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.
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.
Absolute Event Rate: 0.055% vs 0.024%
p-value: p=0.016
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.
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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