Visceral adiposity (VA) is a form of ectopic fat deposition that correlates with cardiometabolic risk in both the general population and among people with human immunodeficiency virus (HIV) (PWH).1 Excess VA (EVA) is prevalent among PWH,2,3 and prevalence rises with age and time on antiretroviral treatment.3 Effective plasma virologic suppression is not protective against EVA and associated comorbidities, possibly due to adverse metabolic effects of certain antiretroviral agents, the low-level expression of HIV gene products within the adipose tissue, and other factos.4~Although EVA has been reported to occur in nearly half of PWH on antiretroviral therapy (ART),2,3 it may go unrecognized or be mischaracterized as generalized obesity. Whereas obesity and EVA both increase waist circumference (WC), they differ in that overweight and obese individuals accumulate fat primarily in subcutaneous depots, whereas individuals with EVA accumulate fat within the abdominal cavity. Ectopic fat accumulation (EFA) also occurs at various other depots, namely around and within various internal organs (e.g., the heart, skeletal muscle, liver, and pancreas).1,5 For purposes of the VAMOS study, EFA is defined as the amount of pericardial fat, skeletal muscle fat, and liver fat the VAMOS study subjects have. VA for the VAMOS study is held separately as it is the primary endpoint.~Because it represents a potentially modifiable cardiovascular risk factor among PWH, simple, practical surrogate markers are needed to identify patients with probable EVA. Anthropometric measurements such as WC correlate with EVA in the general population1, but their predictive value is less well defined for subgroups of PWH.
The Visceral Adiposity Measurement and Observation Study