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

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

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)999-1006
Number of pages8
JournalAIDS
Volume32
Issue number8
DOIs
StatePublished - May 15 2018

Fingerprint

C-Reactive Protein
Cardiovascular Diseases
HIV
Carotid Intima-Media Thickness
Linear Models
Logistic Models
Carotid Stenosis
Carotid Arteries
Blood Proteins
Ultrasonography
Cohort Studies
Retrospective Studies
Odds Ratio
Confidence Intervals

Keywords

  • atherosclerosis
  • C-reactive protein
  • HIV
  • subclinical cardiovascular disease
  • women

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

Moran, C. A., Sheth, A. N., Mehta, C. C., Hanna, D. B., Gustafson, D. R., Plankey, M. W., ... Ofotokun, I. (2018). The association of C-reactive protein with subclinical cardiovascular disease in HIV-infected and HIV-uninfected women. AIDS, 32(8), 999-1006. https://doi.org/10.1097/QAD.0000000000001785

The association of C-reactive protein with subclinical cardiovascular disease in HIV-infected and HIV-uninfected women. / Moran, Caitlin A.; Sheth, Anandi N.; Mehta, C. Christina; 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.

In: AIDS, Vol. 32, No. 8, 15.05.2018, p. 999-1006.

Research output: Contribution to journalArticle

Moran, CA, Sheth, AN, Mehta, CC, Hanna, DB, Gustafson, DR, Plankey, MW, Mack, WJ, Tien, PC, French, AL, Golub, ET, Quyyumi, A, Kaplan, RC & Ofotokun, I 2018, 'The association of C-reactive protein with subclinical cardiovascular disease in HIV-infected and HIV-uninfected women', AIDS, vol. 32, no. 8, pp. 999-1006. https://doi.org/10.1097/QAD.0000000000001785
Moran, Caitlin A. ; Sheth, Anandi N. ; Mehta, C. Christina ; 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. / The association of C-reactive protein with subclinical cardiovascular disease in HIV-infected and HIV-uninfected women. In: AIDS. 2018 ; Vol. 32, No. 8. pp. 999-1006.
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abstract = "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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T1 - The association of C-reactive protein with subclinical cardiovascular disease in HIV-infected and HIV-uninfected women

AU - Moran, Caitlin A.

AU - Sheth, Anandi N.

AU - Mehta, C. Christina

AU - Hanna, David B.

AU - Gustafson, Deborah R.

AU - Plankey, Michael W.

AU - Mack, Wendy J.

AU - Tien, Phyllis C.

AU - French, Audrey L.

AU - Golub, Elizabeth T.

AU - Quyyumi, Arshed

AU - Kaplan, Robert C.

AU - Ofotokun, Ighovwerha

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Y1 - 2018/5/15

N2 - 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.

AB - 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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KW - C-reactive protein

KW - HIV

KW - subclinical cardiovascular disease

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