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To characterize diet quality across a global cohort of people with HIV (PWH).Cross-sectional analysis.Leveraging REPRIEVE data from baseline across five Global Burden of Disease (GBD) regions, we analyzed participant responses to the Rapid Eating Assessment for Participants questionnaire. An overall diet quality score and scores for specific diet components were generated. Higher scores indicate better diet quality.Among 7736 participants (median age 50 years, 30% women, median BMI 25.8 kg/m 2 ) overall diet quality score (max score 30) was optimal in 13% of participants and good, suboptimal or poor in 45%, 38%, and 4% of participants, respectively; saturated fat score (max score 18) was good, suboptimal, or poor in 38%, 40%, or 7% of participants, respectively. Diet quality scores differed across GBD region with the highest scores reported in the South Asia region [median 23 (21-25)] and lowest in the sub-Saharan Africa region [median 15 (12-18)]; 61% of participants in the South Asia region reported optimal diet quality compared with only 6% in the sub-Saharan Africa region. Higher atherosclerotic cardiovascular risk scores were seen with worsening diet quality.Among PWH eligible for primary CVD prevention, diet quality was suboptimal or poor for almost half of participants, and there were substantial variations in diet quality reported by GBD region.NCT02344290.

OBJECTIVE To investigate the association of mild renal impairment and coronary plaque in people living with HIV (PLHIV). METHODS PLHIV and non-HIV controls with serum creatinine less than 1.5 mg/dl were investigated. Estimated glomerular filtration rate (eGFR) (calculated by CKD-EPI formula) was related to coronary plaque indices obtained by CT angiography. RESULTS One hundred and eighty-four PLHIV [HIV viral load, 49 (47,49) copies/ml, CD4+ cell count, median 536 (370, 770) cells/μl, duration HIV, 15 ± 7 years] and 72 HIV-negative controls without known cardiovascular disease (CVD) were studied. The two groups were well matched for traditional CVD risk factors. Serum creatinine (0.9 ± 0.2 vs. 0.9 ± 0.2 mg/dl, P = 0.96) and eGFR (96 ± 22 vs. 96 ± 24 ml/min per 1.73 m(2), P = 0.99) were similar between PLHIV and non-HIV, respectively. In PLHIV, eGFR inversely related to total severity of coronary plaque score (r = -0.27, P = 0.002), total coronary segments with plaque (r = -0.21, P = 0.005), calcified plaque segments (r = -0.15, P = 0.045), and Agatston score (r = -0.21, P = 0.006). Adjusting for total Framingham point score, BMI, and HIV parameters, eGFR remained significantly associated with calcified plaque and Agatston score in PLHIV. In HIV negative controls, eGFR did not correlate with calcified plaque (r = -0.20, P = 0.10) or Agatston score (r = -0.13, P = 0.29). Among PLHIV, those with eGFR less than 90 ml/min per 1.73 m(2) demonstrated increased total severity of coronary plaque score compared with those with eGFR greater than or equal to 90, P = 0.02). This relationship was stronger in PLHIV than the non-HIV group. CONCLUSION Our data highlight a robust relationship between subclinical renal impairment and coronary artery disease among PLHIV. Further research is needed to understand the relationship between mild renal impairment and CVD in HIV.

OBJECTIVE Persons living with HIV (PLWH) well treated on antiretroviral therapies remain at risk for ensuing arterial disease. We investigated the relationship between adipose depots and biomarkers of arterial injury and inflammation to gain insight into the link between body composition and CVD risk. DESIGNS/METHODS One hundred and fifty-five HIV-infected and 70 non-HIV infected individuals were well phenotyped for body composition. Adipose depots were assessed via single-slice abdominal computed tomography (CT). Circulating markers of arterial disease and generalized inflammation [lipoprotein-associated phospholipase A2 (LpPLA2), oxidized low-density lipoprotein (oxLDL), high-sensitivity cardiac troponin T (hs-cTnT), high-sensitivity C-reactive protein (hsCRP)] were evaluated. RESULTS Despite similar BMI and visceral adipose tissue (VAT), HIV-infected individuals had significantly lower subcutaneous adipose tissue [SAT, 199 (126-288) vs. 239 (148-358) cm(2), P = 0.04] than non-HIV infected individuals. Among HIV-infected individuals, reduced SAT inversely correlated with LpPLA2 (ρ = -0.19, P = 0.02) and hs-cTnT (ρ = -0.24, P = 0.004), whereas increased VAT significantly and positively related to LpPLA2 (ρ = 0.25, P = 0.003), oxLDL (ρ = 0.28, P = 0.0005), hs-cTnT (ρ = 0.28, P = 0.0007) and hsCRP (ρ = 0.32, P =

