Oliviero Ugo, Bonadies Giovanni, Apuzzi Valentina, Foggia Maria, Bosso Giorgio, Nappa Salvatore, Valvano Antonio, Leonardi Enrico, Borgia Guglielmo, Castello Giuseppe, Napoli Raffaele, Saccà Luigi
Department of Internal Medicine, University Federico II, Naples, Italy.
Atherosclerosis. 2009 Jun;204(2):586-9. doi: 10.1016/j.atherosclerosis.2008.10.012. Epub 2008 Nov 1.
Premature atherosclerosis in HIV-infected patients has been attributed to highly active antiretroviral therapy (HAART) and the associated metabolic complications. Whether HIV per se plays a role is an unresolved issue. The purpose of this study was to evaluate whether HIV per se exerts atherogenic effects.
We measured carotid intima-media thickness (IMT) and brachial endothelial-dependent (FMD) and endothelial-independent (NMD) vasodilation in 38 naïve untreated HIV-infected patients and 41 healthy control subjects.
Control subjects were selected as to match the HIV patients for metabolic risk factors. Mean carotid IMT was higher in HIV patients (0.85+/-0.2mm; p<0.001) than in controls (0.63+/-0.1mm). In a stepwise multiple regression model, the changes in carotid IMT were predicted by the duration of HIV infection (p<0.001) and CD4 T-cells (p=0.035). Brachial FMD was impaired in HIV patients (8.8+/-3% versus 12.2+/-3% in controls; p<0.001). In contrast, NMD values practically overlapped in the HIV patients and controls. Analysis of the data in relation to viral load showed that FMD was significantly more impaired in the subgroup of patients with viral load values above the median (p<0.001). In addition, there was a highly significant, inverse correlation between FMD and the HIV-RNA copies (p<0.001).
HIV infection causes functional and structural vascular alterations in a very early stage of the infection independent of HAART and metabolic factors. The data lend support to the viral infectious theory of atherosclerosis. Early assessment of the vascular status in HIV-infected patients is suggested.
HIV 感染患者的动脉粥样硬化过早发生被认为与高效抗逆转录病毒治疗（HAART）及相关代谢并发症有关。HIV 本身是否起作用仍是一个未解决的问题。本研究的目的是评估 HIV 本身是否具有致动脉粥样硬化作用。
我们测量了 38 例未经治疗的初治 HIV 感染患者和 41 例健康对照者的颈动脉内膜中层厚度（IMT）以及肱动脉内皮依赖性（FMD）和内皮非依赖性（NMD）血管舒张功能。
选择对照者使其在代谢危险因素方面与 HIV 患者相匹配。HIV 患者的平均颈动脉 IMT 高于对照组（0.85±0.2mm；p<0.001），对照组为（0.63±0.1mm）。在逐步多元回归模型中，颈动脉 IMT 的变化可由 HIV 感染持续时间（p<0.001）和 CD4 T 细胞（p=0.035）预测。HIV 患者的肱动脉 FMD 受损（8.8±3%，而对照组为 12.2±3%；p<0.001）。相比之下，并 HIV 患者和对照组的 NMD 值实际重叠。对与病毒载量相关的数据进行分析显示，病毒载量值高于中位数的患者亚组中 FMD 受损更明显（p<0.001）。此外 FMD 与 HIV-RNA 拷贝数之间存在高度显著的负相关（p<0.001）。
HIV 感染在感染的极早期就会导致血管功能和结构改变，与 HAART 和代谢因素无关。这些数据支持动脉粥样硬化的病毒感染理论。建议对 HIV 感染患者的血管状况进行早期评估。
