scholarly journals Aspartame Intake Relates to Coronary Plaque Burden and Inflammatory Indices in Human Immunodeficiency Virus

2017 ◽  
Vol 4 (2) ◽  
Author(s):  
Leangelo N. Hall ◽  
Laura R. Sanchez ◽  
Jane Hubbard ◽  
Hang Lee ◽  
Sara E. Looby ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cardiac Computed Tomography ◽  
Coronary Plaque ◽  
Plaque Burden ◽  
Artificial Sweetener ◽  
Food Record ◽  
Cvd Risk ◽  
Cardiac Computed Tomography Angiography ◽  
Markers Of Inflammation ◽  
Immunodeficiency Virus

Abstract Background Dietary sweeteners may contribute to metabolic dysregulation and cardiovascular disease (CVD), but this has not been assessed in human immunodeficiency virus (HIV). Methods One hundred twenty-four HIV-infected and 56 non-HIV-infected participants, without history of known coronary artery disease were included. Dietary intake was assessed using a 4-day food record. Coronary plaque was determined using cardiac computed tomography angiography. Results Human immunodeficiency virus-infected participants had significantly greater intake of dietary sweeteners, including total sugar (P = .03) and added sugar (P = .009); intake of aspartame (artificial sweetener) was greater among aspartame consumers with HIV versus non-HIV consumers (P = .03). Among HIV-infected participants, aspartame intake was significantly associated with coronary plaque (P = .002) and noncalcified plaque (P = .007) segments, as well as markers of inflammation/immune activation (monocyte chemoattractant protein 1 and lipoprotein-associated phospholipase A2), which may contribute to increased atherogenesis. In multivariable regression modeling, aspartame remained an independent predictor of plaque in HIV. In contrast, among non-HIV-infected participants, no sweetener type was shown to relate to plaque characteristics. Conclusions We demonstrate increased intake of dietary sweeteners and a potential novel association between aspartame intake, plaque burden, and inflammation in HIV. Our data suggest that aspartame may contribute to CVD risk in HIV. Further studies should address potential mechanisms by which aspartame may contribute to increased plaque burden and cardiovascular benefits of dietary strategies targeting aspartame intake in HIV.

scholarly journals Anatomic Fat Depots and Coronary Plaque Among Human Immunodeficiency Virus-Infected and Uninfected Men in the Multicenter AIDS Cohort Study

2016 ◽  
Vol 3 (2) ◽  
Author(s):  
Frank J. Palella ◽  
Rebeccah McKibben ◽  
Wendy S. Post ◽  
Xiuhong Li ◽  
Matthew Budoff ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Adipose Tissue ◽  
Coronary Plaque ◽  
Multicenter Aids Cohort Study ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Fat Depots ◽  
Immunodeficiency Virus ◽  
Hiv Serostatus ◽  
Subcutaneous Adipose

Abstract Methods.  In a cross-sectional substudy of the Multicenter AIDS Cohort Study, noncontrast cardiac computed tomography (CT) scanning for coronary artery calcium (CAC) scoring was performed on all men, and, for men with normal renal function, coronary CT angiography (CTA) was performed. Associations between fat depots (visceral adipose tissue [VAT], abdominal subcutaneous adipose tissue [aSAT], and thigh subcutaneous adipose tissue [tSAT]) with coronary plaque presence and extent were assessed with logistic and linear regression adjusted for age, race, cardiovascular disease (CVD) risk factors, body mass index (BMI), and human immunodeficiency virus (HIV) parameters. Results.  Among HIV-infected men (n = 597) but not HIV-uninfected men (n = 343), having greater VAT was positively associated with noncalcified plaque presence (odds ratio [OR] = 1.04, P < .05), with a significant interaction (P < .05) by HIV serostatus. Human immunodeficiency virus-infected men had lower median aSAT and tSAT and greater median VAT among men with BMI <25 and 25–29.9 kg/m2. Among HIV-infected men, VAT was positively associated with presence of coronary plaque on CTA after adjustment for CVD risk factors (OR = 1.04, P < .05), but not after additional adjustment for BMI. There was an inverse association between aSAT and extent of total plaque among HIV-infected men, but not among HIV-uninfected men. Lower tSAT was associated with greater CAC and total plaque score extent regardless of HIV serostatus. Conclusions.  The presence of greater amounts of VAT and lower SAT may contribute to increased risk for coronary artery disease among HIV-infected persons.