OBJECTIVE: Monocyte/macrophage activation is increased among people with HIV, and may contribute to the heightened risk of atherosclerosis and neurocognitive dysfunction in this population. Insulin-like growth factor 1 (IGF-1) has been shown to attenuate the innate immune response in animal models of atherosclerosis and inflammatory bowel disease. We investigated for the first time relationships of circulating IGF-1 with monocyte/macrophage-specific indices among HIV-infected individuals and uninfected controls. DESIGN: Observational. METHODS: 131 HIV-infected subjects and 65 well-matched controls without known cardiac disease or viral hepatitis were recruited previously. IGF-1, expressed as a z-score relative to the age- and sex-adjusted population mean, was related to log-transformed inflammatory markers within HIV and non-HIV groups. RESULTS: In HIV, IGF-1 inversely related to sCD163 (r = −0.28, P = 0.002), sCD14 (r = −0.29, P = 0.002), and high-sensitivity IL-6 (r = −0.27, P = 0.006). There was no association of IGF-1 with high-sensitivity CRP, MCP-1, IL-18, or LPS in HIV, or between IGF-1 and any inflammatory marker in controls. Relationships of IGF-1 with sCD163 and sCD14 remained significant in HIV after controlling for age, sex, smoking, body mass index, visceral fat, statin use, viral load, and antiretroviral therapy. For every 1-unit decline in IGF-1 z-score, sCD163 and sCD14 increased by 14% (95% CI, 0.23%, 29%) and 29% (95% CI, 1.4%, 63%), respectively. CONCLUSIONS: Low IGF-1 was robustly associated with high sCD163 and sCD14 in HIV. Prospective studies are needed to investigate augmentation of IGF-1 as a novel strategy to reduce monocyte/macrophage activation in this population.

The well treated HIV population remains at risk for insulin resistance and chronic immune activation. We tested the effects of acute hyperinsulinemia on inflammation in HIV. Twenty HIV-infected and 10 non-HIV-infected individuals well matched for BMI underwent oral glucose tolerance testing to stimulate insulin secretion and assess for changes in circulating soluble CD163, soluble CD14, and monocyte chemoattract protein 1. Soluble CD14 decreased significantly after stimulation of hyperinsulinemia and no significant changes in soluble CD163 or monocyte chemoattract protein 1 were demonstrated in HIV-infected and non-HIV-infected groups.

OBJECTIVE Circulating oxidized low-density lipoprotein (oxLDL) levels are elevated in HIV-infected patients and have been associated with atherosclerosis. Statins have been shown to reduce plaque on coronary computed tomography angiography (cCTA) in HIV-infected individuals. Thus, we investigated the effect of statins on serum oxLDL levels and the relationship between changes in oxLDL and coronary atherosclerosis on cCTA in patients with HIV. DESIGN We previously conducted a 12-month randomized, placebo-controlled trial with atorvastatin in 40 HIV-infected patients on stable antiretroviral therapy with subclinical coronary atherosclerosis and low-density lipoprotein (LDL)-cholesterol less than 130 mg/dl. METHODS In the current analysis, patients underwent cCTA and measurements of serum oxLDL, sCD14, sCD163, lipoprotein phospholipase-A2, and fasting lipids at baseline and end of the study. RESULTS Nineteen patients were randomized to atorvastatin and 21 patients to placebo. Serum oxLDL decreased -22.7% (95% CI -28.7 to -16.7) in the atorvastatin group and increased 7.5% (95% CI -3.3 to 18.4) in the placebo group (P < 0.0001). Change in oxLDL significantly correlated with changes in noncalcified plaque volume, total plaque volume, positively remodeled plaque, and low attenuation plaque. The association between changes in oxLDL and noncalcified plaque volume was independent of the baseline 10-year Framingham risk, LDL, CD4 cell count, and viral load. CONCLUSION Statins lower oxLDL levels in HIV-infected patients, and reductions in oxLDL are related to improvements in coronary atherosclerosis, independent of traditional cardiovascular risk factors. Reductions in oxLDL may be one mechanism through which statins exert beneficial effects on reducing atherosclerosis in HIV-infected individuals.

