Dissertations and Theses

Date of Degree


Document Type


Degree Name

Doctor of Philosophy (Ph.D.)


Community Health and Social Sciences


Christian Grov

Committee Members

Terry T-K Huang

H. Jonathon Rendina

Kit N. Simpson

Subject Categories

Medicine and Health Sciences | Public Health


Cardiovascular health, youth living with HIV, smoking, metabolic synndrome, lipids, substance abuse diagnosis


Background: HIV infection has shown to be associated with increased risk for, and earlier occurrence of cardiovascular disease (CVD). Emerging evidence suggests that detectable viral load (VL) and CD4 ≤ 200 contribute substantially to increased risk of CVD. Cigarette smoking is prevalent in at least 40% of those with HIV, and significantly more common compared to the general population. As many as 33% of adolescents are overweight, and this excess weight leads to lipid abnormalities, and increases in metabolic syndrome. With the newer formulation of antiretroviral therapy (ART) agents available as a component of single tablet regimens (STR), it is important to examine their impact on lipid abnormalities in youth living with HIV (YLH). The cardiovascular risk profile for YLH has yet to be developed. These findings support a cardiovascular risk framework incorporating biomarkers, behavioral measures, and ART medications as independent factors of a single multivariable CVD risk function among YLH in the United States (U.S.). Methods: De-identified electronic health records of YLH who received care in 2016 were extracted from multidisciplinary adolescent HIV clinics across the United States. Two analytic samples were developed based on Cardiac Risk Score1 (n =813) and Cardiac Risk Score2 (n = 398) to examine the association of HIV biomarkers (VL and CD4 cell count) with cardiovascular risk among YLH aged 14-26 (AIM 1). The second analytic sample of 398 was used to examine iv the association of cigarette smoking and metabolic syndrome with VL (AIM 2) and examine the association of STR and detectable VL with lipid abnormalities (AIM 3) among YLH aged 14-26. We used descriptive statistics, chi-square, ANOVA and independent t tests to examine the independent contributions of biomarkers, behavioral measures, and ART medications on cardiovascular risk among YLH in the U.S. We ran a series of multivariable linear regression models and tested the hypotheses that detectable VL and CD4 ≤ 200 will be positively associated with increased cardiovascular risk among YLH (AIM 1). We then tested the hypotheses that smoking and presence of metabolic syndrome will be positively associated with an increased odds of having detectable VL by performing multivariable linear regression models (AIM 2). Finally, we tested the hypotheses that detectable VL will be positively associated with increased risk of having low HDL and high total cholesterol whereas treatment with STR will be positively associated with decreased risk of having low HDL and high total cholesterol by performing multivariable logistic regression models (AIM 3). Results: Detectable VL was significantly associated with increased cardiovascular risk, cigarette smoking, and lipid abnormalities (AIMS 1-3); after simultaneously adjusting for demographic and clinical covariates. CD4 cell count ≤ 200 was not found to be significantly associated with increased cardiovascular risk (AIM 1). Cigarette smoking was associated with increased odds of VL non-suppression; however, the presence of components of metabolic syndrome were not found to be significantly associated with VL non-suppression after adjusting for demographic and clinical covariates (AIM 2). Treatment with single tablet regimen (STR) was associated with decreased odds of having low HDL cholesterol and high total cholesterol (AIM 3). Conclusions: Overall, this dissertation demonstrates that a relationship exists between detectable VL and increased risk of CVD; and it appears that smoking is positively associated with VL non- v suppression, which then is positively and independently associated with lipid abnormalities whereas STR is associated with lipid abnormalities as a protective agent in YLH. The variety of biomedical and behavioral factors that make HIV-positive individuals more susceptible to developing CVD is compelling evidence to reconfigure how the two ailments are addressed. The targeted population YLH carries a lot of interconnected factors that act as a tide in the ocean against seeking them, and it requires a multidisciplinary treatment method to increase its effectiveness in biological, societal, and even psychological way.

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