Coronary Inflammation Assessed by Perivascular Fat Attenuation Index in Patients with Psoriasis: A Propensity Score-Matched Study

Dermatology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Wenrui Bao ◽  
Min Yang ◽  
Zhihan Xu ◽  
Fuhua Yan ◽  
Qi Yang ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Coronary Plaque ◽  
Plaque Burden ◽  
Control Group ◽  
Low Grade ◽  
Cvd Risk ◽  
Control Subjects ◽  
Atherosclerotic Burden ◽  
Attenuation Index ◽  
Perivascular Fat

<b><i>Objectives:</i></b> This study aimed to evaluate coronary inflammation by measuring the perivascular fat attenuation index (FAI) and quantify the atherosclerosis burden in patients with psoriasis and control individuals without psoriasis based on coronary computed tomography angiography (CCTA) images. <b><i>Methods:</i></b> A total of 98 consecutive patients with psoriasis (76 male [77.6%], aged 56.5 years, range 45.5–65.0) were recruited, and 196 patients (157 male [80.1%]; aged 54.6 ± 14.1 years) without established cardiovascular disease (CVD) who underwent CCTA within the same period were enrolled in the control group. Coronary plaque burden was quantified using the computed tomography-adapted Leaman score (CT-LeSc), and the FAI surrounding the proximal of three main epicardial vessels was measured to represent coronary inflammation. <b><i>Results:</i></b> Patients with psoriasis and the control subjects were well matched in CVD risk factors (all <i>p</i> &#x3e; 0.05). Psoriasis patients had a greater overall CT-LeSc (5.86 vs. 4.69, <i>p</i> = 0.030) and lower perivascular FAI (−80.19 ± 7.48 vs. −78.14 ± 7.81 HU, <i>p</i> &#x3c; 0.001). A similar result was found upon comparing psoriasis patients without biological or statin therapy with non-psoriasis individuals without statin treatments. Furthermore, the psoriasis group had a higher prevalence of non-calcified plaques (30.3% in the psoriasis group vs. 20.1% in the control subjects, <i>p</i> = 0.001). No difference in perivascular FAI on either calcified and mixed plaques or non-calcified plaques between the two groups was found. <b><i>Conclusion:</i></b> Patients with psoriasis have a higher atherosclerotic burden as quantified by CT-LeSc and less coronary inflammation as detected by perivascular FAI around the most proximal of the three major epicardial vessels. The usefulness of perivascular FAI for evaluating coronary inflammation in patients with chronic low-grade inflammatory disease such as psoriasis should be verified.

scholarly journals Serum Albumin Is Associated With Higher Inflammation and Carotid Atherosclerosis in Treated Human Immunodeficiency Virus Infection

2018 ◽  
Vol 5 (11) ◽  
Author(s):  
Sahera Dirajlal-Fargo ◽  
Manjusha Kulkarni ◽  
Emily Bowman ◽  
Lingpeng Shan ◽  
Abdus Sattar ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Serum Albumin ◽  
Carotid Atherosclerosis ◽  
Ldl Cholesterol ◽  
Surrogate Marker ◽  
Density Lipoprotein ◽  
Mixed Effect ◽  
Baseline Serum ◽  
Markers Of Inflammation ◽  
Immunodeficiency Virus

Abstract Background This study was conducted to explore the associations between serum albumin and markers of inflammation and cardiovascular disease in treated human immunodeficiency virus (HIV)-infected adults. Methods We conducted a nested study within in the SATURN-HIV trial in which 147 HIV+ adults on stable antiretroviral therapy were (1) virally suppressed, (2) had a low-density lipoprotein (LDL)-cholesterol level &lt;130 mg/dL, and (3) were randomized to 10 mg daily rosuvastatin or placebo. Measures of serum albumin, carotid intima media thickness ([cIMT] surrogate marker of atherosclerosis), inflammation, T cells, monocyte activation, and gut integrity were assessed at baseline, 48 and 96 weeks later. Spearman correlations and linear mixed-effect models were used to assess associations with serum albumin. Results Mean age was 45 years, 80% of participants were male, and 69% were African American. Mean serum albumin was similar between the groups at all time points (4.01–4.09 g/dL in statin arm vs 4.02–4.11 g/dL in placebo arm; P = .08–0.35). Lower baseline serum albumin significantly predicted larger changes in cIMT, interleukin 6, D-dimer, tumor necrosis factor α receptor 1, fibrinogen, and high-sensitivity C-reactive protein (P ≤ .03) over 96 weeks independently of statin therapy. After adjusting for age, gender, smoking, body mass index, creatinine clearance, and LDL cholesterol, every 1 g/dL decrease in serum albumin at baseline remained associated with a 0.05-mm increase in cIMT over 96 weeks (P = .05). Conclusions Lower serum albumin in controlled HIV is associated with higher markers of chronic inflammation and hypercoagulation, which could explain the prior observation that serum albumin predicts nonacquired immune deficiency syndrome events in HIV. Serum albumin may predict progression of carotid atherosclerosis independent of traditional risk factors.

