期刊
JOURNAL OF THE AMERICAN HEART ASSOCIATION
卷 1, 期 2, 页码 -出版社
WILEY
DOI: 10.1161/JAHA.111.000422
关键词
AIDS; carotid arteries; inflammation; atherosclerosis
资金
- Doris Duke Charitable Foundation
- National Institutes of Health [K23 AI066885, K24AI069994, R01 HL095130, R01 AI052745, R01 CA119903, P30 AI27763, RO1 AI087145, MO1 RR000083]
- UCSF CFAR [PO AI27763]
- UCSF CTSI [UL1 RR024131]
- amfAR [106710-40-RGRL]
- Ragon Institute
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.)
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