Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Artery Atherosclerosis in HIV-Infected Women and Men

Hanna, David B.; Lin, Juan; Post, Wendy S.; Hodis, Howard N.; Xue, Xiaonan; Anastos, Kathryn; Cohen, Mardge H.; Gange, Stephen J.; Haberlen, Sabina; Heath, Sonya L.; Lazar, Jason; Liu, Chenglong; Mack, Wendy J.; Ofotokun, Igho; Palella, Frank J.; Tien, Phyllis C.; Witt, Mallory D.; Landay, Alan; Kingsley, Lawrence; Tracy, Russell P.; Kaplan, Robert C.

doi:10.1093/infdis/jix082

Cited by 94 publications

(70 citation statements)

References 49 publications

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“…This study supports previous work demonstrating elevated concentrations of inflammatory biomarkers among HIV controllers and LTNPs compared to HIV‐uninfected individuals . Levels of monocyte activation markers sCD163 and sCD14 have been associated with subclinical atherosclerosis in the MACS, WIHS and other cohorts . Despite elevated concentrations of sCD163 and sCD14 in HIV controllers and LTNPs compared to HIV‐uninfected individuals, we found similar prevalences of carotid and coronary subclinical atherosclerosis.…”

Section: Discussionmentioning

confidence: 98%

“…Inflammatory biomarker concentrations were collected for an ancillary study among 1281 individuals from MACS and WIHS who had serial carotid ultrasound scans . Characteristics of this cohort have been previously described . Biomarkers were chosen based on their established association with CVD risk .…”

Section: Methodsmentioning

confidence: 99%

“…Characteristics of this cohort have been previously described . Biomarkers were chosen based on their established association with CVD risk . Concentrations of soluble CD163 (sCD163), soluble CD14 (sCD14), interleukin‐6 (IL‐6), galectin‐3 (Gal‐3) and galectin‐3 binding protein (Gal‐3BP) were measured using ELISA in stored frozen sera collected at the core study visit closest to the vascular study visit.…”

Section: Methodsmentioning

confidence: 99%

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Subclinical cardiovascular disease in HIV controller and long‐term nonprogressor populations

et al. 2019

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Objectives Elite controllers (ECs), viraemic controllers (VCs), and long‐term nonprogressors (LTNPs) control HIV viral replication or maintain CD4 T‐cell counts without antiretroviral therapy, but may have increased cardiovascular disease (CVD) risk compared to HIV‐uninfected persons. We evaluated subclinical carotid and coronary atherosclerosis and inflammatory biomarker levels among HIV controllers, LTNPs and noncontrollers and HIV‐uninfected individuals in the Multicenter AIDS Cohort Study (MACS) and the Women’s Interagency HIV Study (WIHS). Methods We measured carotid plaque presence and common carotid artery intima‐media thickness (IMT) in 1729 women and 1308 men, and the presence of coronary artery calcium and plaque in a subgroup of men. Associations between HIV control category and carotid and coronary plaque prevalences were assessed by multivariable regression analyses adjusting for demographics and CVD risk factors. Serum inflammatory biomarker concentrations [soluble CD163 (sCD163), soluble CD14 (sCD14), galectin‐3 (Gal‐3), galectin‐3 binding protein (Gal‐3BP) and interleukin (IL)‐6] were measured and associations with HIV control category assessed. Results We included 135 HIV controllers (30 ECs) and 135 LTNPs in the study. Carotid plaque prevalence and carotid IMT were similar in HIV controllers, LTNPs and HIV‐uninfected individuals. HIV controllers and LTNPs had lower prevalences of carotid plaque compared to viraemic HIV‐infected individuals. The prevalence of coronary atherosclerosis was similar in HIV controllers/LTNPs compared to HIV‐uninfected and viraemic HIV‐infected men. Controllers and LTNPs had higher concentrations of sCD163 and sCD14 compared to HIV‐uninfected persons. Conclusions Subclinical CVD was similar in HIV controllers, LTNPs and HIV‐uninfected individuals despite elevated levels of some inflammatory biomarkers. Future studies of HIV controllers and LTNPs are needed to characterize the risk of CVD among HIV‐infected persons.

