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Impaired Cardiac Strain and Biomarkers of Immune Activation in HIV
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Reported by Jules Levin
CROI 2015 Feb 23-26, Seattle, WA
Colleen Hadigan1, Julia Purdy1, Diana Thiara1, Louisa Howard1, Chia-Ying Liu1, Fabio Raman1, Sabrina Mangat1, David Bluemke1, Christopher Sibley3
1 NIAID, National Institutes of Health (NIH), Bethesda, Maryland, United States;3 Oregon Health and Sciences University, Portland, Oregon, United States
Conclusions: HIV-infected subjects demonstrate subclinical impairment in systolic function and this is associated with markers of chronic immune activation, inflammation and tissue remodeling. Similar to patients with chronic heart failure, increased levels of MCP-1, a chemokine important in the regulation of macrophage migration and a marker of immune activation, was a strong independent predictor of impairment in cardiac function. LBP, an acute phase protein made in response to LPS, and TIMP-1, a marker of tissue remodeling, were also associated with impaired cardiac strain. Our findings indicate that subclinical impairment in cardiac strain tracks with markers of chronic inflammation and immune activation, which may serve as targets for future therapeutic strategies to optimize long-term cardiovascular health in persons living with HIV.
Conclusions
--> Strain indices, a marker of systolic dysfunction, were decreased in HIV-infected subjects
--> Diffuse myocardial fibrosis, a potential early marker of LV impairment, is increased in asymptomatic HIV compared to controls
--> Subclinical impairment in cardiac strain tracks with markers of chronic inflammation and chronic immune activation, which may serve as targets for future therapeutic strategies to optimize long-term cardiovascular health in persons living with HIV
program abstract
Background: Chronic HIV infection is associated with an increased risk of cardiovascular disease (CVD). Subclinical cardiac dysfunction can be assessed through MRI measurements of cardiac strain and myocardial fibrosis. In order to investigate the underlying etiology of CVD in HIV, we performed cardiac MRI in conjunction with biomarkers of inflammation and immune activation in a cohort of HIV+ adults without known CVD.
Methods: This is a prospective cross-sectional study of 95 HIV+ adults and 30 age, sex, race-matched healthy controls. Myocardial fibrosis (quantified as extracellular volume index) and regional cardiac strain were measured by MRI. Laboratory determinations included serologic biomarkers of inflammation, coagulation, and immune activation (e.g. C-reactive protein [CRP], D-dimer, pro-brain natriuretic peptide [pro-BNP], monocyte chemoattractant protein-1 [MCP-1], lipopolysaccharide binding protein [LBP], tissue inhibitor of metalloproteinase-1 [TIMP-1]).
Results: Radial strain and epicardial-endocardial circumferential strain were significantly decreased in HIV+ compared to controls (Table 1). Among the HIV+ group, radial strain impairment was strongly correlated with increased levels of MCP-1 (r=-0.43, p
Conclusions: HIV-infected subjects demonstrate subclinical impairment in systolic function and this is associated with markers of chronic immune activation, inflammation and tissue remodeling. Similar to patients with chronic heart failure, increased levels of MCP-1, a chemokine important in the regulation of macrophage migration and a marker of immune activation, was a strong independent predictor of impairment in cardiac function. LBP, an acute phase protein made in response to LPS, and TIMP-1, a marker of tissue remodeling, were also associated with impaired cardiac strain. Our findings indicate that subclinical impairment in cardiac strain tracks with markers of chronic inflammation and immune activation, which may serve as targets for future therapeutic strategies to optimize long-term cardiovascular health in persons living with HIV.
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