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      Cardiovascular manifestations of HIV infection in children

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          Abstract

          HIV infection in children is now considered as a chronic condition, in which various non-infectious complications may occur, including those affecting the developing cardiovascular system. As children are expected to survive well into adulthood, understanding childhood as well as potential future cardiovascular complications is of major importance.

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          Associations between HIV infection and subclinical coronary atherosclerosis.

          Coronary artery disease (CAD) has been associated with HIV infection, but data are not consistent.
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            Relationship between inflammatory markers, endothelial activation markers, and carotid intima-media thickness in HIV-infected patients receiving antiretroviral therapy.

            Human immunodeficiency virus (HIV)-infected patients are at increased risk of cardiovascular disease, which may be related to chronic inflammation and endothelial dysfunction despite virological control with antiretroviral therapy. The relationship between carotid intima-media thickness (IMT), a surrogate marker for cardiovascular disease, proinflammatory cytokines, and endothelial activation markers has not been fully explored in HIV-infected patients who are receiving antiretroviral therapy. We conducted a prospective, cross-sectional, observational study of treated HIV-infected patients and healthy control subjects to evaluate the relationship between carotid IMT, proinflammatory cytokines, endothelial activation biomarkers, and metabolic parameters in treated HIV-infected patients, compared with healthy control subjects. We enrolled 73 HIV-infected patients and 21 control subjects. Common carotid artery and internal carotid artery IMT measurements, as well as tumor necrosis factor-alpha, high-sensitivity C-reactive protein, interleukin-6, myeloperoxidase, and soluble vascular cell adhesion molecule-1 levels were higher in the HIV-infected group. High-sensitivity C-reactive protein was the only biomarker that was positively correlated with carotid IMT in both groups. In the HIV-infected group, soluble vascular cell adhesion molecule-1 was positively correlated with all inflammatory cytokine levels. In multiple regression analysis, soluble vascular cell adhesion molecule-1, myeloperoxidase, and tumor necrosis factor-alpha levels were all associated with internal carotid artery IMT in the HIV-infected group, whereas age was associated with both common carotid artery and internal carotid artery IMT. Enhanced endothelial activation, inflammation, and increased carotid IMT occur in HIV-infected patients despite antiretroviral therapy. Inflammatory markers are associated with endothelial activation, and both are associated with internal carotid artery IMT, supporting a potential role of inflammation in endothelial activation and cardiovascular disease in HIV infection.
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              Effects of HIV disease on lipid, glucose and insulin levels: results from a large antiretroviral-naive cohort.

              With the use of potent antiretroviral therapy in patients with HIV disease, changes in lipid parameters and glucose homeostasis have been noted. However, these effects have been difficult to interpret because of the varied demographic and treatment characteristics of the cohorts and the complexity of differentiating the effect of HIV disease from that of the drugs used in its treatment. This study was designed to explore these issues. Demographic information and fasting blood samples were collected from 419 antiretroviral-naive HIV-1-infected patients. The average age of the participants was 38.2 years, with 21% being female, 60% being African American, and 14% having a history of injection drug use. The mean CD4 lymphocyte count was 216 cells/microL, the mean baseline log10 HIV viral load was 4.98 HIV-1 RNA copies/mL, and 26% of patients had a history of AIDS-defining events. Women and African Americans had significantly higher levels of high-density lipoprotein (HDL) cholesterol, and older age was associated with higher total cholesterol levels. Lower CD4 lymphocyte counts and higher HIV RNA levels were independently associated with lower HDL cholesterol levels. Additionally, higher HIV RNA level was associated with lower levels of low-density lipoprotein (LDL) cholesterol and higher levels of very-low-density lipoprotein (VLDL) cholesterol and triglycerides. A history of AIDS-defining events was associated with higher total cholesterol, VLDL cholesterol and triglyceride concentrations. With respect to glucose homeostasis, a higher CD4 lymphocyte count was associated with less evidence of insulin resistance. However, a higher body mass index was associated with higher lipid levels and with more evidence of insulin resistance. Both HIV disease and demographic characteristics were found to influence lipid values and glucose homeostasis in the absence of antiretroviral treatment. More advanced HIV disease was associated with less favourable lipid and glucose homeostatic profiles. The independent association between HIV RNA levels and various lipid parameters suggests that viral replication had a direct effect on lipid levels. Interpretation of the effects of various HIV treatment regimen and drugs on metabolic parameters must take into account the stage of HIV disease and the demographic characteristics of the population studied.
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                Author and article information

                Journal
                European Journal of Preventive Cardiology
                Eur J Prev Cardiolog
                SAGE Publications
                2047-4873
                2047-4881
                September 26 2014
                November 2015
                November 14 2014
                November 2015
                : 22
                : 11
                : 1452-1461
                Affiliations
                [1 ]Department of Child Health/Centre for Clinical Epidemiology and Evidence Based Medicine (CEEBM), Faculty of Medicine University of Indonesia – Cipto Mangunkusumo Hospital, Jakarta, Indonesia
                [2 ]Julius Global Health, Julius Center for Health Science and Primary Care, The University Medical Center, Utrecht, The Netherlands
                [3 ]Department of Pediatrics, University of Melbourne, Australia
                [4 ]Murdoch Children Research Institute, Royal Children’s Hospital, Melbourne, Australia
                [5 ]Department of Paediatrics, Monash University, Australia
                Article
                10.1177/2047487314560086
                25398702
                c0ec120f-31d3-4e28-8e9d-f8a59a9667e0
                © 2015

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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