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Higher epicardial fat in older adults living with HIV with viral suppression and relationship with liver steatosis, coronary calcium and cardiometabolic risks
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Abstract
Objectives:
HIV infection is associated with ectopic fat deposition, which leads to chronic inflammation and cardiometabolic dysregulation. We assessed the epicardial adipose tissue (EAT) volume and its associated factors among people with HIV (PWH).
Design:
A cross-sectional study.
Methods:
We conducted a cross-sectional study among PWH aged at least 50 years and age-matched and sex-matched HIV-negative older individuals in Bangkok, Thailand. Participants underwent a noncontrast, cardiac computed tomography (CT) scan to assess coronary artery calcium (CAC) score and EAT between March 2016 and June 2017. Multivariate linear regression analyses were used to investigate HIV-related factors, cardiac and metabolic markers associated with EAT volume.
Results:
Median age was 55 years [interquartile range (IQR) 52-60] and 63% were men. Median duration of antiretroviral therapy (ART) was 16 years with 97% had HIV-1 RNA less than 50 copies/ml and median CD4+ cell count of 617 cells/μl. Median EAT volume was significantly higher in PWH [99 (IQR 75-122) cm3] than HIV-negative individuals [93 (IQR 69-117) cm3], P = 0.022. In adjusted model, factors associated with EAT volume included male sex (P = 0.045), older age (P < 0.001), abnormal waist circumference (P < 0.001) and HOMA-IR (P = 0.01). In addition, higher CAC score was independently associated with EAT volume. Higher mean EAT volume was seen in PWH with severe liver steatosis than those without steatosis (P = 0.018). In adjusted PWH-only model, duration of HIV was significantly associated with higher EAT volume (P = 0.028).
Conclusion:
In an aging cohort, PWH had higher EAT volume than HIV-negative controls. EAT was also independently associated with central fat accumulation, insulin resistance, liver steatosis and CAC score.
Epicardial adipose tissue (EAT) is located within the pericardial sac that surrounds the heart and it has the same arterial supply as the coronary arteries [6]. EAT has been shown to influence myocardial function and to be associated with atherosclerotic cardiovascular diseases [7]. Previous studies in HIV-negative population have suggested EAT was associated with cardiovascular risk factors including metabolic syndrome, insulin resistance [8] and sub-clinical coronary atherosclerosis markers, such as coronary calcium and plaque formation [9,10]. Moreover, recent studies have also described the associations of EAT volume with liver fibrosis and nonalcoholic fatty liver diseases [11,12], as epicardial fat and visceral fat share the same embryonic origin: brown fat [13].
A few studies have also described the association of EAT with metabolic parameters, immune activation and systemic inflammation in PWH population [14,15]. However, little is known regarding the EAT among elderly PWH who are on suppressive ART. Therefore, in this study, we investigated the EAT using cardiac computed tomography (CT) scans among PWH older than 50 years treated with a median of 16 years of ART, matched with HIV-negative individuals, and explored the factors associated with EAT volume, including liver-related parameters, such as liver fibrosis and steatosis.
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Association of epicardial fat with noncalcified coronary plaque volume and with low attenuation plaque in people with HIV
Abstract
Objectives:
People with HIV are exposed to a higher risk of coronary artery disease (CAD) compared with the general population. Epicardial fat may play a unique role in promoting coronary atherosclerosis. We measured epicardial fat in participants living with HIV and controls and investigated its association with coronary plaque volume and low attenuation plaque, a marker of plaque vulnerability.
Design:
This is a cross-sectional study, nested in the Canadian HIV and Aging Cohort Study, a large prospective cohort actively following participants with HIV and controls. Participants with low/intermediate cardiovascular risk without symptoms/history of CAD were invited to undergo cardiac computed tomography (CT).
Methods:
Volume of epicardial fat, coronary plaque and low attenuation component of the plaque were measured. Association between epicardial fat, coronary plaque volume and low attenuation component was tested using adjusted regression analysis.
Results:
A total of 169 participants with HIV and 81 controls underwent cardiac CT. Participants with HIV had a greater epicardial fat volume compared with controls (P = 0.019). In participants with HIV, epicardial fat volume was positively associated with duration of nonnucleoside reverse transcriptase inhibitors (NNRTI) (β=2.19, P = 0.004). After adjustment for cardiovascular risk factors, epicardial fat volume was positively associated to noncalcified plaque volume [odds ratio (OR) = 1.09, P = 0.028] and to the low-attenuation plaque component portion (β=0.38, P = 0.026).
Conclusion:
The association of epicardial fat volume to noncalcified plaque volume and to low attenuation component plaque may suggest a potential mechanism by which epicardial fat could be a silent driver of CAD in the HIV population.
Cardiovascular disease is one of the most important cause of death in people with HIV (PWH) receiving antiretroviral therapy (ART) [1,2]. An increased risk of coronary artery disease (CAD) in this population has been demonstrated in several large cohort studies [3-5]. More recently, studies using coronary computed tomography (CT) angiography (CCTA) have allowed noninvasive characterization of coronary atherosclerosis in PWH [6-9]. Most studies showed a higher prevalence of noncalcified coronary plaques as well as plaques with CT markers of vulnerability (high-risk plaques) in individuals with HIV compared with controls [6-9]. Noncalcified plaques and high-risk plaques have been associated with an increased risk of cardiovascular events [10,11]. Reasons for higher prevalence of high-risk plaques in HIV are still imprecise, although ART [12] and HIV infection itself may be involved.
People with HIV are known to experience changes in body fat distribution characterized by visceral fat accumulation [13,14]. Epicardial fat is the visceral fat of the heart, and ex-vivo and in-vivo studies suggest that this adipose tissue depot may play a unique role in CAD because of its proximity to the coronary arteries. Epicardial fat secretes active mediators in direct vicinity to the coronary arteries that are known to promote inflammation and atherosclerosis [15-18]. Recent studies have shown an association between epicardial fat and the presence and progression of coronary artery disease in the general population [19-22]. In PWH, studies have demonstrated an association between epicardial fat and coronary artery calcium score, noncalcified plaques and adverse cardiovascular events [23-25].
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