrombolysis (2024). https://doi.org/10.1007/s11239-024-02982-3

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