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Excess Epicardial Fat Tied to Noncalcified Plaque in Women With HIV
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Conference on Retroviruses and Opportunistic Infections (CROI), February 13-16, 2017, Seattle
Mark Mascolini
Analysis of 82 women with and without HIV linked excess epicardial fat to immune activation, arterial inflammation, and noncalcified plaque in the HIV group [1]. The study did not tie excess epicardial fat to traditional cardiovascular risk factors.
[Epicardial fat (EF) is a visceral fat deposit, located between the heart and the pericardium, which shares many of the pathophysiological properties of other visceral fat deposits, It also potentially causes local inflammation and likely has direct effects on coronary atherosclerosis....https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998169/]
Researchers from Massachusetts General Hospital and other centers noted that reasons for higher myocardial infarction risk in women with HIV remain unclear. A potential contributing factor may be epicardial adipose tissue (EAT), which sits in the pericardial sac and shares a blood supply with the coronary arteries it surrounds. The researchers proposed that cytokines secreted by EAT may increase arterial inflammation and accelerate atherogenesis.
To address these issues, the investigators measured EAT volume in HIV-positive and negative women without known cardiovascular disease who had undergone cardiac computed tomography angiography (CCTA). The analysis involved 55 women with HIV and 27 age-matched HIV-negative women. All women were between 18 and 60 years old, and the HIV group had taken a stable antiretroviral regimen for at least 3 months. All study participants had fasting samples drawn to measure metabolic, inflammatory, immune activation, and cardiac markers.
The HIV and non-HIV groups did not differ significantly in average age (47 years in both groups), proportions of whites (33% and 37%) or current smokers (49% and 56%), or proportions with hypertension, abnormal lipids, current statin use, or diabetes. The HIV-negative group had a higher proportion with a family history of coronary heart disease (42% versus 20%, P = 0.04). Blood pressure, glucose, cholesterol, triglycerides, body mass index, and visceral and subcutaneous adipose tissue were similar in the HIV-positive and negative groups, as was EAT volume (54 and 65 cm(3), P = 0.31). The HIV group had been diagnosed for an average 15 years, 98% were taking antiretrovirals, current CD4 count averaged 599, and current viral load lay below 100 copies.
Markers of monocyte activation and arterial inflammation were highest in HIV-positive women with excess EAT when compared with HIV-positive women without excess EAT and to HIV-negative women with or without excess EAT. For example, for log-transformed sCD163, an activation marker, levels averaged 3.24 ng/mL in HIV-positive women above the median EAT, 3.14 ng/mL in HIV-positive women below the median EAT, 3.12 ng/mL in HIV-negative women above the median EAT, and 2.93 ng/mL in HIV-negative women below the median EAT (P = 0.004).
Proportions of women with detectable coronary plaque did not differ significantly across those four groups. But HIV-positive women above the median EAT had the highest proportion of arterial segments with dangerous noncalcified coronary plaque (78% versus 71% in the other HIV group, 19% in the HIV-negative group above the median EAT, and 33% in the non-HIV group below the median EAT, P = 0.009).
Among women with HIV, EAT was not associated with traditional cardiovascular risk factors but was associated with several HIV-specific variables, including duration of nucleoside use (r = 0.27, P = 0.045) and visceral adipose tissue (r = 0.58, P < 0.0001). In a multivariate model adjusted for age and nucleoside duration, visceral adipose tissue remained an independent predictor of EAT in women with HIV (beta estimate = 0.2527, P = 0.0002).
The researchers conclude that excess EAT is associated with immune activation, arterial inflammation, and noncalcified plaque in women with HIV. They propose that "future treatment strategies aimed at reducing ectopic fat among HIV-infected women may have potential to dampen systemic immune activation and favorably influence plaque morphology."
[ectopic fat. Ectopic means "not where it's supposed to be". It accumulates in the abdominal region (beer belly), the liver, muscle tissue including the heart, the pancreas, and perhaps in lipid-rich deposits in the arteries.Dec 7, 2008....subcutaneous fat (or peripheral fat). It accumulates right under the skin and is evenly distributed over the body's surface area, including extremities. The second is called ectopic fat. Ectopic means "not where it's supposed to be". It accumulates in the abdominal region (beer belly), the liver, muscle tissue including the heart, the pancreas, and perhaps in lipid-rich deposits in the arteries. Subcutaneous fat can be measured by taking skinfold thickness in different places on the body, or sometimes by measuring arm or leg circumference. Ectopic fat can be measured by taking waist circumference. http://wholehealthsource.blogspot.com/2008/12/peripheral-vs-ectopic-fat.html]
Reference
1. Srinivasa S, Lu M, Fitch KV, et al. Epicardial fat, immune activation, and coronary plaque among HIV+ and HIV- women. Conference on Retroviruses and Opportunistic Infections (CROI), February 13-16, 2017, Seattle. Abstract 627.
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