Objective Some intestinal microbiota-generated metabolites of phosphatidylcholine are recognized to be proatherogenic. As the HIV population is vulnerable to cardiovascular disease and can develop intestinal dysbiosis associated with systemic inflammation, we investigated the novel relationship between microbiota-derived metabolites of phosphatidylcholine and coronary atherosclerosis in HIV. Design/methods One hundred and fifty-five HIV-infected and 67 non-HIV-infected individuals without known history of cardiovascular disease were previously recruited to assess coronary plaque by computed tomography angiography. In the current study, we evaluate whether serum choline, trimethylamine (TMA), or trimethylamine-N-oxide (TMAO) levels are associated with plaque features. Results Young, asymptomatic HIV-infected patients (age 47 ± 7 years) demonstrated significantly higher prevalence of plaque (53 vs. 35%, P = 0.01) and number of total plaque segments (1.8 ± 2.5 vs. 1.2 ± 2.2, P = 0.03) when compared with well matched noninfected individuals with similar comorbidities. TMA was significantly associated with calcium score (r = 0.22, P = 0.006), number of total (r = 0.20, P = 0.02) and calcified (r = 0.18, P = 0.03) plaque segments, and calcium plaque volume (r = 0.19, P = 0.02) and mass (r = 0.22, P = 0.009) in the HIV cohort only. In multivariate modeling among HIV-infected patients, TMA remained significantly associated with calcium score (P = 0.008), number of total (P = 0.005) and calcified (P = 0.02) plaque segments, and calcium plaque volume (P = 0.01) and mass (P = 0.007), independent of Framingham risk score. In contrast, there was no association of TMAO to coronary plaque features in either cohort. Conclusion A link between TMA and atherosclerosis has not previously been established. The current study suggests that TMA may be a nontraditional risk factor related to the number of plaque segments and severity of calcified plaque burden in HIV.

Background The 2013 American College of Cardiology/American Heart Association (ACC/AHA) cholesterol guidelines are being applied to HIV-infected patients but have not been validated in this at-risk population, which is known to have a high prevalence of subclinical high-risk morphology (HRM) coronary atherosclerotic plaque. Objective To compare recommendations for statins among HIV-infected subjects with/without HRM coronary plaque according to 2013 ACC/AHA versus 2004 Adult Treatment Panel III guidelines. Methods/design Data from 108 HIV-infected subjects without known cardiovascular disease (CVD) or lipid-lowering treatment who underwent contrast-enhanced computed tomography angiography were analyzed. Recommendations for statin therapy according to 2013 versus 2004 guidelines were assessed among those with/without HRM coronary plaque. Results Among all subjects, 10-year atherosclerotic cardiovascular disease (ASCVD) risk score was 3.3% (1.6, 6.6), yet 36% of subjects had HRM coronary plaque. Among those with HRM coronary plaque, statins would be recommended for 26% by 2013 guidelines versus 10% by 2004 guidelines (P = 0.04). Conversely, among those without HRM coronary plaque, statins would be recommended for 19% by 2013 guidelines versus 7% by 2004 guidelines (P = 0.005). In multivariate modeling, while 10-year ASCVD risk score related to HRM coronary plaque burden (P = 0.02), so too did other factors not incorporated into 2013 guidelines. Conclusion The 2013 ACC/AHA cholesterol guidelines recommend statin therapy for a higher percentage of subjects with and without HRM coronary plaque relative to 2004 guidelines. However, even by 2013 guidelines, statin therapy would not be recommended for the majority (74%) of HIV-infected subjects with subclinical HRM coronary plaque. Outcome studies are needed to determine the utility of new statin recommendations and the contribution of HRM coronary plaque to CVD events among HIV-infected subjects.

