Inflammatory activity of pericoronary adipose tissue may affect plaque composition in patients with acute coronary syndrome without persistent ST-segment elevation: preliminary results

Abstract

The extravascular expression of inflammatory mediators may adversely influence coronary lesion formation and plaque stability through outside-to-inside signalling. It has been shown that the maximal standardised uptake value (SUV) of 18-fluorodeoxyglucose detected by positron emission tomography (PET/CT) is proportional to macrophage density. To investigate whether the inflammatory activity of pericoronary adipose tissue (PVAT) may influence plaque composition in acute coronary syndrome without persistent ST-segment elevation (NSTE-ACS) patients. In a prospective study, 36 coronary arteries (LM, RCA, LCX, LAD) were investigated in non-diabetic patients with a low or intermediate risk of NSTE-ACS (GRACE ≤ 140). SUV was measured in fat surrounding coronary arteries on the sections corresponding to proximal and medial segments (Siemens biograph 64-PET/CT system). Additionally, SUV was measured in subcutaneous fat (SC), visceral thoracic fat (VS), and epicardial fat over the right ventricle (EPI). Virtual histology intravascular ultrasound (VH-IVUS) was performed to assess plaque composition (Volcano, USA). PET/CT sections were further examined in segments corresponding to coronary plaques. PVAT SUV in NSTE-ACS patients was significantly greater than in other fat locations (LM SUV: 1.60; RCA SUV: 1.54; LCX SUV: 1.94; LAD SUV: 2.37 vs. 0.57; VS SUV: 0.77; EPI SUV: 0.98; p < 0.001; ANOVA). PVAT SUV positively correlated with plaque burden (r = 0.49, p < 0.05) and necrotic core plaque rate (r = 0.68, p < 0.05), and negatively correlated with fibrous plaque rate (r = -0.52, p < 0.05). The inflammatory activity of PVAT reflected by SUV is greater than in subcutaneous, visceral thoracic, or epicardial tissue in NSTE-ACS patients; PVAT SUV correlates with the plaque burden and necrotic core component of coronary plaque.