Epicardial adipose tissue and atherogenesis: EAT your heart out.

Cardiovascular disease (CVD) is increasingly recognized among HIV-infected patients, and carefully performed cohort studies show increased relative risk ratios of 1.5–2.0 [1,2]. Moreover, these studies suggest that traditional risk factors, while accounting for some degree of this increase in relative risk, do not account for all or even a major portion of the increased risk [1]. Insights into the mechanisms of this disease have been forthcoming from imaging studies, in which increased noncalcified plaque has been shown among HIV-infected men and also in HIV-infected women compared with age and BMI-matched controls [3,4]. This observation is significant because noncalcified plaque may be more vulnerable and prone to rupture. In contrast, although calcium score is itself a marker for increased CVD risk, it may represent a process by which plaque becomes more fibrotic and mechanically more stable, and thus, less prone to rupture. Recent studies assessing detailed measures of plaque morphology take these observations one step further and suggest that HIV-infected patients (men in this instance), demonstrate increased features of high-risk morphology plaque, including positive remodeling and low attenuation, fatty lesions [5]. In prior studies, traditional risk factors, such as age, hypertension, cholesterol and Framingham score, were shown to segregate more with calcified plaque, and non-traditional risk factors, such as increased immune activation indices (sCD163 and sCD14), with noncalcified plaque and high-risk morphology plaque [3,5]. Moreover, recent studies suggest increased arterial inflammation in HIVinfected patients, a reflection of macrophage infiltration,