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

ABSTRACT

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/mm³) 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.

KEYWORDS:

• HIV
• stroke
• atherosclerosis
• stroke mechanism
• small artery disease

Disclosure statement

M. T. Y. reports personal fees from Gilead Sciences and Viiv outside the submitted work. J. G. reports grants from the Campbell Foundation and the NIH during the conduct of the study and personal fees from Pfizer and ProPhase, outside the submitted work. He has also received personal fees while working as a medico-legal consultant outside the submitted work. All other authors report no conflicts.

ORCID

Jose Gutierrez http://orcid.org/0000-0002-2175-8078

Additional information

Funding

This work was supported by Campbell Foundation; National Institute of Allergy and Infectious Diseases: [grant number 5T32AI007387-27].