Fourie C M T, Schutte A E, Smith W, Kruger A, van Rooyen J M
Hypertension in Africa Research Team (HART), North-West University, Potchefstroom 2520, South Africa.
MRC Research Unit for Hypertension and Cardiovascular Disease, North-West University, Potchefstroom 2520, South Africa.
Atherosclerosis. 2015 May;240(1):154-60. doi: 10.1016/j.atherosclerosis.2015.03.015. Epub 2015 Mar 14.
The role the human immunodeficiency virus (HIV) and antiretroviral treatment on endothelial activation, and the subsequent relationship with cardiovascular disease, is not well understood. We investigated endothelial activation, inflammatory and cardiometabolic profiles, and measures of vascular structure and function of 66 antiretroviral treated (ART), 78 never-treated (no-ART) HIV infected and 165 HIV free Africans.
Blood samples were obtained for biochemical analysis and blood pressure, pulse wave velocity (PWV) and carotid intima-media thickness (IMT) measurements were performed.
The HIV infection duration was at least five years and the treatment 2.86±0.13 years. The intracellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) levels were elevated in the HIV infected groups compared to the controls. The odds of higher adhesion molecule levels were increased when HIV infected (especially in the no-ART group); OR no-ART vs. no-HIV: ICAM 3.92 (2.2-7.0); VCAM 16.2 (7.5-35). ICAM and VCAM associated with HIV status and interleukin-6 (IL-6) in the total group (all p<0.01). In both HIV infected groups VCAM associated inversely with CD4 counts (no-ART: β=-0.28, p=0.01; ART: β=-0.22, p=0.07) and TC (no-ART: β=-0.36, p<0.01; ART: β=-0.27, p=0.03). The ART group had an unfavourable lipid profile compared to the no-ART group. The inflammatory markers (C-reactive protein (CRP) and IL-6), PWV and IMT did not differ between the three groups.
HIV infected Africans showed endothelial activation when compared to HIV free controls. The endothelial activation was not accompanied by increased inflammation (as measured with CRP and IL-6), arterial stiffness or sub-clinical atherosclerosis.
人类免疫缺陷病毒（HIV）及抗逆转录病毒治疗对内皮细胞活化的作用，以及其与心血管疾病的后续关系，目前尚不清楚。我们调查了66例接受抗逆转录病毒治疗（ART）、78例未接受治疗（未接受ART）的HIV感染者以及165例未感染HIV的非洲人的内皮细胞活化、炎症和心脏代谢特征，以及血管结构和功能指标。
采集血样进行生化分析，并测量血压、脉搏波速度（PWV）和颈动脉内膜中层厚度（IMT）。
HIV感染持续时间至少为5年，治疗时间为2.86±0.13年。与对照组相比，HIV感染组的细胞间黏附分子（ICAM）和血管细胞黏附分子（VCAM）水平升高。HIV感染时（尤其是在未接受ART组），黏附分子水平升高的几率增加；未接受ART组与未感染HIV组相比：ICAM为3.92（2.2 - 7.0）；VCAM为16.2（7.5 - 35）。在总人群中，ICAM和VCAM与HIV状态及白细胞介素-6（IL-6）相关（所有p<0.01）。在两个HIV感染组中，VCAM均与CD4细胞计数呈负相关（未接受ART组：β=-0.28，p=0.01；接受ART组：β=-图22，p=0.07）以及与总胆固醇（未接受ART组：β=-0.36，p<0.01；接受ART组：β=-0.27，p=0.03）呈负相关。与未接受ART组相比，接受ART组的血脂谱较差。三组之间的炎症标志物（C反应蛋白（CRP）和IL-6）、PWV和IMT没有差异。
与未感染HIV的对照组相比，感染HIV的非洲人表现出内皮细胞活化。内皮细胞活化并未伴有炎症增加（以CRP和IL-6衡量）、动脉僵硬度增加或亚临床动脉粥样硬化。
