Perivascular fat, inflammation, and cardiovascular risk in HIV-infected patients on antiretroviral therapy
Abstract Background HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown. Methods In a...
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Published in | International journal of cardiology Vol. 168; no. 4; pp. 4039 - 4045 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Ireland Ltd
09.10.2013
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Abstract | Abstract Background HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown. Methods In a cross-sectional study, epicardial (EAT) and thoracic periaortic (TAT) adipose tissue volumes were measured by computed tomography in 100 HIV-infected adults, on stable ART, with LDL-cholesterol ≤ 130 mg/dL and evidence of heightened T-cell activation (CD8+CD38+HLA-DR+ ≥ 19%) or increased inflammation (high sensitivity C-reactive protein ≥ 2 mg/L). Results Overall, 77% were males and 70% African American. Mean (standard deviation) age and body mass index were 47 (10) years and 28 (6.4) kg/m2 , respectively. All subjects had HIV-1 RNA < 1000 copies/mL with mean (standard deviation) CD4 + T cell count of 665 (280) cells/μL; 50% were on a protease inhibitor. EAT and TAT were correlated with each other (r = 0.766, p < 0.0001). Both were associated with metabolic syndrome, atherogenic lipid profile, insulin resistance, total and central body fat, serum biomarkers of inflammation, and soluble CD163, but not with cellular immune activation markers. In multivariable models that adjusted for age, sex, and other measures of adiposity, both perivascular fat depots were independently associated with the presence of coronary calcium. Conclusions Perivascular fat is associated with soluble CD163, biomarkers of inflammation, insulin resistance, and subclinical atherosclerosis in this population of virologically suppressed HIV-infected patients on ART. The association of perivascular fat with coronary artery calcification appears to be independent of other measures of adiposity. |
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AbstractList | HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown.
In a cross-sectional study, epicardial (EAT) and thoracic periaortic (TAT) adipose tissue volumes were measured by computed tomography in 100 HIV-infected adults, on stable ART, with LDL-cholesterol ≤130 mg/dL and evidence of heightened T-cell activation (CD8+CD38+HLA-DR+ ≥19%) or increased inflammation (high sensitivity C-reactive protein ≥2 mg/L).
Overall, 77% were males and 70% African American. Mean (standard deviation) age and body mass index were 47 (10) years and 28 (6.4) kg/m(2), respectively. All subjects had HIV-1 RNA <1000 copies/mL with mean (standard deviation) CD4+ T cell count of 665 (280) cells/μL; 50% were on a protease inhibitor. EAT and TAT were correlated with each other (r = 0.766, p < 0.0001). Both were associated with metabolic syndrome, atherogenic lipid profile, insulin resistance, total and central body fat, serum biomarkers of inflammation, and soluble CD163, but not with cellular immune activation markers. In multivariable models that adjusted for age, sex, and other measures of adiposity, both perivascular fat depots were independently associated with the presence of coronary calcium.
