Key result
HIV infection was associated with a greater rate of carotid intima-media thickness progression compared with controls (0.055 vs. 0.024 mm/year, P=0.016), preferentially at the bifurcation region.
Why the study?
Does HIV infection accelerate carotid intima-media thickness progression and plaque development compared to uninfected controls?
Cohort (n=347)
Does HIV infection accelerate carotid intima-media thickness progression and plaque development compared to uninfected controls?
HIV infection is associated with accelerated atherosclerosis, particularly at the carotid bifurcation, which is predicted by elevated hsCRP levels.
HIV-associated IMT progression at the bifurcation may signal heightened local risk; leaves open whether inflammation modulation slows site-specific atherosclerosis.
BACKGROUND: Shear stress gradients and inflammation have been causally associated with atherosclerosis development in carotid bifurcation regions. The mechanism underlying higher levels of carotid intima-media thickness observed among HIV-infected individuals remains unknown. METHODS AND RESULTS: We measured carotid intima-media thickness progression and development of plaque in the common carotid, bifurcation region, and internal carotid artery in 300 HIV-infected persons and 47 controls. The median duration of follow-up was 2.4 years. When all segments were included, the rate of intima-media thickness progression was greater in HIV-infected subjects compared with controls after adjustment for traditional risk factors (0.055 vs. 0.024 mm/year, P=0.016). Rate of progression was also greater in the bifurcation region (0.067 vs. 0.025 mm/year, P=0.042) whereas differences were smaller in the common and internal regions. HIV-infected individuals had a greater incidence of plaque compared with controls in the internal (23% vs. 6.4%, P=0.0037) and bifurcation regions (34% vs. 17%, P=0.014). Among HIV-infected individuals, the rate of progression in the bifurcation region was more rapid compared with the common carotid, internal, or mean intima-media thickness; in contrast, progression rates among controls were similar at all sites. Baseline hsCRP was elevated in HIV-infected persons and was a predictor of progression in the bifurcation region. CONCLUSIONS: Atherosclerosis progresses preferentially in the carotid bifurcation region in HIV-infected individuals. hsCRP, a marker of inflammation, is elevated in HIV and is associated with progression in the bifurcation region. These data are consistent with a model in which the interplay between hemodynamic shear stresses and HIV-associated inflammation contribute to accelerated atherosclerosis. (J Am Heart Assoc. 2012;1:jah3-e000422 doi: 10.1161/JAHA.111.000422.) CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov. Unique identifier: NCT01519141.
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Hsue et al. (2012) conducted a cohort in HIV infection (n=347). HIV infection vs. Uninfected controls was evaluated on Rate of intima-media thickness progression (all segments) (p=0.016). HIV infection was associated with a greater rate of carotid intima-media thickness progression compared with controls (0.055 vs. 0.024 mm/year, P=0.016), preferentially at the bifurcation region.
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