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T-cell activation, both pre- and post-HAART levels, correlates with carotid artery stiffness over 6.5 years among HIV-infected women in the WIHS.

ABSTRACT: T-cell activation is a major pathway driving HIV disease progression. Little is known regarding the impact of T-cell activation on HIV-associated atherosclerosis and cardiovascular disease, a common comorbidity in HIV infection. We hypothesized that T-cell activation will predict vascular stiffness, a measure of subclinical atherosclerosis.Linear regression models evaluated the covariate-adjusted association of T-cell activation with vascular stiffness.CD38 and HLA-DR expression on CD4? and CD8? T cells was assessed by flow cytometry among 59 HIV-negative and 376 HIV-infected (185 hepatitis C coinfected) women in the Women's Interagency HIV Study. T-cell activation was defined by CD8?CD38?DR+ and CD4?CD3?8DR+. Multiple activation assessments over 6.5 years were averaged. In 140 women, T-cell activation was measured before and after highly active antiretroviral therapy (HAART) initiation. Carotid artery ultrasounds were completed a median of 6.5 years after last measurement of T-cell activation and carotid artery stiffness including distensibility and elasticity were calculated.Percentages of CD4? and CD8? T-cell activation were significantly higher in HIV- infected compared with HIV-negative women. Among HIV-negative women, T-cell activation was not associated with carotid artery stiffness. Among HIV-infected women, higher CD4? T-cell activation levels significantly predicted increased arterial stiffness independent of CD4? cell count and HIV RNA. The association was stronger among HIV/hepatitis C-coinfected women compared with HIV-monoinfected women; however, the difference was not statistically significant (P for interaction >0.05). Pre- and post-HAART levels of CD4? T-cell activation significantly predicted carotid artery stiffness.Persistent T-cell activation, even after HAART initiation, can contribute to structural and/or functional vascular damage accelerating atherogenesis in HIV infection. These results need to be confirmed in a longitudinal prospective study.

SUBMITTER: Karim R

PROVIDER: S-EPMC4197806 | biostudies-other | 2014 Nov

REPOSITORIES: biostudies-other

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T-cell activation, both pre- and post-HAART levels, correlates with carotid artery stiffness over 6.5 years among HIV-infected women in the WIHS.

Karim Roksana R Mack Wendy J WJ Kono Naoko N Tien Phyllis C PC Anastos Kathryn K Lazar Jason J Young Mary M Desai Seema S Golub Elizabeth T ET Kaplan Robert C RC Hodis Howard N HN Kovacs Andrea A

Journal of acquired immune deficiency syndromes (1999) 20141101 3

<h4>Objective</h4>T-cell activation is a major pathway driving HIV disease progression. Little is known regarding the impact of T-cell activation on HIV-associated atherosclerosis and cardiovascular disease, a common comorbidity in HIV infection. We hypothesized that T-cell activation will predict vascular stiffness, a measure of subclinical atherosclerosis.<h4>Design</h4>Linear regression models evaluated the covariate-adjusted association of T-cell activation with vascular stiffness.<h4>Method ...[more]

PMID: 25314253

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Project description:Background Carotid artery stiffness is associated with cognitive impairment and dementia, but the underlying mechanisms remain unknown. We examined the associations of carotid artery stiffness with cerebral small-vessel disease markers, cognition, and dementia subtypes in a memory clinic cohort. Methods and Results A total of 272 participants underwent carotid ultrasonography, 3 Tesla brain magnetic resonance imaging, and neuropsychological assessment. Carotid ultrasonography was used to assess β-index, pressure-strain elastic modulus, and pulse-wave velocity-β. Brain magnetic resonance images were graded for cerebral small-vessel disease markers, including white matter hyperintensities, lacunes, and cerebral microbleeds. Participants were classified as having no cognitive impairment, cognitive impairment and no dementia, or dementia subtyped as Alzheimer disease and vascular dementia. Cognition was assessed using National Institute of Neurological Disorders and Stroke-Canadian Stroke Network harmonization battery. After adjusting for age, sex, cardiovascular risk factors, and diseases, multivariable models showed that β-index (β=0.69; P=0.002), elastic modulus (β=0.78; P<0.001), and pulse-wave velocity-β (β=0.80; P<0.001) were associated with white matter hyperintensities, and elastic modulus (odds ratio [OR], 1.39 [95% CI, 1.04-1.85]) and pulse-wave velocity-β (OR, 1.47 [95% CI, 1.10-1.98]) were independently associated with lacunes. Similarly, β-index (OR, 2.04 [95% CI, 1.14-4.13]), elastic modulus (OR, 2.22 [95% CI, 1.25-4.42]), and pulse-wave velocity-β (OR, 2.50 [95% CI, 1.36-5.18]) were independently associated with vascular dementia. Carotid stiffness measures were independently associated with worse performance in global cognition, visuomotor speed, visuospatial function, and executive function. These associations became largely nonsignificant after further adjusting for cerebral small-vessel disease markers. Conclusions In memory clinic patients, carotid artery stiffness was associated with white matter hyperintensities and lacunes, impairment in global and domain-specific cognition, and causative subtypes of dementia, particularly vascular. The effects of carotid stiffness on cognition were not independent of, and were partially mediated by, cerebral small-vessel disease.

Project description:ObjectivesPhysical activity is negatively associated with arterial stiffness. However, the relationship between sedentary behaviour and arterial stiffness is poorly understood. In this study, we aimed to investigate the association of sedentary behaviour with arterial stiffness among young adults.DesignCross-sectional.Setting34 study clinics across Australia during 2004-2006.Participants2328 participants (49.4% male) aged 26-36 years who were followed up from a nationally representative sample of Australian schoolchildren in 1985.MeasurementsArterial stiffness was measured by carotid ultrasound. Sitting time per weekday and weekend day, and physical activity were self-reported by questionnaire. Cardiorespiratory fitness was estimated as physical work capacity at a heart rate of 170 bpm. Anthropometry, blood pressure, resting heart rate and blood biochemistry were measured. Potential confounders, including strength training, education, smoking, diet, alcohol consumption and parity, were self-reported. Rank correlation was used for analysis.ResultsSitting time per weekend day, but not per weekday, was correlated with arterial stiffness (males r=0.11 p<0.01, females r=0.08, p<0.05) and cardiorespiratory fitness (males r?=?-0.14, females r?=?-0.08, p<0.05), and also with fatness and resting heart rate. One additional hour of sitting per weekend day was associated with 5.6% (males p=0.046) and 8.6% (females p=0.05) higher risk of having metabolic syndrome. These associations were independent of physical activity and other potential confounders. The association of sitting time per weekend day with arterial stiffness was not mediated by resting heart rate, fatness or metabolic syndrome.ConclusionsOur study demonstrates a positive association of sitting time with arterial stiffness. The greater role of sitting time per weekend day in prediction of arterial stiffness and cardiometabolic risk than that of sitting time per weekday may be due to better reflection of discretionary sitting behaviour.

Dataset Information

T-cell activation, both pre- and post-HAART levels, correlates with carotid artery stiffness over 6.5 years among HIV-infected women in the WIHS.

Publications

T-cell activation, both pre- and post-HAART levels, correlates with carotid artery stiffness over 6.5 years among HIV-infected women in the WIHS.

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