title: Traditional risk factors and D-dimer predict incident cardiovascular disease events in chronic HIV infection.
abstract: OBJECTIVE
  Cardiovascular disease (CVD) contributes significantly to HIV-related morbidity and mortality. Chronic immune activation and inflammation are thought to augment the progression of atherosclerotic disease. In this retrospective, case-control study of HIV-infected individuals, we investigated the association of traditional cardiac risk factors, HIV-related disease, and inflammation with CVD events.
  
  
  METHODS
  HIV-infected individuals who experienced an incident CVD event while enrolled in National Institutes of Health clinical protocols from 1995 to 2009 were matched 2: 1 to HIV-infected individuals without known CVD. Markers of inflammation and cell activation were measured in serum or plasma using ELISA-based assays and peripheral mononuclear cells by four-color flow cytometry.
  
  
  RESULTS
  Fifty-two patients experienced an incident CVD event. Events were related to smoking, dyslipidemia, hyperglycemia, and family history as well as elevated D-dimer, soluble vascular cell adhesion molecule-1, tissue inhibitor of metalloproteinase-1, and soluble tissue factor, but not high-sensitivity C-reactive protein. No significant differences in antiviral therapy, CD4 T-cell count, or CD38 and human leukocyte antigen-DR expression were identified between patients and controls. In multivariable analysis, smoking, family history, D-dimer, and glucose were independently related to CVD risk.
  
  
  CONCLUSIONS
  In this cohort, CVD risk was related to traditional CVD risk factors and markers of thrombosis and endothelial damage, but not to high-sensitivity C-reactive protein or markers of T-cell activation such as CD38/human leukocyte antigen-DR coexpression. D-dimer may help identify HIV-infected patients at elevated CVD risk.
authors.affiliation: National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Emily S
authors.initials: ES
authors.lastname: Ford
authors.forename: Jamieson H
authors.initials: JH
authors.lastname: Greenwald
authors.forename: Aaron G
authors.initials: AG
authors.lastname: Richterman
authors.forename: Adam
authors.initials: A
authors.lastname: Rupert
authors.forename: Lauren
authors.initials: L
authors.lastname: Dutcher
authors.forename: Yunden
authors.initials: Y
authors.lastname: Badralmaa
authors.forename: Ven
authors.initials: V
authors.lastname: Natarajan
authors.forename: Catherine
authors.initials: C
authors.lastname: Rehm
authors.forename: Colleen
authors.initials: C
authors.lastname: Hadigan
authors.forename: Irini
authors.initials: I
authors.lastname: Sereti
mesh_terms: D050197:Atherosclerosis / Q000209:etiology / Q000276:immunology*; D018791:CD4 Lymphocyte Count; D016022:Case-Control Studies; D002908:Chronic Disease; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000276:immunology*; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000276:immunology*
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D019010:Vascular Cell Adhesion Molecule-1; C036309:fibrin fragment D