Peri-coronary adipose tissue attenuation and its association with plaque vulnerability and clinical outcomes in coronary artery disease using combined CCTA and OCT

Abstract

Vascular inflammation plays a pivotal role in the pathogenesis of atherosclerotic plaques, driving their progression from a stable to an unstable phenotype. Previous research has identified a relationship between peri-coronary adipose tissue (PCAT) attenuation, as assessed by coronary computed tomography angiography (CCTA), and the degree of coronary inflammation, which is associated with an elevated risk of cardiovascular mortality. Nevertheless, the interplay between PCAT attenuation, as determined by CCTA, and plaque characterization via optical coherence tomography (OCT), alongside clinical outcomes, remains inadequately explored. In this study, we retrospectively analyzed data from 111 patients with coronary artery disease who underwent a sequential diagnostic workup comprising CCTA, coronary angiography (CAG), and OCT from January 2022 to May 2023. Patients were stratified into two groups based on a PCAT attenuation threshold of -70.1 Hounsfield units (HU): a high-PCAT attenuation group (n = 39) and a low-PCAT attenuation group (n = 72). The cohort was further divided into major adverse cardiac event (MACE) and non-MACE groups, depending on whether a MACE occurred during a median follow-up period of 504 days. Compared to the low-PCAT attenuation group, patients in the high-PCAT attenuation group were younger (55.77 ± 9.33 vs. 60.07 ± 9.88; p < 0.028) and exhibited a higher incidence of acute coronary syndrome (ACS) (30.8% vs. 13.9%; p = 0.033). Additionally, lipid-rich plaques (84.6% vs. 52.8%; p = 0.001), macrophages (79.5% vs. 51.4%; p = 0.004), thin-cap fibrous atherosclerotic plaques (TCFA) (43.6% vs. 25.0%; p = 0.044), and red blood clots (33.3% vs. 15.3%; p = 0.027) were more prevalent in the high-attenuation group. Multivariate logistic regression analysis revealed that high PCAT attenuation was an independent predictor of lipid plaques, macrophage presence, and TCFA. During the follow-up period, 22 patients (19.8%) experienced a primary clinical endpoint event. Patients in the MACE group demonstrated higher levels of PCAT attenuation compared to those in the non-MACE group (- 69.67 [- 74.75, - 65.59] HU vs. - 73.67 [- 76.67, - 69.50] HU, p = 0.037). Multivariate Cox proportional hazards regression modeling further substantiated that elevated PCAT attenuation was independently associated with an increased risk of MACE. In conclusion, the high-attenuation group exhibited more OCT-detected features indicative of vulnerable plaques and a higher frequency of MACE events relative to the low-attenuation group. These findings suggest a significant association between elevated vascular inflammation, as reflected by PCAT attenuation, vulnerable plaque characteristics identified by OCT, and poorer clinical outcomes.

Keywords: Clinical outcomes; Optical coherence tomography; Peri-coronary adipose tissue; Plaque vulnerability.

Fig. 1

Two representative images of PCAT attenuation differences between patients with and without MACE measured by CCTA. (A) A 57-year-old patient (male) with MACE, the PCAT attenuation was − 70HU. (B) A 42-year-old patient (male) without MACE, the PCAT attenuation was − 84HU. CCTA = coronary computed tomography angiography, HU = hounsfield unit, MACE = major adverse cardiovascular event, PCAT = peri-coronary adipose tissue.

Fig. 2

Representative OCT images are shown in Fig. 2. (A) Lipid plaque. (B) Calcified plaque. (C) TCFA. (D) Plaque rupture. (E) Plaque erosion. (F) NV. (G) Macrophages. (H) Red thrombus. TCFA = Thin-cap fibrous atherosclerotic, NV = Neovascularization.

Fig. 3

Flowchart showing the study design. CAG = Coronary Arteriography, CCTA = coronary computed tomography angiography, MACE = major adverse cardiac events, OCT = Optical coherence tomography, PCAT = peri-coronary adipose tissue.

Fig. 4

Differences on PCAT attenuation between optical coherence tomography plaque. (A). PCAT attenuation was significantly higher in patients with lipid plaque (+) than in those with lipid plaque (-). (B). PCAT attenuation was significantly higher in patients with Macrophages (+) than in those with Macrophages (-). (C). PCAT attenuation was significantly higher in patients with TCFA (+) than in those with TCFA (-). (D). PCAT attenuation showed no statistically significant difference between the two groups regarding red thrombus; however, there was an observable trend towards an increase in the incidence of red thrombus in the high attenuation group. Student’s t-test was applied to obtain P values. PCAT = peri-coronary adipose tissue, TCFA = thin-cap fibroatheroma.

Fig. 5

Kaplan-Meier curves for the primary outcome of major adverse cardiovascular events.