Journal of the American Heart Association · 2012 · 101 citations · 40 references
Veterinary MedicineInfectious DiseasesHiv PreventionInfectious Disease EpidemiologyInflammationCarotid Artery DiseaseHiv EpidemiologyInflammation In Infectious DiseaseInflammatory MediatorsAtherosclerosis RiskAtherosclerotic ProgressionBifurcationCarotid Artery AtherosclerosisCarotid Plaque MorphologyCommon Carotid ArteryInternal Carotid Artery SegmentsPlaque Inflammation
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.
40
Hemodynamic Shear Stress and Its Role in Atherosclerosis
Adel M. Malek · JAMA · 1999 · 3.6K citations
David N. Ku, Don P. Giddens, Christopher K. Zarins et al. · Arteriosclerosis An Official Journal of the American Heart Association Inc · 1985 · 2.7K citations · Full text
Lloyd E. Chambless, Gerardo Heiss, A. R. Folsom et al. · American Journal of Epidemiology · 1997 · 2K citations · Full text
Virginia A. Triant, Hang Lee, Colleen Hadigan et al. · The Journal of Clinical Endocrinology & Metabolism · 2007 · 1.6K citations · Full text