Epicardial and pericoronary fat volume and attenuation, lipid lowering therapy and coronary high risk coronary plaque burden. (3rd October 2022)

• Record Type: Journal Article
• Authors: Balcer, B; Ranjbar, N; Dykun, I; Schlosser, T; Rassaf, T; Mahabadi, A A
• Is Part Of: European heart journal. Volume 43(2022)Supplement 2
• Publication Date: 2022-10-03
• Subjects: Cardiology -- Periodicals; Heart -- Diseases -- Periodicals; 616.12005
• DOI: 10.1093/eurheartj/ehac544.211
• Languages: English
• ISSNs: 0195-668X

Abstract

Abstract: Background: Epicardial (EAT) and pericoronary adipose tissue (PCAT) are known as risk predictors of subclinical atherosclerosis and coronary artery disease. We aimed to evaluate the association of EAT and PCAT volume and attenuation with the presence of high risk coronary plaque burden in patients with vs. without lipid lowering therapy. Methods: In the present retrospective analysis a total of 321 patients undergoing coronary CTA at the XXX were included. EAT and PCAT were manually traced from CT imaging for assessment of fat volume and attenuation. According to the SCCT guidelines for the interpretation of coronary CTA, each coronary segment was evaluated for the presence of high risk plaque features (napkin ring sign, spotty calcification, positive remodeling, and low attenuation plaque). Results: Overall data from 321 patients (mean age: 55.5±14.7 years, 62% male) and a total of 5778 coronary segments were included in our analysis. The cohorts consists of 116 patients without plaque and stenosis, 96 patients with plaque but no significant stenosis and 109 patients with obstructive coronary stenosis. Highest rates of the presence of coronary plaque were detected in proximal LAD (17.9%), followed by mid LAD (12.9%) and proximal RCA (10.8%). Coronary stenosis was also most common in proximal LAD (14.6%), followed by mid LAD (12.1%) and proximal RCA (11%). High risk plaque features were found in 401 segments and were most frequently located in the proximal LAD (21.4%). EAT volume increased with higher rates of stenosis and plaque (44.7±25.2ml vs. 68, 2±28, 5ml vs. 85.2±31.7ml, p<0.001). Prevalence of high risk plaque increased by higher EAT volume (OR [95% CI]: 3.17 [2.33–4.33], p<0.0001) and remains stable after upon adjustment for risk factors (2.32 [1.46–3.7], p<0.0001). EAT attenuation also significantly associated with the presence of high risk plaques with 0.68-folded risk in the unadjusted (0.68 [0.53–0.88], p=0.003), and 0.62-folded risk in the multivariate (MV) adjusted regression analysis (0.62 [0.45–0.85], p=0.003). However, for PCAT only its volume but not its attenuation was significantly associated with presence of high risk plaques in MV-adjusted regression analysis (PCAT volume: 2.25 [1.02–4.96], p=0.044; PCAT attenuation: 0.84 [0.63–1.12], p=0.24). Furthermore, patients receiving lipid-lowering therapy showed a significantly lower probability for high risk plaque detection (0.17 [0.14–0.21], p<0.0001). These findings remained stable after multivariate adjustment (0.27 [0.21–0.35], p<0.0001). Conclusion: EAT volume and attenuation as well as PCAT volume associate with high risk plaques independent of traditional cardiovascular risk factors. In contrast, we found no significant association of PCAT attenuation with high risk coronary atherosclerosis. Our results encourage further research to evaluate the interplay of lipid-lowering therapy and EAT on plaque composition. Funding Acknowledgement: Type of funding sources: None.