OBJECTIVES To investigate the effects of aging and smoking on carotid intima-media thickness (cIMT) among patients with and without HIV. METHODS Data from a community sample of HIV-infected and HIV-uninfected participants were analyzed. Carotid intima-media thickness was measured via carotid ultrasound and smoking history was obtained via patient interview. RESULTS Data on 166 male and female participants with stable HIV-infection and 152 healthy HIV-uninfected participants were analyzed. Among the HIV-infected and HIV-uninfected participants, a significant association was observed between age and cIMT [r = 0.51, P < 0.0001 (HIV), r = 0.39, P < 0.0001, (non-HIV)], and between smoking burden and cIMT [r = 0.42, P < 0.0001 (HIV), r = 0.24, P = 0.003 (non-HIV)]. In multivariate regression modeling among all participants (HIV and non-HIV), a significant three-way interaction was observed between age, smoking burden, and HIV status with respect to cIMT (P < 0.010), controlling for sex, race, and traditional cardiovascular disease (CVD) risk factors, such that increased cIMT was associated with increased smoking burden and age to a greater degree among HIV-infected vs. HIV-uninfected participants. Among HIV-infected participants a significant interaction between smoking burden and age with respect to cIMT was seen (P = 0.027) controlling for race, sex, CVD risk factors, immunological function, and antiretroviral therapy use. CONCLUSION A significant interaction between HIV, age, and smoking on cIMT was observed, suggesting that HIV-infection modifies the relationship of age and smoking on cIMT in this population. These findings emphasize the need to encourage smoking cessation in this population, due to its deleterious effect on subclinical atherosclerosis in older HIV-infected patients.

HIV-1 elite controllers spontaneously maintain suppressed levels of viremia, but exhibit significant immune activation. We investigated coronary atherosclerosis by coronary computed tomography angiography (CTA) in elite controllers, nonelite controller, chronically HIV-1 infected, antiretroviral therapy (ART)-treated patients with undetectable viral load ('chronic HIV'), and HIV-negative controls. Prevalence of atherosclerosis (78 vs. 42%, P < 0.05) and markers of immune activation were increased in elite controllers compared with HIV-negative controls. sCD163, a monocyte activation marker, was increased in elite controllers compared with chronic HIV-1 (P < 0.05) and compared with HIV-negative controls (P < 0.05). These data suggest a significant degree of coronary atherosclerosis and monocyte activation among elite controllers.

Objective To evaluate dietary intake and its relationship to lipid parameters in HIV-infected patients with metabolic abnormalities. Method We prospectively determined dietary intake (4-day food records or 24-h recall) in 356 HIV-infected patients and 162 community-derived HIV-negative controls evaluated for metabolic studies between 1998-2005. Differences in dietary intake between HIV-infected patients and non-HIV-infected controls, in relation to the established 2005 USDA (United States Department of Agriculture) Recommended Dietary Guidelines, were determined. The relationship between dietary fat intake and serum lipid levels among HIV-infected individuals was also evaluated. Results Assessment of dietary intake in this group of HIV-infected patients demonstrated increased intake of total dietary fat (P 10%/day) (76.0% HIV vs. 60.9% controls, P = 0.003), and cholesterol (> 300 mg/day) (49.7% HIV vs. 37.9% controls, P = 0.04). Saturated fat intake was strongly associated with triglyceride level [triglyceride level increased 8.7 mg/dl (parameter estimate) per gram of increased saturated fat intake, P = 0.005] whereas total fat was inversely associated with triglyceride level [triglyceride level decreased 3.0 mg/dl (parameter estimate) per gram of increased total fat intake, P = 0.02] among HIV-infected individuals. Conclusions Increased intake of saturated fat is seen and contributes to hypertriglyceridemia among HIV-infected patients who have developed metabolic abnormalities. Increased saturated fat intake should be targeted for dietary modification in this population.

