BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND:Human immunodeficiency virus (HIV)-infectedpatients 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-infectedpatients who are receiving antiretroviral therapy. METHODS: We conducted a prospective, cross-sectional, observational study of treated HIV-infectedpatients and healthy control subjects to evaluate the relationship between carotid IMT, proinflammatory cytokines, endothelial activation biomarkers, and metabolic parameters in treated HIV-infectedpatients, compared with healthy control subjects. RESULTS: We enrolled 73 HIV-infectedpatients 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. CONCLUSIONS: Enhanced endothelial activation, inflammation, and increased carotid IMT occur in HIV-infectedpatients 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.
Authors: M Bongiovanni; M Casana; P Cicconi; M Pisacreta; R Codemo; M Pelucchi; A d'Arminio Monforte; T Bini Journal: J Antimicrob Chemother Date: 2007-11-12 Impact factor: 5.790
Authors: Avni H Thakore; Chao-Yu Guo; Martin G Larson; Diane Corey; Thomas J Wang; Ramachandran S Vasan; Ralph B D'Agostino; Izabella Lipinska; John F Keaney; Emelia J Benjamin; Christopher J O'Donnell Journal: Am J Cardiol Date: 2007-04-18 Impact factor: 2.778
Authors: Co Hileman; Ct Longenecker; Tl Carman; Gl Milne; D E Labbato; Nj Storer; Ca White; Ga McComsey Journal: HIV Med Date: 2012-05-25 Impact factor: 3.180
Authors: Grace A McComsey; Douglas Kitch; Paul E Sax; Camlin Tierney; Nasreen C Jahed; Kathleen Melbourne; Belinda Ha; Todd T Brown; Anthony Bloom; Neal Fedarko; Eric S Daar Journal: J Acquir Immune Defic Syndr Date: 2014-02-01 Impact factor: 3.731