Plaque Rupture, Compared With Plaque Erosion, Is Associated With a Higher Level of Pancoronary Inflammation.

Objectives: The aim of this study was to compare the level of coronary inflammation between plaque rupture and plaque erosion using pericoronary adipose tissue (PCAT) attenuation.
Background: Vascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. PCAT attenuation determined using computed tomography has emerged as a marker specific for coronary artery inflammation.
Methods: Patients with non-ST-segment elevation acute coronary syndromes who underwent preintervention coronary computed tomographic angiography and optical coherence tomographic culprit lesion imaging were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries.
Results: Among 198 patients, plaque rupture was the underlying mechanism in 107 (54.0%) and plaque erosion in 91 (46.0%). Plaque rupture had higher PCAT attenuation than plaque erosion both at the culprit plaque level (-65.8 ± 7.5 HU vs -69.5 ± 11.4 HU; P = 0.010) and at the culprit vessel level (-67.1 ± 7.1 HU vs -69.6 ± 8.2 HU; P = 0.024). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in patients with plaque rupture than in plaque erosion, indicating a higher level of inflammation (-67.9 ± 5.7 HU vs -69.9 ± 6.8 HU; P = 0.030). In multivariable analysis, plaque rupture was significantly associated with high PCAT attenuation.
Conclusions: PCAT attenuation in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results suggest that pancoronary inflammation plays a more significant role in plaque rupture than in plaque erosion. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194).
Competing Interests: Funding Support and Author Disclosures Dr Jang’s research was supported by Mr and Mrs Allan and Gill Gray and by Mr and Mrs Michael and Kathryn Park. Dr Dey is supported by National Heart, Lung, and Blood Institute grants (1R01HL148787-01A1 and 1R01HL151266). The funders had no role in the design or conduct of this research. Dr Jang has received educational grant support from Abbott Vascular; and consulting fees from Svelte Medical Systems and Mitobridge. Outside the present study, Dr Dey has received software royalties from Cedars-Sinai Medical Center; and has a patent. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)