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Inflammatory Markers Associated with Coronary Heart Disease in Persons with HIV Infection
1Division of Infectious Diseases, University of Cincinnati College of Medicine, 231 Albert Sabin Way, PO Box 670560, Cincinnati, OH, 45267-0560, USA, Carl.fichtenbaum@uc.edu.
Insights
HIV infection causes chronic inflammation, increasing coronary heart disease (CHD) risk. Antiretroviral therapy may not fully suppress this inflammation, highlighting the importance of monitoring CHD biomarkers in HIV patients.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- Coronary heart disease (CHD) is a chronic inflammatory condition.
- HIV infection is linked to chronic inflammation and elevated CHD risk markers.
- Antiretroviral therapy (ART) may not fully resolve inflammation in HIV patients.
Purpose of the Study:
- To review biomarkers of inflammation associated with CHD development in HIV-infected individuals.
- To discuss the impact of ART on CHD risk and inflammation.
Main Methods:
- Review of current literature on CHD, HIV, inflammation, and biomarkers.
- Analysis of studies investigating inflammatory mediators (e.g., IL-6, D-dimer) in HIV-positive individuals.
- Examination of the association between specific ART agents and cardiovascular events.
Main Results:
- HIV infection elevates CHD risk biomarkers even with controlled viral replication.
- The SMART study linked ART interruption to increased mortality and CHD events.
- Certain ART drugs (e.g., abacavir) may increase myocardial infarction risk and inflammatory markers.
Conclusions:
- Chronic inflammation in HIV contributes to increased CHD risk.
- Monitoring inflammatory biomarkers is crucial for managing cardiovascular health in HIV patients.
- Further research is needed to optimize ART strategies for reducing CHD risk in HIV.
Abstract:
Coronary heart disease (CHD) is an inflammatory process that takes decades to develop. In HIV-seronegative persons, high-sensitivity C-reactive protein is a biologic marker of CHD risk. HIV infection induces chronic inflammation, despite adequate suppression of HIV replication with antiretroviral therapy, resulting in elevations of several biologic markers associated with CHD risk in HIV-seronegative persons. Indeed, the SMART study demonstrated that interruption in antiretroviral therapy is associated with higher mortality and CHD events postulated to be related to inflammatory mediators such as interleukin-6 and D-dimer. Specific antiretroviral agents (eg, abacavir) have been associated with higher rates of myocardial infarctions and elevations in markers of inflammation such as interleukin-6 and D-dimer in persons with CHD events. This article reviews the current understanding of biomarkers of inflammation associated with the development of CHD in the setting of HIV infection and the use of antiretroviral therapy.
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