Perivascular fat is associated with soluble CD163, biomarkers of inflammation, insulin resistance, and subclinical atherosclerosis in this population of virologically suppressed HIV-infected patients on ART. The association of perivascular fat with coronary artery calcification appears to be independent of other measures of adiposity. Abstract Background HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown. Methods In a cross-sectional study, epicardial (EAT) and thoracic periaortic (TAT) adipose tissue volumes were measured by computed tomography in 100 HIV-infected adults, on stable ART, with LDL-cholesterol ≤ 130 mg/dL and evidence of heightened T-cell activation (CD8+CD38+HLA-DR+ ≥ 19%) or increased inflammation (high sensitivity C-reactive protein ≥ 2 mg/L). Results Overall, 77% were males and 70% African American. Mean (standard deviation) age and body mass index were 47 (10) years and 28 (6.4) kg/m2 , respectively. All subjects had HIV-1 RNA < 1000 copies/mL with mean (standard deviation) CD4 + T cell count of 665 (280) cells/μL; 50% were on a protease inhibitor. EAT and TAT were correlated with each other (r = 0.766, p < 0.0001). Both were associated with metabolic syndrome, atherogenic lipid profile, insulin resistance, total and central body fat, serum biomarkers of inflammation, and soluble CD163, but not with cellular immune activation markers. In multivariable models that adjusted for age, sex, and other measures of adiposity, both perivascular fat depots were independently associated with the presence of coronary calcium. Conclusions Perivascular fat is associated with soluble CD163, biomarkers of inflammation, insulin resistance, and subclinical atherosclerosis in this population of virologically suppressed HIV-infected patients on ART. The association of perivascular fat with coronary artery calcification appears to be independent of other measures of adiposity. Background: HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown. HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown. In a cross-sectional study, epicardial (EAT) and thoracic periaortic (TAT) adipose tissue volumes were measured by computed tomography in 100 HIV-infected adults, on stable ART, with LDL-cholesterol ≤130mg/dL and evidence of heightened T-cell activation (CD8+CD38+HLA-DR+ ≥19%) or increased inflammation (high sensitivity C-reactive protein ≥2mg/L). Overall, 77% were males and 70% African American. Mean (standard deviation) age and body mass index were 47 (10) years and 28 (6.4) kg/m2, respectively. All subjects had HIV-1 RNA <1000copies/mL with mean (standard deviation) CD4+ T cell count of 665 (280) cells/μL; 50% were on a protease inhibitor. EAT and TAT were correlated with each other (r=0.766, p<0.0001). Both were associated with metabolic syndrome, atherogenic lipid profile, insulin resistance, total and central body fat, serum biomarkers of inflammation, and soluble CD163, but not with cellular immune activation markers. In multivariable models that adjusted for age, sex, and other measures of adiposity, both perivascular fat depots were independently associated with the presence of coronary calcium. Perivascular fat is associated with soluble CD163, biomarkers of inflammation, insulin resistance, and subclinical atherosclerosis in this population of virologically suppressed HIV-infected patients on ART. The association of perivascular fat with coronary artery calcification appears to be independent of other measures of adiposity. |
Author | Lederman, Michael M Labbato, Danielle E Funderburg, Nicholas T Jiang, Ying Debanne, Sara McComsey, Grace A Storer, Norma Yun, Chun-Ho Bezerra, Hiram G Longenecker, Chris T |
AuthorAffiliation | 3 Division of Cardiology, Mackay Memorial Hospital, Taipei, Taiwan 4 Division of Infectious Diseases, Case Western Reserve University, Cleveland, OH, USA 2 Department of Biostatistics, Case Western Reserve University, Cleveland, OH, USA 1 University Hospitals Harrington Heart & Vascular Institute, Division of Cardiology, Case Western Reserve University, Cleveland, OH, USA |
