title: Reduced ovarian reserve relates to monocyte activation and subclinical coronary atherosclerotic plaque in women with HIV.
abstract: OBJECTIVE
  To investigate differences in subclinical coronary atherosclerotic plaque and markers of immune activation among HIV-infected and non-HIV-infected women categorized by degree of ovarian reserve and menopause status.
  
  
  METHODS
  Cross-sectional evaluation.
  
  
  METHODS
  Seventy-four women (49 HIV-infected, 25 non-HIV-infected) without known cardiovascular disease (CVD) were classified as premenopausal, premenopausal with reduced ovarian reserve, or postmenopausal based on menstrual history and anti-Müllerian hormone (AMH) levels. Participants underwent contrast-enhanced coronary computed tomography angiography and immune phenotyping. Comparisons in coronary atherosclerotic plaque burden and immune markers were made between the HIV-infected and non-HIV-infected women overall and within the HIV-infected and non-HIV-infected women by reproductive classification group.
  
  
  RESULTS
  Among the overall group of HIV-infected women, the women with reduced ovarian reserve (undetectable AMH) had a higher prevalence of coronary atherosclerotic plaque (52 versus 6%, P = 0.0007) and noncalcified plaque (48 versus 6%, P = 0.002), as well as higher levels of log sCD163 (P = 0.0004) and log MCP-1 (P = 0.006), compared with the premenopausal women with measurable AMH. Furthermore, reduced ovarian reserve in the HIV-infected group related to noncalcified plaque, controlling for traditional CVD risk factors (P = 0.04) and sCD163 (P = 0.03).
  
  
  CONCLUSIONS
  HIV-infected women with reduced ovarian reserve have increased subclinical coronary atherosclerotic plaque compared with premenopausal women in whom AMH is measurable. This relationship holds when controlling for CVD risk factors (including age) and immune activation. Our findings demonstrate that reduced ovarian reserve may contribute to CVD burden in HIV-infected women and support a comprehensive assessment of CVD risk prior to completion of menopause in this population.
authors.affiliation: aProgram in Nutritional Metabolism, Massachusetts General Hospital bHarvard Medical School, Boston, Massachusetts cDavid Geffen School of Medicine at University of California, Los Angeles, California, USA.
authors.forename: Sara E
authors.initials: SE
authors.lastname: Looby
authors.forename: Kathleen V
authors.initials: KV
authors.lastname: Fitch
authors.forename: Suman
authors.initials: S
authors.lastname: Srinivasa
authors.forename: Janet
authors.initials: J
authors.lastname: Lo
authors.forename: Danielle
authors.initials: D
authors.lastname: Rafferty
authors.forename: Amanda
authors.initials: A
authors.lastname: Martin
authors.forename: Judith C
authors.initials: JC
authors.lastname: Currier
authors.forename: Steven
authors.initials: S
authors.lastname: Grinspoon
authors.forename: Markella V
authors.initials: MV
authors.lastname: Zanni
mesh_terms: D000328:Adult; D000792:Angiography; D058070:Asymptomatic Diseases; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000276:immunology*; D006801:Humans; D016130:Immunophenotyping; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D065851:Ovarian Reserve; D058226:Plaque, Atherosclerotic / Q000473:pathology*; D014057:Tomography, X-Ray Computed