Divisions of Cardiology, University of California San Francisco (P.Y.H., A.S., A.F.B., K.M., P.G., S.C.K.).
J Am Heart Assoc. 2012 Apr;1(2). doi: 10.1161/JAHA.111.000422. Epub 2012 Apr 24.
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.
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.
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.)
URL: http://clinicaltrials.gov. Unique identifier: NCT01519141.
剪切力梯度和炎症与颈动脉分叉区动脉粥样硬化的发展有因果关系。在 HIV 感染者中观察到的颈动脉内膜中层厚度较高的机制尚不清楚。
我们测量了 300 名 HIV 感染者和 47 名对照者的颈总动脉、分叉区和颈内动脉的颈动脉内膜中层厚度进展和斑块形成。中位随访时间为 2.4 年。当所有节段均包括在内时，在调整传统危险因素后，与对照组相比，HIV 感染者的内膜中层厚度进展率更高（0.055 比 0.024mm/年，P=0.016）。在分叉区的进展率也更高（0.067 比 0.025mm/年，P=0.042），而在颈总动脉和颈内动脉的差异较小。与对照组相比，HIV 感染者的内部（23%比 6.4%，P=0.0037）和分叉区（34%比 17%，P=0.014）发生斑块的发生率更高。在 HIV 感染者中，与颈总动脉、颈内动脉或平均内膜中层厚度相比，分叉区的进展速度更快；相比之下，对照组在所有部位的进展率相似。基线 hsCRP 在 HIV 感染者中升高，是分叉区进展的预测因子。
在 HIV 感染者中，颈动脉分叉区的动脉粥样硬化进展更快。hsCRP，炎症的标志物，在 HIV 中升高，并与分叉区的进展相关。这些数据与血流剪切应力与 HIV 相关炎症相互作用导致加速动脉粥样硬化的模型一致。
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