scholarly journals Leveraging a Landmark Trial of Primary Cardiovascular Disease Prevention in Human Immunodeficiency Virus: Introduction From the REPRIEVE Coprincipal Investigators

2020 ◽  
Vol 222 (Supplement_1) ◽  
pp. S1-S7 ◽  
Author(s):  
Steven K Grinspoon ◽  
Pamela S Douglas ◽  
Udo Hoffmann ◽  
Heather J Ribaudo
Keyword(s):  
Cardiovascular Disease ◽  
Human Immunodeficiency Virus ◽  
Disease Prevention ◽  
Gender Diversity ◽  
Coronary Plaque ◽  
Cardiovascular Disease Prevention ◽  
Population Characteristics ◽  
Vascular Events ◽  
Global Epidemic ◽  
Immunodeficiency Virus

Abstract The Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) is the largest study of cardiovascular disease in human immunodeficiency virus. Enrolling 7770 participants from 2015 to 2019 with sites across 5 continents, REPRIEVE will assess the effects of a statin as a cardiovascular disease prevention strategy in people with HIV (PWH) receiving antiretroviral therapy (ART). Although the primary purpose of REPRIEVE, and its substudy assessing coronary plaque, is to assess cardiovascular outcomes, the trial is a rich source of data on population characteristics and critical comorbidities in PWH, particularly across Global Burden of Disease (GBD) regions, reflective of the ethnic, racial, and gender diversity in this global epidemic. The purpose of this Supplement is to leverage the rich phenotyping in REPRIEVE, to provide data on detailed patterns of baseline ART and immune function by GBD region, reproductive aging among cisgender women, and data on the participation and clinical characteristics of transgender participants. We also leveraged REPRIEVE to assess critical comorbidities, including renal dysfunction, muscle function and frailty, and myocardial steatosis. REPRIEVE is a remarkable collaboration between funders, trial networks, clinical research sites, clinical and data coordinating centers, and willing participants who devoted their time to make the trial possible.

scholarly journals Impact of the American College of Cardiology/American Heart Association Cholesterol Guidelines on Statin Eligibility Among Human Immunodeficiency Virus-Infected Individuals

2018 ◽  
Vol 5 (12) ◽  
Author(s):  
Mosepele Mosepele ◽  
Susan Regan ◽  
Joseph Massaro ◽  
James B Meigs ◽  
Markella V Zanni ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Statin Therapy ◽  
American Heart Association ◽  
American Heart ◽  
Clinical Care ◽  
Heart Association ◽  
Cvd Risk ◽  
Immunodeficiency Virus ◽  
Statin Prescription ◽  
Cholesterol Guidelines

Abstract Background Individuals with human immunodeficiency virus (HIV) face elevated cardiovascular disease (CVD) risk. There are limited data regarding the application of the American College of Cardiology/American Heart Association (ACC/AHA) cholesterol guidelines in HIV compared with non-HIV patients. Methods Human immunodeficiency virus-infected and demographically similar control patients were assessed for statin recommendation status by ACC/AHA and the National Cholesterol Education Program Adult Treatment Program III (ATPIII), indication for statin recommendation, actual statin prescription, and CVD event. Outcomes were atherosclerotic CVD for ACC/AHA and coronary heart disease for ATPIII. Results In a clinical care cohort of 1394 patients infected with HIV, 38.6% (538 of 1394) of patients were recommended for statin therapy by the ACC/AHA guidelines compared with 20.1% (280 of 1394) by the ATPIII guidelines. Of those recommended for statin therapy, actual statin prescription rates were 42.8% (230 of 538) for ACC/AHA and 66.4% (186 of 280) for ATPIII. Among patients infected with HIV with an incident CVD event during follow-up, statin therapy was recommended for 59.2% (42 of 71) of patients by ACC/AHA and 35.2% (25 of 71) by ATPIII, versus 71.6% (141 of 197) by ACC/AHA and 43.1% (85 of 197) by ATPIII in the control group. Conclusions In an HIV clinical care cohort, the ACC/AHA cholesterol guidelines recommend a higher proportion of patients for statin therapy and identify an increased proportion of patients with a CVD event compared with ATPIII. However, 40% of patients with a CVD event would not have been recommended for statin therapy by ACC/AHA, compared with 29% for controls. This gap in identification of patients infected with HIV at high CVD risk underscores the need for HIV-specific cardiovascular prevention strategies.