Objective: A large percentage of HIV-infected patients receiving highly active antiretroviral therapy demonstrate the metabolic syndrome. In this study, we sought to determine whether lifestyle modification improves metabolic syndrome criteria, including waist circumference, blood pressure, fasting blood sugar, triglycerides, and HDL among HIV-infected patients with the metabolic syndrome. Design: We conducted a randomized, 6-month study in HIVinfected patients with metabolic syndrome as defined by the National Cholesterol Education Program (NCEP). Subjects were randomized to an intensive lifestyle modification program modelled after the Diabetes Prevention Program, which included weekly one-on-one counseling sessions with a registered dietician, or observation (control group). Methods: Metabolic syndrome criteria and cardiovascular parameters including blood pressure, body composition, sub-maximal stress testing, lipids, hemoglobin A1C and other biochemical parameters were determined. Results: Thirty-four patients were randomized and 28 subjects completed the study. Compared to the control group, subjects randomized to the lifestyle modification program demonstrated significant decreases in waist circumference (-2.6 ±1.1 versus 1.2 ±1.0 cm, P=0.022), systolic blood pressure (-13 ±4 versus 4 ±4 mmHg, P=0.008), HgbA1C (-0.1 ±0.1 versus 0.2 ±0.1%, P=0.017), lipodystrophy score (-1.2 ±0.3 versus 0.9 ±0.6, P=0.006) and increased activity (17.7 ±14.3 METS versus -33.1 ±12.7 METS, P=0.014) as measured by the Modifiable Activity Questionnaire, but lipid levels did not improve. Conclusions: These data demonstrate that intensive lifestyle modification significantly improved important cardiovascular risk indices in HIV-infected patients with the metabolic syndrome. Lifestyle modification may be a useful strategy to decrease cardiovascular risk in this population.

OBJECTIVE To investigate differences in subclinical coronary atherosclerotic plaque and markers of immune activation among HIV-infected and non-HIV-infected women categorized by degree of ovarian reserve and menopause status. DESIGN Cross-sectional evaluation. METHODS Seventy-four women (49 HIV-infected, 25 non-HIV-infected) without known cardiovascular disease (CVD) were classified as premenopausal, premenopausal with reduced ovarian reserve, or postmenopausal based on menstrual history and anti-Mullerian hormone (AMH) levels. Participants underwent contrast-enhanced coronary computed tomography angiography and immune phenotyping. Comparisons in coronary atherosclerotic plaque burden and immune markers were made between the HIV-infected and non-HIV-infected women overall and within the HIV-infected and non-HIV-infected women by reproductive classification group. RESULTS Among the overall group of HIV-infected women, the women with reduced ovarian reserve (undetectable AMH) had a higher prevalence of coronary atherosclerotic plaque (52 versus 6%, P = 0.0007) and noncalcified plaque (48 versus 6%, P = 0.002), as well as higher levels of log sCD163 (P = 0.0004) and log MCP-1 (P = 0.006), compared with the premenopausal women with measurable AMH. Furthermore, reduced ovarian reserve in the HIV-infected group related to noncalcified plaque, controlling for traditional CVD risk factors (P = 0.04) and sCD163 (P = 0.03). CONCLUSION HIV-infected women with reduced ovarian reserve have increased subclinical coronary atherosclerotic plaque compared with premenopausal women in whom AMH is measurable. This relationship holds when controlling for CVD risk factors (including age) and immune activation. Our findings demonstrate that reduced ovarian reserve may contribute to CVD burden in HIV-infected women and support a comprehensive assessment of CVD risk prior to completion of menopause in this population.