Medical Service, Department of Veterans Affairs Medical Center, University of California, San Francisco, California 94121, USA.
AIDS. 2009 Sep 10;23(14):1841-9. doi: 10.1097/QAD.0b013e32832d3b85.
Cardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors.
Cross-sectional study of HIV-infected participants and controls without pre-existing CVD from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA). Preclinical atherosclerosis was assessed by carotid intima-medial thickness (cIMT) measurements in the internal/bulb and common regions in HIV-infected participants and controls after adjusting for traditional CVD risk factors.
For internal carotid, mean IMT was 1.17 +/- 0.50 mm for HIV-infected participants and 1.06 +/- 0.58 mm for controls (P < 0.0001). After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected participants vs. controls was 0.188 mm [95% confidence interval (CI) 0.113-0.263, P < 0.0001]. Further adjustment for traditional CVD risk factors modestly attenuated the HIV association (0.148 mm, 95% CI 0.072-0.224, P = 0.0001). For the common carotid, HIV infection was independently associated with greater IMT (0.033 mm, 95% CI 0.010-0.056, P = 0.005). The association of HIV infection with IMT was similar to that of smoking, which was also associated with greater IMT (internal 0.173 mm, common 0.020 mm).
Even after adjustment for traditional CVD risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by IMT. The stronger association of HIV infection with IMT in the internal/bulb region compared with the common carotid may explain previous discrepancies in the literature. The association of HIV infection with IMT was similar to that of traditional CVD risk factors, such as smoking.
心血管疾病（CVD）是感染 HIV 的患者发病率和死亡率不断增加的一个原因。然而，HIV 感染是否会导致动脉粥样硬化加速，而不考虑传统的 CVD 危险因素，这一点仍存在争议。
这项研究是一项横断面研究，纳入了来自 HIV 脂肪再分布和代谢变化研究（FRAM）和动脉粥样硬化多民族研究（MESA）的无预先存在 CVD 的 HIV 感染参与者和对照者。在调整了传统 CVD 危险因素后，通过对 HIV 感染参与者和对照者的内颈动脉（ICA）和总颈动脉（CCA）内/球部和总部位进行颈动脉内膜中层厚度（cIMT）测量，评估了亚临床动脉粥样硬化。
对于 ICA，HIV 感染参与者的平均 IMT 为 1.17±0.50mm，而对照者的平均 IMT 为 1.06±0.58mm（P<0.0001）。经多变量调整人口统计学特征后，HIV 感染参与者与对照者之间的平均差异为 0.188mm[95%置信区间（CI）0.113-0.263，P<0.0001]。进一步调整传统 CVD 危险因素后，这种 HIV 相关性略有减弱（0.148mm，95%CI 0.072-0.224，P=0.0001）。对于 CCA，HIV 感染与更大的 IMT 独立相关（0.033mm，95%CI 0.010-0.056，P=0.005）。HIV 感染与 IMT 的相关性与吸烟相似，吸烟也与更大的 IMT 相关（ICA 0.173mm，CCA 0.020mm）。
即使在调整了传统 CVD 危险因素后，HIV 感染仍伴有通过 IMT 测量的更广泛的动脉粥样硬化。与 CCA 相比，HIV 感染与 ICA 内/球部区域的 IMT 相关性更强，这可能解释了文献中的先前差异。HIV 感染与 IMT 的相关性与传统 CVD 危险因素（如吸烟）相似。