Abstract 17992: Observed versus Predicted Myocardial Infarction Among Individuals With Human Immunodeficiency Virus by American College of Cardiology/American Heart Association Pooled Cohort Equation Risk Strata: Center for AIDS Research Network of Integrated Clinical Systems

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Matthew J Feinstein ◽  
Daniel R Drozd ◽  
Hongyan Ning ◽  
Joseph A Delaney ◽  
Robin Nance ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Human Immunodeficiency Virus ◽  
Risk Prediction ◽  
White Men ◽  
Cvd Risk ◽  
Immunodeficiency Virus ◽  
Ascvd Risk ◽  
Risk Estimator ◽  
Aids Research ◽  
Clinical Systems

Background: Human immunodeficiency virus (HIV)-infected individuals are at elevated risk for cardiovascular disease (CVD) due to an interplay between traditional CVD risk factors, chronic inflammation persisting despite HIV viral suppression, and side effects of antiretroviral therapy. Previous studies evaluating CVD risk prediction models in HIV populations have generally been small in size and assessed non-U.S. cohorts. The 2013 ACC/AHA ASCVD Risk Estimator has not been evaluated in a large, multi-center HIV cohort. Hypothesis: Our primary hypothesis was that the ACC/AHA ASCVD Risk Estimator would underestimate ASCVD risk across risk strata for HIV-infected patients. Methods: We evaluated this risk prediction tool in the Centers for AIDS Research (CFAR) Network of Integrated Clinical Systems (CNICS) multi-center U.S.-based cohort of approximately 30,000 HIV-infected adults with rigorous central adjudication of myocardial infarction (MI) and differentiation between type I and II MI. We compared MI and ASCVD risks predicted by the ASCVD Risk Estimator to actual rates of MI observed in the CNICS cohort. Results: A total of 132 MIs were observed during follow-up, compared with 103 MIs that would have been expected based on the ASCVD risk estimator. Observed MI rates were higher than expected across most predicted risk levels, particularly among black participants and those with low (<5%) predicted 10-year ASCVD risk. This under-prediction was relatively uniform across risk strata among white men; the observed MI rates were 68%, 68%, 67%, and 67% greater than expected, respectively, for white men with <5%, 5% to <7.5%, 7.5% to <10%, and 10% or greater predicted 10-year ASCVD risk. Conclusions: These data suggest that the ACC/AHA Risk Estimator under-predicts MI risk among HIV-infected individuals. The under-prediction was relatively uniform across risk strata for white men. These data highlight the need for accurate HIV-specific CVD risk prediction tools.

scholarly journals Clinical Outcomes and Immunologic Characteristics of Coronavirus Disease 2019 in People With Human Immunodeficiency Virus

2020 ◽  
Author(s):  
Hsi-en Ho ◽  
Michael J Peluso ◽  
Colton Margus ◽  
Joao Pedro Matias Lopes ◽  
Chen He ◽  
...  
Keyword(s):  
At Risk ◽  
Human Immunodeficiency Virus ◽  
Inflammatory Markers ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Markers Of Inflammation ◽  
Cell Counts ◽  
Immunodeficiency Virus ◽  
Factor Α ◽  
Necrosis Factor

Abstract We performed a retrospective study of coronavirus disease 2019 (COVID-19) in people with human immunodeficiency virus (PWH). PWH with COVID-19 demonstrated severe lymphopenia and decreased CD4+ T cell counts. Levels of inflammatory markers, including C-reactive protein, fibrinogen, D-dimer, interleukin 6, interleukin 8, and tumor necrosis factor α were commonly elevated. In all, 19 of 72 hospitalized individuals (26.4%) died and 53 (73.6%) recovered. PWH who died had higher levels of inflammatory markers and more severe lymphopenia than those who recovered. These findings suggest that PWH remain at risk for severe manifestations of COVID-19 despite antiretroviral therapy and that those with increased markers of inflammation and immune dysregulation are at risk for worse outcomes.

