Abstract 377: Inflammation in Peri-Coronary Adipose Tissue May Stimulate Atherosclerotic Leasions Formation in Patients With Stable Angina
Background: Extravascular expression of inflammatory mediators may adversely influence coronary lesions formation and plaque stability through outside-to-inside signaling. Additionally, maximal standardized uptake value (SUV) of fluorodeoxyglucose (FDG) detected by positron emission tomography is proportional to macrophage density. Accordingly, we examined peri-coronary adipose tissue (PAT) inflammatory activity using FDG-PET/CT in patients with stable coronary artery disease (CAD) and in controls.
Methods: 24 consecutive, non-diabetic patients with angiographicaly confirmed CAD underwent FDG-PET/CT. SUV was measured in subcutaneous fat (SC), visceral thoracic fat (VS), epicardial fat over right ventricle (EPI), and in fat surrounding three main coronary arteries on the sections corresponding to proximal segments (RCA, LCX, LAD, respectively). Similar measurements of SUV were taken in a group of healthy volunteers matched for age and BMI (n=13). In the group of CAD, associations of SUV with gender, age, body mass index (BMI), serum glucose, were further analyzed. Extent of CAD was determined by % stenosis in QCA (segments corresponding to PET/CT sections).
Results: The SUV surrounding coronary arteries (PAT SUV) was significantly greater than SUV in other fat locations for both CAD patients and controls. PAT SUV was significantly greater in CAD patients than in the controls (table⇓). PAT SUV was not related to gender, age, BMI, or serum glucose. Finally, PAT SUV was positively related to % stenosis of respective coronary artery (RCA: 0.38; p<0.02; LCX 0.60; p<0.0001; LAD 0.53; p<0.001).
Inflammatory activity of PAT is greater than in CS, VS, or EPI;
SUV in PAT is higher in CAD patients, than in non-CAD controls;
PAT SUV correlates with the extent of the disease.
In conclusion, the greater pro-inflammatory activity of PAT in patients with CAD compared to healthy controls may contribute to plaque formation, and vessel narrowing;