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

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.