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Role of pre-stroke immunity in ischemic stroke mechanism among patients with HIV

机译:患有艾滋病毒患者缺血性脑卒中机制中卒中前免疫的作用

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Individuals with HIV are at a higher risk of stroke compared to uninfected populations. The role of HIV-related immunosuppression in stroke mechanism is uncertain. Our aim is to test the hypothesis that stroke mechanisms among HIV+ individuals vary according to preceding CD4 counts. We carried out a retrospective chart review of inpatient admissions for ICD-9 defined ischemic events (TIA or stroke) in HIV+ individuals from 2002 to 2016 at a tertiary care center. Stroke mechanisms were ascertained based on radiographic and clinical presentation, and adjudicated by the treating team and confirmed separately by a vascular neurologist. Vascular risk factors, use of antiretroviral drugs (ARVs), nadir CD4 and current CD4 counts (cells/mm(3)) were captured to build logistic regressions and generalized linear models to calculate the odds ratios (OR) and beta estimates with their respective 95% confidence intervals. We found that among 115 cases (median age 52, 64% men), stroke mechanisms were 22% due to large artery atherosclerosis (LAA), 17% small artery disease, 16% infectious, 8% cardioembolic, 21% cryptogenic, and 16% other etiologies. The median nadir CD4-count was 153 (IQR 22-274), and 312 (IQR 88-518) at the time of stroke, and 53% were on ARVs. LAA was more common with longer HIV infection (OR 1.1 per year, 1.0-1.2) and nadir CD4 counts 200 (OR 6.7, 1.4-31.9). Stroke due to LAA was associated with higher CD4 count the year prior to stroke (B = 0.009, P = 0.06 for the interaction) independent of CD4 nadir 200 (B = 1.88, P = 0.035). We concluded that in this sample, LAA was the most frequent stroke mechanism among HIV+ individuals with nadir CD4 200 but higher CD4 counts near the time of stroke. Determining the association between pre-stroke immune status and stroke mechanisms may allow a targeted approach to stroke prevention.
机译:与未感染的人群相比,艾滋病毒的个体患有较高的行程风险。 HIV相关免疫抑制在卒中机制中的作用是不确定的。我们的宗旨是测试HIV +个人中风机制的假设根据前面的CD4计数而变化。我们对2002年至2016年在第三级护理中心的艾滋病毒+个人中对ICD-9定义缺血事件(TIA或Strows)的住院入住入住入住入住途径的回顾性审查。基于射线照相和临床介绍确定中风机制,并由治疗团队判决并由血管神经科医生分开证实。捕获血管危险因素,抗逆转录病毒药物(ARV),Nadir CD4和当前CD4计数(细胞/ mm(3))被捕获以构建逻辑回归和广义的线性模型,以计算各自的差距比率(或)和β估计95%的置信区间。我们发现,由于大动脉动脉粥样硬化(LAA),17%的小动脉疾病,16%感染,8%的心脏病,21%Clyptogenic,21%Clyptogenic,21%Clyptogenic,21%Clyptogenic,21%Clyptogenic,21%Clyptogenic,21%Cryptogenic,21%Chexogenic,21%Cryptogenic,21%Clyptogenic,21%Chexogenic和16件%其他病因。中位数CD4计数为153(IQR 22-274),卒中时312(IQR 88-518),53%在ARV上。 LAA更常见,较长的HIV感染(或每年1.1,1.0-1.2)和Nadir CD4计数& 200(或6.7,1.4-31.9)。由于LAA由于CD4Nadir而不是LAA,LAA引起的卒中与较高的CD4计数(B = 0.009,P = 0.06)相关联(B = 0.009,P = 0.06)。我们得出结论,在该样品中,LAA是艾滋病毒+个体中最常见的卒中机制,Nadir CD4& 200但高级CD4靠近行程时的计数。确定预卒中预防免疫状态和中风机制之间的关联可以允许靶向方法预防。

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