Hanna David B, Post Wendy S, Deal Jennifer A, Hodis Howard N, Jacobson Lisa P, Mack Wendy J, Anastos Kathryn, Gange Stephen J, Landay Alan L, Lazar Jason M, Palella Frank J, Tien Phyllis C, Witt Mallory D, Xue Xiaonan, Young Mary A, Kaplan Robert C, Kingsley Lawrence A
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York.
Department of Medicine, Johns Hopkins University School of Medicine Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
Clin Infect Dis. 2015 Aug 15;61(4):640-50. doi: 10.1093/cid/civ325. Epub 2015 Apr 22.
Individuals infected with human immunodeficiency virus (HIV) live longer as a result of effective treatment, but long-term consequences of infection, treatment, and immunological dysfunction are poorly understood.
We prospectively examined 1011 women (74% HIV-infected) in the Women's Interagency HIV Study and 811 men (65% HIV-infected) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004-2013. Outcomes included changes in right common carotid artery intima-media thickness (CCA-IMT) and new focal carotid artery plaque formation (IMT >1.5 mm) over median 7 years. We assessed the association between HIV serostatus and progression of subclinical atherosclerosis, adjusting for demographic, behavioral, and cardiometabolic risk factors.
Unadjusted mean CCA-IMT increased (725 to 752 µm in women, 757 to 790 µm in men), but CCA-IMT progression did not differ by HIV serostatus, either in combined or sex-specific analyses. Focal plaque prevalence increased from 8% to 15% in women and 25% to 34% in men over 7 years. HIV-infected individuals had 1.6-fold greater risk of new plaque formation compared with HIV-uninfected individuals (relative risk [RR] 1.61, 95% CI, 1.12-2.32), adjusting for cardiometabolic factors; the association was similar by sex. Increased plaque occurred even among persistently virologically suppressed HIV-infected individuals compared with uninfected individuals (RR 1.56, 95% CI, 1.07-2.27). HIV-infected individuals with baseline CD4+ ≥ 500 cells/µL had plaque risk not statistically different from uninfected individuals.
HIV infection is associated with greater increases in focal plaque among women and men, potentially mediated by factors associated with immunodeficiency or HIV replication at levels below current limits of detection.
由于有效治疗，感染人类免疫缺陷病毒（HIV）的个体寿命延长，但对感染、治疗及免疫功能障碍的长期后果了解甚少。
我们前瞻性地研究了参与女性机构间HIV研究的1011名女性（74%感染HIV）和多中心艾滋病队列研究的811名男性（65%感染HIV），这些人在2004年至2013年期间接受了多次B型颈动脉超声成像检查。结果包括右侧颈总动脉内膜中层厚度（CCA-IMT）的变化以及在中位7年时间里新的局灶性颈动脉斑块形成（IMT>1.5毫米）。我们评估了HIV血清学状态与亚临床动脉粥样硬化进展之间的关联，并对人口统计学、行为学和心脏代谢危险因素进行了校正。
未经校正的平均CCA-IMT有所增加（女性从725微米增至752微米，男性从757微米增至790微米），但在综合分析或按性别分析中，CCA-IMT进展在HIV血清学状态方面并无差异。局灶性斑块患病率在7年中女性从8%增至15%，男性从25%增至34%。校正心脏代谢因素后，与未感染HIV的个体相比，感染HIV的个体出现新斑块形成的风险高1.6倍（相对风险[RR]1.61，95%CI，1.12-2.32）；按性别分析，该关联相似。与未感染个体相比，即使在病毒学持续抑制的HIV感染个体中也出现了更多斑块（RR 1.56，95%CI，1.07-2.27）。基线CD4+≥500细胞/微升的HIV感染个体的斑块风险与未感染个体无统计学差异。
HIV感染与男性和女性局灶性斑块的更大增加有关联，可能由与免疫缺陷或低于当前检测水平的HIV复制相关的因素介导。
