Ortiz G, Koch S, Romano J G, Forteza A M, Rabinstein A A
Department of Neurology, University of Miami School of Medicine, FL, USA.
Neurology. 2007 Apr 17;68(16):1257-61. doi: 10.1212/01.wnl.0000259515.45579.1e.
To evaluate the types and mechanisms of stroke in a large population of HIV-infected patients.
We reviewed records of consecutive HIV-infected patients with acute stroke admitted to a large metropolitan hospital between 1996 and 2004. Stroke mechanism was defined by consensus between two cerebrovascular neurologists using TOAST classification.
A total of 82 patients were included, 77 with ischemic stroke and 5 with intracerebral hemorrhage. Mean age was 42 years and 89% were African American. Previous diagnosis of HIV infection was documented in 91% and AIDS diagnosis in 80%. Mean CD4 count was 113 cells/mm(3) and 85% had CD4 count <200 cells/mm(3). A total of 61% of patients had received combination antiretroviral treatment (CART). The mechanism of ischemic stroke was large artery atherosclerosis in 12%, cardiac embolism in 18%, small vessel occlusion in 18%, other determined etiology in 23%, and undetermined in 29% (including 19% with incomplete evaluation). Vasculitis was deemed responsible for the stroke in 10 patients (13%) and hypercoagulability in 7 (9%). Protein S deficiency was noted in 10/22 (45%) and anticardiolipin antibodies in 9/31 (29%) tested patients. When comparing patients with large or small vessel disease (atherothrombotic strokes) vs the rest of the population, there were no differences in exposure to CART or CD4 count, but patients with non-atherothrombotic strokes were younger (p = 0.04). Recent cocaine exposure was less common among patients with atherothrombotic strokes (p = 0.02). Strokes were fatal or severely disabling in 35% of cases.
Stroke mechanisms are variable in HIV-infected patients, with a relatively high incidence of vasculitis and hypercoagulability. In our population of severely immunodepressed patients, exposure to combination antiretroviral treatment did not significantly influence the mechanism of stroke.
评估大量感染人类免疫缺陷病毒(HIV)患者的中风类型及机制。
我们回顾了1996年至2004年间入住一家大型都市医院的连续性急性中风HIV感染患者的记录。中风机制由两位脑血管神经科医生根据TOAST分类法达成共识后确定。
共纳入82例患者,其中77例为缺血性中风,5例为脑出血。平均年龄为42岁,89%为非裔美国人。91%的患者有HIV感染既往诊断记录,80%有艾滋病诊断记录。平均CD4细胞计数为113个/立方毫米,85%的患者CD4细胞计数<200个/立方毫米。共有61%的患者接受了联合抗逆转录病毒治疗(CART)。缺血性中风的机制为大动脉粥样硬化占12%,心源性栓塞占18%,小血管闭塞占18%,其他明确病因占23%,未明确占29%(包括19%评估不完整者)。血管炎被认为是10例患者(13%)中风的原因,高凝状态是7例患者(9%)中风的原因。检测的患者中,10/22(45%)有蛋白S缺乏,9/31(29%)有抗心磷脂抗体。比较大血管或小血管疾病(动脉粥样硬化性血栓形成性中风)患者与其他患者时,CART暴露或CD4细胞计数无差异,但非动脉粥样硬化性血栓形成性中风患者更年轻(p = 0.04)。近期使用可卡因在动脉粥样硬化性血栓形成性中风患者中较少见(p = 0.02)。35%的病例中风是致命的或导致严重残疾。
HIV感染患者的中风机制各不相同,血管炎和高凝状态的发生率相对较高。在我们这群严重免疫抑制的患者中,联合抗逆转录病毒治疗的暴露并未显著影响中风机制。