Seaberg Eric C, Benning Lorie, Sharrett A Richey, Lazar Jason M, Hodis Howard N, Mack Wendy J, Siedner Mark J, Phair John P, Kingsley Lawrence A, Kaplan Robert C
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Stroke. 2010 Oct;41(10):2163-70. doi: 10.1161/STROKEAHA.110.583856. Epub 2010 Aug 26.
Individuals with human immunodeficiency virus (HIV) who use highly active antiretroviral therapy (HAART) may have an increased risk for cardiovascular-related events, although the underlying mechanism remains unclear. We tested the hypothesis that carotid arterial stiffness was higher among persons using HAART compared to HAART-naïve and HIV-uninfected persons.
Between 2004 and 2006, we performed high-resolution B-mode ultrasound on 2789 HIV-infected and HIV-uninfected participants of the Women's Interagency HIV Study (1865 women) and the Multicenter AIDS Cohort Study (924 men) and determined carotid arterial distensibility, which is a direct measure of carotid arterial stiffness. We used generalized estimating equations to evaluate the association between distensibility and HIV infection, CD4(+) cell count, and exposure to HAART adjusted for demographic, behavioral, and clinical characteristics.
In multivariable analysis, distensibility was 4.3% lower (95% confidence interval, -7.4% to -1.1%) among HIV-infected vs uninfected participants. Among HIV-infected participants with <200 CD4(+) cells, distensibility was 10.5% lower (95% confidence interval, -14.5% to -6.2%) than that among HIV-uninfected participants, and this effect did not differ significantly by cohort or race. Concurrent HAART use was independently associated with lower distensibility among Multicenter AIDS Cohort Study participants but not among Women's Interagency HIV Study participants.
Our finding that advanced HIV-related immunosuppression was associated with increased carotid arterial stiffness independent from the effects of traditional atherosclerosis risk factors suggests that the etiologic mechanism underlying reports of an increased cardiovascular disease risk among HIV-infected individuals might involve HIV-related immunosuppression leading to vascular dysfunction and arterial stiffening.
使用高效抗逆转录病毒疗法（HAART）的人类免疫缺陷病毒（HIV）感染者发生心血管相关事件的风险可能会增加，但其潜在机制仍不清楚。我们检验了这样一个假设：与未使用HAART的HIV感染者和未感染HIV的人相比，使用HAART的人的颈动脉僵硬度更高。
在2004年至2006年期间，我们对妇女机构间HIV研究（1865名女性）和多中心艾滋病队列研究（924名男性）中的2789名HIV感染者和未感染HIV的参与者进行了高分辨率B型超声检查，并测定了颈动脉扩张性，这是颈动脉僵硬度的直接指标。我们使用广义估计方程来评估扩张性与HIV感染、CD4(+)细胞计数以及在根据人口统计学、行为学和临床特征进行调整后接触HAART之间的关联。
在多变量分析中，HIV感染者与未感染者相比，扩张性降低了4.3%（95%置信区间，-7.4%至-1.1%）。在CD4(+)细胞数<200的HIV感染者中，扩张性比未感染HIV的参与者低10.5%（95%置信区间，-14.5%至-6.2%），并且这种效应在不同队列或种族之间没有显著差异。在多中心艾滋病队列研究的参与者中，同时使用HAART与较低的扩张性独立相关，但在妇女机构间HIV研究的参与者中并非如此。
我们的研究发现，与传统动脉粥样硬化危险因素的影响无关，晚期HIV相关免疫抑制与颈动脉僵硬度增加有关，这表明HIV感染者心血管疾病风险增加报告背后的病因机制可能涉及HIV相关免疫抑制导致血管功能障碍和动脉僵硬。
