Mosepele Mosepele, Mohammed Terence, Mupfumi Lucy, Moyo Sikhulile, Bennett Kara, Lockman Shahin, Hemphill Linda C, Triant Virginia A
Department of Medicine, Faculty of Medicine, University of Botswana, Gaborone, Botswana; Botswana-Harvard AIDS Institute Partnership, Gaborone, Botswana. Email:
Botswana-Harvard AIDS Institute Partnership, Gaborone, Botswana.
Cardiovasc J Afr. 2018;29(3):155-161. doi: 10.5830/CVJA-2018-003. Epub 2018 May 14.
Untreated HIV infection is associated with increased biomarkers of endothelial dysfunction. However, the predictors and degree of endothelial dysfunction among virally suppressed HIV-infected adults on long-term antiretroviral therapy (ART) have not been well studied in sub-Saharan Africa (SSA).
We enrolled 112 HIV-infected adults with virological suppression on long-term ART and 84 HIV-uninfected controls in Botswana. We measured plasma levels of markers of endothelial injury [soluble vascular adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1) and E-selectin] and plasma levels of biomarkers of inflammation [interleukin 6 (IL-6)] and monocyte activation (sCD163). Baseline traditional cardiovascular disease (CVD) risk factors and bilateral common carotid intima-media thickness (cIMT) were also available for all participants. We assessed whether HIV status (despite virological suppression on ART) was associated with biomarkers of endothelial dysfunction after controlling for traditional CVD risk factors in linear regression models. We additionally assessed the association between IL-6, sCD163 and cIMT with endothelial dysfunction in separate multivariate linear regression models, controlling for cIMT, among virally suppressed HIV-infected participants only.
In multivariate analysis, HIV infection was significantly associated with increased VCAM-1 (p < 0.01) and ICAM-1 (p = 0.03) but not E-selectin (p = 0.74) levels. Within the HIV-positive group, higher sCD163 levels were associated with decreased ICAM-1 and E-selectin (p < 0.01 and p = 0.01, respectively) but not VCAM-1 (p = 0.13) levels. IL-6 was not associated with any of the biomarkers of endothelial dysfunction.
HIV disease was associated with biomarkers of endothelial dysfunction among virally suppressed adults in Botswana on long-term ART after controlling for traditional CVD risk factors. Future work should explore the clinical impact of persistent endothelial dysfunction following long-term HIV viral suppression on the risk of CVD clinical endpoints among HIV-infected patients in this setting.
未经治疗的HIV感染与内皮功能障碍生物标志物升高有关。然而，在撒哈拉以南非洲（SSA），长期接受抗逆转录病毒治疗（ART）且病毒得到抑制的HIV感染成年人中，内皮功能障碍的预测因素和程度尚未得到充分研究。
我们在博茨瓦纳招募了112名长期接受ART且病毒学得到抑制的HIV感染成年人以及84名未感染HIV的对照者。我们测量了内皮损伤标志物[可溶性血管细胞黏附分子1（VCAM-1）、细胞间黏附分子1（ICAM-1）和E-选择素]的血浆水平以及炎症生物标志物[白细胞介素6（IL-6）]和单核细胞活化（sCD163）的血浆水平。所有参与者还提供了基线传统心血管疾病（CVD）危险因素和双侧颈总动脉内膜中层厚度（cIMT）数据。我们在多元线性回归模型中控制传统CVD危险因素后，评估HIV状态（尽管接受ART后病毒学得到抑制）是否与内皮功能障碍生物标志物相关。我们还在单独的多元线性回归模型中，仅在病毒得到抑制的HIV感染参与者中，控制cIMT后，评估IL-6、sCD163与cIMT与内皮功能障碍之间的关联。
在多变量分析中，HIV感染与VCAM-1水平升高（p < 0.01）和ICAM-1水平升高（p = 0.03）显著相关，但与E-选择素水平无关（p = 0.74）。在HIV阳性组中，较高的sCD163水平与ICAM-1和E-选择素水平降低相关（分别为p < 0.01和p = 0.01），但与VCAM-1水平无关（p = 0.13）。IL-6与任何内皮功能障碍生物标志物均无关联。
在博茨瓦纳，长期接受ART且病毒得到抑制的成年人中，控制传统CVD危险因素后，HIV疾病与内皮功能障碍生物标志物相关。未来的工作应探讨长期HIV病毒抑制后持续的内皮功能障碍对该环境下HIV感染患者CVD临床终点风险的临床影响。
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