The Relation of Epicardial Adipose Tissue and Cardiovascular Disease in HIV-Positive and HIV-Negative Patients: The Liverpool HIV-Heart Project

Aims: We sought to assess and compare the association of epicardial adipose tissue (EAT) with cardiovascular disease (CVD) in HIV-positive and HIV-negative groups. Methods and Results: Using existing clinical databases we analysed 700 patients (195 HIV-positive, 505 HIV-negative). CVD was quantified by the presence of coronary calcification from both dedicated cardiac computed tomography (CT) and non-dedicated CT of the thorax. Epicardial adipose tissue (EAT) was quantified using dedicated software. The HIV-positive group had lower mean age (49.2 versus 57.8, p<0.005), higher proportion of male sex (75.9% versus 48.1%, p<0.005) and lower rates of coronary calcification (29.2% versus 58.2%, p<0.005). Mean EAT volume was also lower in the HIV-positive group (68mm3 versus 118.3mm3, p<0.005). Multiple linear regression demonstrated EAT volume was associated hepatosteatosis (HS) in the HIV-positive group but no the HIV-negative group after adjustment for BMI (p<0.005 versus p=0.066). In the multivariate analysis, after adjustment for CVD risk factors, age, sex, statin use and body mass index (BMI), EAT volume and hepatosteatosis were significantly associated with coronary calcification (odds ratio [OR] 1.14, p<0.005 and OR 3.17, p<0.005 respectively). In the HIV-negative group the only significant association with EAT volume after adjustment was total cholesterol (OR 0.75, p=0.012). Conclusions: We demonstrated a strong and significant independent association of EAT volume and coronary calcium, after adjustment, in HIV-positive group but not in the HIV-negative group. This result hints at differences in the mechanistic drivers of atherosclerosis between HIV-positive and HIV-negative groups. Funding Information: No funding was given for this research. Declaration of Interests: T.H.: received speaking fees from Merck Sharp & Dohme and Gilead and received investigator-sponsored research grant from Gilead Sciences S.M.: received speaking fees from Gilead Sciences; G.L.: consultant and speaker for BMS/P!zer, Boehringer Ingelheim, and Daiichi-Sankyo. No fees received personally. DD: NIH/NHLBI grant 1R01HL133616. S.K.: received grants from Gilead Sciences, Merck Sharp & Dohme, and Janssen and received grants and speaking fees from ViiV Healthcare. The remaining authors have no funding or conflicts of interest to disclose Ethics Approval Statement: The project was approved by the Liverpool University Hospital Foundation Trust audit committee. Ethical approval was not sought as this data is purely retrospective and exists in clinical databases.