Details

Autor(en) / Beteiligte

• Moran, Caitlin A
• Sheth, Anandi N
• Mehta, C C
• Hanna, David B
• Gustafson, Deborah R
• Plankey, Michael W
• Mack, Wendy J
• Tien, Phyllis C
• French, Audrey L
• Golub, Elizabeth T
• Quyyumi, Arshed
• Kaplan, Robert C
• Ofotokun, Ighovwerha

Titel

The association of C-reactive protein with subclinical cardiovascular disease in HIV-infected and HIV-uninfected women

Ist Teil von

• AIDS (London), 2018-05, Vol.32 (8), p.999-1006

Ort / Verlag

England: Copyright Wolters Kluwer Health, Inc

Erscheinungsjahr

2018

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• OBJECTIVE:HIV is a cardiovascular disease (CVD) risk factor. However, CVD risk is often underestimated in HIV-infected women. C-reactive protein (CRP) may improve CVD prediction in this population. We examined the association of baseline plasma CRP with subclinical CVD in women with and without HIV. DESIGN:Retrospective cohort study. METHODS:A total of 572 HIV-infected and 211 HIV-uninfected women enrolled in the Womenʼs Interagency HIV Study underwent serial high-resolution B-mode carotid artery ultrasonography between 2004 and 2013 to assess carotid intima–media thickness (CIMT) and focal carotid artery plaques. We used multivariable linear and logistic regression models to assess the association of baseline high (≥3 mg/l) high-sensitivity (hs) CRP with baseline CIMT and focal plaques, and used multivariable linear and Poisson regression models for the associations of high hsCRP with CIMT change and focal plaque progression. We stratified our analyses by HIV status. RESULTS:Median (interquartile range) hsCRP was 2.2 mg/l (0.8–5.3) in HIV-infected, and 3.2 mg/l (0.9–7.7) in HIV-uninfected, women (P = 0.005). There was no statistically significant association of hsCRP with baseline CIMT [adjusted mean difference −3.5 μm (95% confidence interval:−19.0 to 12.1)] or focal plaques [adjusted odds ratio1.31 (0.67–2.67)], and no statistically significant association of hsCRP with CIMT change [adjusted mean difference 11.4 μm (−2.3 to 25.1)]. However, hsCRP at least 3 mg/l was positively associated with focal plaque progression in HIV-uninfected [adjusted rate ratio5.97 (1.46–24.43)], but not in HIV-infected [adjusted rate ratio0.81 (0.47–1.42)] women (P = 0.042 for interaction). CONCLUSION:In our cohort of women with similar CVD risk factors, higher baseline hsCRP is positively associated with carotid plaque progression in HIV-uninfected, but not HIV-infected, women, suggesting that subclinical CVD pathogenesis may be different HIV-infected women.