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Antiviral Therapy and Smoking Associated with Coronary Vessel Wall Thickening in HIV-Infected Youth
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Reported by Jules Levin
CROI 2014 March 3-6 Boston, MA
"Vessel wall thickness and quantification of plaque in coronary vessels may be more predictive of cardiovascular events than other indicators of CVD.....this study is a prospective cross-sectional study of 35 youth and young adults who acquired HIV in early life and 11 sex and race matched healthy controls, all free of active CVD.....HIV infection (p=0.02) remained a significant independent predictor of RCA vessel wall thickness in a model including age, sex, and BMI and HIV status......Duration of ART (p<0.05) and smoking pack-years (p=0.01) were independent predictors of RCA [proximal right coronary artery]wall thickness in the HIV-infected patients after adjusting for age, sex, and BMI......There was also no association between vessel wall thickness and: the presence of coronary plaque, levels of CRP, d-dimer, pro-BNP, or homocysteine for either study group.....Among the HIV-infected subjects, duration of antiretroviral therapy corresponded to vessel wall thickness (r=0.38, p=0.02) and duration of stavudine was most closely correlated to RCA thickness (r=0.43, p<0.01). These associations remained significant after adjusting for age, BMI and smoking pack years, which also was consistently associated with RCA thickness."
A. Unsal1, K. Z. Abd-Elmoniem2, S. Eshera2, J. B. Purdy3, R. Hazra4, C. Hadigan1, A. M. Gharib2
1National Institute of Allergy and Infectious Disease, 2National Institute of Digestive and Kidney Diseases, 3Critical Care Medicine, Clinical Center, 4Eunice Kennedy Shriver National Institute of Child Health and Human Development
National Institutes of Health, Bethesda, MD
Program Abstract-
Background: Individuals infected with HIV early in life may be at higher risk for premature vasculopathy and cardiovascular disease. Whether this increased
cardiovascular disease risk is associated with chronic HIV-infection or with long-term antiretroviral therapy has yet to be elucidated. The purpose of this
study therefore was to assess subclinical coronary vessel wall thickening and plaque burden in patients infected with HIV early in life compared to healthy
controls.
Methodology: This is a prospective cross-sectional study of 35 youth and young adults who acquired HIV in early life and 11 uninfected healthy controls,
all free of active cardiovascular disease. Phase-sensitive dual inversion-recovery black-blood vessel wall imaging was utilized for MR imaging of the
proximal right coronary artery (RCA) and CT angiography was performed for determination of coronary plaque burden.
Results: HIV-infected subjects (mean age 22; range 15-29 years; 54% male) had significantly increased proximal RCA thickness compared to uninfected
controls (mean age 25; 22-29 years; 27% male). RCA thickness in HIV+ was 1.32±0.21 mm vs. 1.09±0.12 mm in controls (p=0.002). HIV status
remained a significant predictor of RCA thickness (p=0.01), as did smoking pack years (p=0.004), in a multivariate regression adjusting for age, sex, and
BMI. The difference in proximal RCA thickness also remained significant in a sub-analysis which excluded HIV+ subjects <20 y (p=0.002). Atherosclerotic
plaque was present in the coronary vessels among 45% of controls, but only 19% of HIV-infected subjects (p=0.1) and plaque was not associated
with proximal RCA thickness. There was no association between vessel wall thickness and levels of CRP, d-dimer, pro-BNP, or homocysteine for either
study group. Among the HIV-infected subjects, duration of antiretroviral therapy corresponded to vessel wall thickness (r=0.38, p=0.02) and duration
of stavudine was most closely correlated to RCA thickness (r=0.43, p<0.01). These associations remained significant after adjusting for age, BMI and
smoking pack years, which also was consistently associated with RCA thickness.
Conclusions: This investigation provides evidence of vascular injury in individuals infected with HIV early in life compared to healthy volunteers, as shown
by coronary vessel wall thickness. Among HIV-infected subjects, increased duration of antiretroviral therapy, in particular stavudine, and smoking pack
years were strong indicators of proximal RCA thickening. However, coronary vessel wall thickening was independent of atherosclerotic plaque, indicating
that vessel wall thickening related to antiretroviral therapy exposure occurs through a mechanism distinctive from traditional atherogenesis.
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