Key result
High hsCRP is linked to ~497% greater carotid plaque progression in HIV-uninfected women.
Why the study?
CVD risk is often underestimated in HIV-infected women, and the potential of CRP to improve CVD prediction in this population was unclear.
Does high baseline hsCRP predict subclinical cardiovascular disease progression in HIV-infected and HIV-uninfected women?
Cohort (n=783)
Does high baseline hsCRP predict subclinical cardiovascular disease progression in HIV-infected and HIV-uninfected women?
Relative Risk: 5.97 (95% CI 1.46–24.43)
p-value: p=0.042 for interaction
High baseline hsCRP predicts carotid plaque progression in HIV-uninfected women but not in HIV-infected women, suggesting different mechanisms of subclinical cardiovascular disease pathogenesis.
hsCRP may not mark plaque progression risk in HIV-infected women; leaves open HIV-specific modifiers of inflammation.
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 Women's 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 ratio: 1.31 (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 ratio: 5.97 (1.46-24.43)], but not in HIV-infected [adjusted rate ratio: 0.81 (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.
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Moran et al. (2018) conducted a cohort in Subclinical cardiovascular disease (n=783). High baseline high-sensitivity C-reactive protein (≥3 mg/l) vs. hsCRP <3 mg/l was evaluated on Focal plaque progression in HIV-uninfected women (adjusted rate ratio 5.97, 95% CI 1.46-24.43, p=0.042 for interaction). High baseline hsCRP (≥3 mg/l) was positively associated with carotid focal plaque progression in HIV-uninfected women (adjusted RR 5.97; 95% CI 1.46-24.43), but not in HIV-infected women.
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