AuthorAffiliation_xml | – name: 3 Division of Cardiology, Mackay Memorial Hospital, Taipei, Taiwan – name: 1 University Hospitals Harrington Heart & Vascular Institute, Division of Cardiology, Case Western Reserve University, Cleveland, OH, USA – name: 2 Department of Biostatistics, Case Western Reserve University, Cleveland, OH, USA – name: 4 Division of Infectious Diseases, Case Western Reserve University, Cleveland, OH, USA |
Author_xml | – sequence: 1 fullname: Longenecker, Chris T – sequence: 2 fullname: Jiang, Ying – sequence: 3 fullname: Yun, Chun-Ho – sequence: 4 fullname: Debanne, Sara – sequence: 5 fullname: Funderburg, Nicholas T – sequence: 6 fullname: Lederman, Michael M – sequence: 7 fullname: Storer, Norma – sequence: 8 fullname: Labbato, Danielle E – sequence: 9 fullname: Bezerra, Hiram G – sequence: 10 fullname: McComsey, Grace A |
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Keywords | Inflammation Adipose tissue HIV Macrophages Atherosclerosis Antiretroviral agent Cardiovascular disease Vascular disease Antiviral Cardiology Immunopathology Retroviridae AIDS Immune deficiency Lentivirus Infection Virus Chemotherapy Treatment Viral disease Risk factor Cardiovascular risk Fat Human immunodeficiency virus Macrophage |
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28 Nair (10.1016/j.ijcard.2013.06.059_bb0110) 1999; 29 Hirata (10.1016/j.ijcard.2013.06.059_bb0175) 2011; 58 Ho (10.1016/j.ijcard.2013.06.059_bb0130) 2012; 26 Pou (10.1016/j.ijcard.2013.06.059_bb0160) 2007; 116 Triant (10.1016/j.ijcard.2013.06.059_bb0140) 2010; 55 Zanni (10.1016/j.ijcard.2013.06.059_bb0190) 2012; 77 Yun (10.1016/j.ijcard.2013.06.059_bb0090) 2012; 81 Sporrer (10.1016/j.ijcard.2013.06.059_bb0185) 2009; 39 Lehman (10.1016/j.ijcard.2013.06.059_bb0070) 2010; 210 Grundy (10.1016/j.ijcard.2013.06.059_bb0100) 2004; 109 Floris-Moore (10.1016/j.ijcard.2013.06.059_bb0120) 2009; 23 Seminari (10.1016/j.ijcard.2013.06.059_bb0145) 2002; 7 Subramanian (10.1016/j.ijcard.2013.06.059_bb0080) 2012; 308 Bays (10.1016/j.ijcard.2013.06.059_bb0150) 2011; 57 Lake (10.1016/j.ijcard.2013.06.059_bb0025) 2011; 23 Lichtenstein (10.1016/j.ijcard.2013.06.059_bb0135) 2010; 51 Samaras (10.1016/j.ijcard.2013.06.059_bb0020) 2009; 17 Tilson (10.1016/j.ijcard.2013.06.059_bb0115) 2006; 1085 Burdo (10.1016/j.ijcard.2013.06.059_bb0195) 2011; 204 Fox (10.1016/j.ijcard.2013.06.059_bb0075) 2010; 3 Mazurek (10.1016/j.ijcard.2013.06.059_bb0045) 2003; 108 Stein (10.1016/j.ijcard.2013.06.059_bb0095) 2008; 21 Baker (10.1016/j.ijcard.2013.06.059_bb0035) 2006; 5 |
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Snippet | Abstract Background HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated... HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated... Background: HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with... |
SourceID | pubmedcentral proquest crossref pubmed pascalfrancis elsevier |
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SubjectTerms | Adipose tissue Adipose Tissue - drug effects Adipose Tissue - pathology Adult Anti-Retroviral Agents - adverse effects Anti-Retroviral Agents - pharmacology Antibiotics. Antiinfectious agents. Antiparasitic agents Antiviral agents Atherosclerosis Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cardiovascular Cardiovascular Diseases - chemically induced Cardiovascular Diseases - diagnosis Cardiovascular Diseases - epidemiology Cross-Sectional Studies Double-Blind Method Female Heart HIV HIV Infections - drug therapy HIV Infections - epidemiology Human viral diseases Humans Infectious diseases Inflammation Inflammation - chemically induced Inflammation - diagnosis Inflammation - epidemiology Macrophages Male Medical sciences Middle Aged Pericardium - drug effects Pericardium - pathology Pharmacology. Drug treatments Risk Factors Vascular Calcification - chemically induced Vascular Calcification - diagnosis Vascular Calcification - epidemiology Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids |
Title | Perivascular fat, inflammation, and cardiovascular risk in HIV-infected patients on antiretroviral therapy |
URI | https://www.clinicalkey.es/playcontent/1-s2.0-S0167527313011133 https://dx.doi.org/10.1016/j.ijcard.2013.06.059 https://www.ncbi.nlm.nih.gov/pubmed/23886531 https://search.proquest.com/docview/1520366240 https://pubmed.ncbi.nlm.nih.gov/PMC3805774 |
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