Armah, Kaku
(2013)
Cornonary Heart Disease Risk and HIV Infection: The Roles of Inflammation and Co-Morbid Disease.
Doctoral Dissertation, University of Pittsburgh.
(Unpublished)
Abstract
My research interest is the intersection of communicable and non-communicable (chronic) disease. Human immunodeficiency virus (HIV) infection and coronary heart disease (CHD) provide an interesting model to study this intersection because 1) treated HIV infected people are living long enough to die from non-AIDS causes 2) ischemic heart disease is the leading cause of death worldwide and 3) HIV/AIDS is among the top 10 causes of death. It is therefore of public health importance to examine the mechanisms by which HIV contributes to CHD. This dissertation focuses on the roles that co-morbdity and inflammation play within this intersection.
The first intersection, lipid and lipoprotein dysregulation, is a great place to start because it 1) co-occurs with HIV (and other) infections, 2) is an important risk factor for atherosclerotic CHD and 3) is modifiable with existing, inexpensive therapy. We review lipid and lipoprotein metabolism alterations in untreated HIV infection.
The second intersection is inflammation, an immune response process and an integral component of atherosclerosis. Prior work was limited by comparisons of inflammatory biomarkers in HIV infected and (typically healthier) uninfected populations from different cohorts and limited adjustment for comorbid conditions that also influence these biomarkers. Paper 1 compares inflammatory biomarkers between HIV infected and behaviorally and demographically similar uninfected Veterans with similar burdens of comorbid disease.
The third intersection focuses on other diseases co-morbid with HIV that also contribute to CHD risk. Specifically, Paper 2 compares inflammatory biomarkers between HIV infected people with or without hepatitis C co-infection as an example of HIV-related comorbidity. Paper 3 compares risk for acute myocardial infarction by blood pressure and HIV status as an example of comorbidity that is not directly related to HIV infection.
In summary, this dissertation contributes insights into the pathogenesis of CHD in the setting of HIV infection. It emphasizes the importance of studying HIV as a disease with pleiotropic effects (on biomarkers and organ systems) that can interact with each other, modifying their independent contributions to CHD risk.
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Details
| Item Type: |
University of Pittsburgh ETD
|
| Status: |
Unpublished |
| Creators/Authors: |
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| ETD Committee: |
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| Date: |
27 June 2013 |
| Date Type: |
Publication |
| Defense Date: |
13 March 2013 |
| Approval Date: |
27 June 2013 |
| Submission Date: |
3 April 2013 |
| Access Restriction: |
No restriction; Release the ETD for access worldwide immediately. |
| Number of Pages: |
134 |
| Institution: |
University of Pittsburgh |
| Schools and Programs: |
School of Public Health > Epidemiology |
| Degree: |
PhD - Doctor of Philosophy |
| Thesis Type: |
Doctoral Dissertation |
| Refereed: |
Yes |
| Uncontrolled Keywords: |
HIV, CHD, biomarkers, co-morbid disease |
| Date Deposited: |
27 Jun 2013 18:10 |
| Last Modified: |
15 Nov 2016 14:12 |
| URI: |
http://d-scholarship.pitt.edu/id/eprint/18590 |
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