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Inflammatory Markers Associated With Subclinical Coronary Artery Disease: The Multicenter AIDS Cohort Study
Hossein Bahrami1, Matthew Budoff2, Sabina A Haberlen3
1Division of Cardiovascular Medicine, Keck School of Medicine of University of Southern California, Los Angeles, CA Cardiovascular Institute and Division of Cardiovascular Medicine, Stanford University, Stanford, CA hbahrami@usc.edu.
Insights
HIV+ men show higher coronary artery disease risk due to elevated inflammatory markers like interleukin-6. These markers correlate with increased coronary stenosis and calcification, highlighting the need for further research into these pathways.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- HIV infection is linked to increased coronary artery disease (CAD) risk.
- Mechanisms underlying CAD in HIV+ individuals remain unclear.
- Subclinical atherosclerosis assessment is crucial for understanding CAD risk.
Purpose of the Study:
- To investigate the association between inflammatory markers and subclinical coronary artery disease (CAD) in HIV+ men.
- To compare CAD markers between HIV+ and HIV- men.
- To identify specific inflammatory pathways contributing to CAD in HIV+ individuals.
Main Methods:
- Utilized data from 923 Multicenter AIDS Cohort Study participants (575 HIV+, 348 HIV-).
- Assessed coronary artery calcification (CAC) using noncontrast computed tomography (CT).
- Analyzed coronary plaque characteristics and stenosis severity via coronary CT angiography (CCTA).
Main Results:
- HIV+ men exhibited higher levels of interleukin-6 (IL-6), intercellular adhesion molecule-1, C-reactive protein, and soluble-tumor necrosis factor-α receptors (sTNFαR) I and II.
- A greater prevalence of noncalcified plaque was observed in HIV+ men (63% vs. 54%).
- Elevated IL-6, intercellular adhesion molecule-1, sTNFαR I, and sTNFαR II were significantly associated with increased coronary stenosis and CAC score in HIV+ men.
Conclusions:
- Higher inflammatory marker levels correlate with increased coronary stenosis prevalence in HIV+ men.
- Inflammatory pathways play a significant role in CAD development among HIV+ individuals.
- Further research is needed to elucidate the precise relationships between inflammation and CAD in the context of HIV infection.
Background:
Despite evidence for higher risk of coronary artery disease among HIV+ individuals, the underlying mechanisms are not well understood. We investigated associations of inflammatory markers with subclinical coronary artery disease in 923 participants of the Multicenter AIDS Cohort Study (575 HIV+ and 348 HIV- men) who underwent noncontrast computed tomography scans for coronary artery calcification, the majority (n=692) also undergoing coronary computed tomography angiography.
Methods And Results:
Outcomes included presence and extent of coronary artery calcification, plus computed tomography angiography analysis of presence, composition, and extent of coronary plaques and severity of coronary stenosis. HIV+ men had significantly higher levels of interleukin-6 (IL-6), intercellular adhesion molecule-1, C-reactive protein, and soluble-tumor necrosis factor-α receptor (sTNFαR) I and II (all P<0.01) and a higher prevalence of noncalcified plaque (63% versus 54%, P=0.02) on computed tomography angiography. Among HIV+ men, for every SD increase in log-interleukin-6 and log intercellular adhesion molecule-1, there was a 30% and 60% increase, respectively, in the prevalence of coronary stenosis ≥50% (all P<0.05). Similarly, sTNFαR I and II in HIV+ participants were associated with an increase in prevalence of coronary stenosis ≥70% (P<0.05). Higher levels of interleukin-6, sTNFαR I, and sTNFαR II were also associated with greater coronary artery calcification score in HIV+ men (P<0.01).
Conclusions:
Higher inflammatory marker levels are associated with greater prevalence of coronary stenosis in HIV+ men. Our findings underscore the need for further study to elucidate the relationships of inflammatory pathways with coronary artery disease in HIV+ individuals.
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