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Section: Discussionmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Subclinical cardiovascular disease in HIV controller and long‐term nonprogressor populations

et al. 2019

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“…Several physiology studies performed in all-male or predominantly male (>90% male) cohorts have revealed relationships between systemic markers of monocyte activation (sCD163, sCD14) and surrogates of atherosclerotic cardiovascular disease (ASCVD) risk including subclinical carotid artery atherosclerosis(21), aortic inflammation(22) (23), subclinical coronary atherosclerotic plaque(24) (25) (26), and pathologically remodeled coronary atherosclerotic plaque(27) (28). Separate physiology studies among WLHIV have confirmed parallel relationships between systemic immune activation markers and ASCVD risk surrogates, including subclinical carotid atherosclerosis(29) (30) (31) and the percent of non-calcified coronary atherosclerotic plaque(32). Cells of monocyte/macrophage lineage may also engender myocardial edema and fibrosis, presaging diastolic dysfunction and heart failure with preserved ejection fraction(33) (34).…”

Section: Sex-specific Mechanisms Underlying Heightened Cvd Risk Amongmentioning

confidence: 94%

Cardiovascular disease risk among women living with HIV in North America and Europe

Stone

Looby

Zanni

2017

Current Opinion in HIV and AIDS

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Purpose of review To examine the epidemiology and mechanistic underpinnings of heightened cardiovascular disease (CVD) risk among women living with HIV (WLHIV) in North America and Europe. Recent Findings WLHIV in North America and Europe exhibit high CVD incidence rates, on par with those of compatriot men living with HIV (MLHIV). Compared with uninfected women, WLHIV in these regions face a two- to four-fold increased relative risk for myocardial infarction (MI), stroke, and heart failure. HIV-associated CVD risk is fuelled by a negative synergy of traditional cardiometabolic risk factors and heightened systemic immune activation/inflammation. Among WLHIV, female sex and endogenous sex hormone production influence both traditional cardiometabolic risk factors and patterns of systemic immune activation/inflammation. WLHIV in North America and Europe may also experience heightened CVD risk in relation to a relatively increased prevalence of behavioral and psychosocial CVD risk factors, coupled with suboptimal therapeutic targeting of known traditional cardiometabolic risk factors. Summary Additional research on sex-specific mechanisms of HIV-associated CVD - based not only out of North America and Europe but also and especially out of Africa, Asia, and South America - will inform the development of CVD prediction algorithms and prevention guidelines clinically relevant to the 17 million women aging with HIV globally.

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“…The extent to which these processes are synergistic and the mechanisms are largely unknown; however, it is possible they explain some of the extrahepatic manifestations of liver disease (and these viral infections). For example, cardiovascular disease incidence appears to be increased with HIV and HCV infection as well as nonalcoholic fatty liver disease (NAFLD), and macrophage activation has been linked to coronary and carotid artery inflammation . Clearly more work is needed to disentangle these associations and particularly to guide approaches to reducing the residual risk of inflammation that appears to be present in persons on long‐term ART.…”

Section: Pathogenesis/immunobiology Of Liver Disease In Patients Infementioning

confidence: 99%

Human immunodeficiency virus and liver disease: A comprehensive update

Sherman

Peters

Thomas

2017

Hepatology Communications

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Among persons living with human immunodeficiency virus (HIV) infection, liver disease remains a major cause of morbidity and mortality. While the etiologies are varied and often overlapping in the individual patient, the underlying mechanisms, including oxidative stress, direct activation of stellate cells, HIV interaction with hepatocytes, and bacterial translocation with systemic immune activation, seem to be unifying characteristics. Early and fully suppressive HIV antiretroviral therapy is a mainstay of management either before or concurrent with treatment of etiologic cofactors, including hepatitis C virus, hepatitis B virus, and nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Significant barriers to care that still exist include liver disease recognition, appropriate linkage to care, ongoing substance abuse, and psychiatric comorbidities in the HIV‐infected population. Emerging issues in these patients include acute and chronic hepatitis E, underreported hepatitis D, and a rising incidence of hepatocellular carcinoma. (Hepatology Communications 2017;1:987–1001)

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Association of Macrophage Inflammation Biomarkers With Progression of Subclinical Carotid Artery Atherosclerosis in HIV-Infected Women and Men

Cited by 94 publications

References 49 publications

Subclinical cardiovascular disease in HIV controller and long‐term nonprogressor populations

Subclinical cardiovascular disease in HIV controller and long‐term nonprogressor populations

Cardiovascular disease risk among women living with HIV in North America and Europe

Human immunodeficiency virus and liver disease: A comprehensive update

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