Abstract P040: GlycA, a Novel Inflammatory Marker, and Subclinical Coronary Atherosclerosis in the Multicenter AIDS Cohort Study (MACS)

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Oluwaseun E Fashanu ◽  
Martin Tibuakuu ◽  
Di Zhao ◽  
James D Otvos ◽  
Todd T Brown ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Coronary Atherosclerosis ◽  
Inflammatory Marker ◽  
Prevalence Ratio ◽  
Coronary Plaque ◽  
Plaque Burden ◽  
Cvd Risk ◽  
Cross Sectional ◽  
Calcified Plaque ◽  
Mixed Plaque

Background: Inflammation may link HIV infection to cardiovascular disease (CVD). GlycA, a novel nuclear magnetic resonance (NMR) biomarker of systemic inflammation, has been associated with incident CVD events in the general population. The relation between GlycA and the presence, extent and composition of subclinical coronary plaque in men with HIV infection (HIV+) or at risk for HIV (HIV-) is unknown. Methods: This is a cross-sectional analysis of 935 men enrolled in MACS with plasma measurement of GlycA and non-contrast cardiac CT and/or coronary CT angiography. We used multivariable adjusted Poisson and linear regression to assess associations of GlycA with prevalent coronary atherosclerosis and plaque extent, respectively. Results: Mean ± SD age was 54 ± 7 yrs; 31% were black, and 63% HIV+ with 81% having undetectable viral load (VL). GlycA levels were higher in HIV+ compared to HIV- men (397 ± 68 vs 380 ± 60 μmol/L, p=0.0001), and higher for those with detectable VL vs. undetectable (413 ± 79 vs 393 ± 65 μmol/L, p=0.004). After adjusting for demographic and CVD risk factors, every 1 SD increment in GlycA was associated with an increased prevalence of coronary artery calcium (CAC>0) (prevalence ratio: 1.09, 95% CI: 1.03-1.15), coronary stenosis ≥ 50% (1.20, 1.02-1.41), and calcified plaque (1.12, 1.02-1.23); p for all < 0.03. These associations remained significant after adjusting for other inflammatory markers and did not differ by HIV status. Among men with plaque, GlycA was positively associated with the extent of CAC, total plaque and mixed plaque ( Table ). Associations were weaker in HIV+ men for total and mixed plaque (P interaction = 0.003 and 0.03, respectively). GlycA was not associated with non-calcified plaque. Conclusion: HIV+ men have higher levels of GlycA than HIV- men. Higher GlycA is positively and independently associated with subclinical coronary atherosclerosis. Whether modification of GlycA through lifestyle or pharmacotherapy can reduce coronary plaque burden and future CVD events requires further study.

scholarly journals Human Immunodeficiency Virus Is Associated With Higher Levels of Systemic Inflammation Among Kenyan Adults Despite Viral Suppression

2020 ◽  
Author(s):  
Sarah J Masyuko ◽  
Stephanie T Page ◽  
Stephen J Polyak ◽  
John Kinuthia ◽  
Alfred O Osoti ◽  
...  
Keyword(s):  
Risk Factors ◽  
Human Immunodeficiency Virus ◽  
Inflammatory Markers ◽  
Inflammatory Biomarkers ◽  
Hiv Status ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Hiv Negative

Abstract Background Systemic inflammation independently predicts future cardiovascular events and is associated with a 2-fold increase in cardiovascular disease (CVD) risk among persons living with human immunodeficiency virus (PLHIV). We examined the association between inflammatory markers, HIV status, and traditional CVD risk factors. Methods We conducted a cross-sectional study of Kenyan adults with and without HIV seeking care at Kisumu County Hospital. Using a multiplex immunoassay, we measured interleukin (IL) 1β, IL-6, tumor necrosis factor α (TNF-α), and high-sensitivity C-reactive protein (hsCRP) concentrations. We compared inflammatory marker concentrations by HIV status using the Wilcoxon rank-sum test. Multivariable linear regression was used to evaluate associations between inflammatory biomarkers and HIV status, adjusting for CVD risk factors. Results We enrolled 286 PLHIV and 277 HIV-negative participants. Median duration of antiretroviral therapy for PLHIV was 8 years (interquartile range, 4–10) and 96% were virally suppressed. PLHIV had a 51% higher mean IL-6 concentration (P &lt; .001), 39% higher mean IL-1β (P = .005), 40% higher mean TNF-α (P &lt; .001), and 27% higher mean hsCRP (P = .008) compared with HIV-negative participants, independent of CVD risk factors. Male sex, older age, and obesity were associated with higher concentrations of inflammatory markers. Restricting to PLHIV, viral load of ≥1000 copies/mL was associated with higher TNF-α levels (P = .013). Conclusions We found higher levels of systemic inflammatory biomarkers among PLHIV who were virally suppressed, and this was independent of traditional CVD risk factors. Further longitudinal analyses to determine whether these inflammatory markers predict future CVD events, and are possible therapeutic targets among PLHIV, are warranted.

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