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Published on: January 12, 2016
Risk of cerebrovascular events in persons with and without HIV: a Danish nationwide population-based cohort study
Line D Rasmussen1, Frederik N Engsig, Hanne Christensen
1Department of Infectious Diseases, Odense University Hospital, Denmark. linedahlerup@hotmail.com
Insights
HIV infection increases cerebrovascular event (CVE) risk, especially with injection drug use (IDU) and low CD4 counts. Abacavir exposure also elevates risk, but highly active antiretroviral therapy (HAART) does not.
Area of Science:
- Epidemiology
- Infectious Diseases
- Neurology
Background:
- HIV infection is associated with various comorbidities.
- Cerebrovascular events (CVEs) are a significant concern in HIV-infected populations.
- Understanding risk factors for CVEs in HIV is crucial for patient management.
Purpose of the Study:
- To assess the risk of CVEs in individuals with HIV.
- To evaluate the impact of injection drug use (IDU), immunodeficiency, and highly active antiretroviral therapy (HAART) on CVE risk.
- To investigate the role of specific antiretroviral drugs and family-related factors in CVE development.
Main Methods:
- A nationwide, population-based cohort study design was employed.
- Included Danish HIV-infected individuals and a comparison cohort.
- Incidence rate ratios (IRRs) and time-dependent Cox regression analyses were used to assess risk factors and drug impacts.
Main Results:
- HIV-infected individuals showed an increased risk of CVEs (IRR 1.60 for non-IDU, 3.94 for IDU).
- Low CD4 cell count (<200 cells/μl) and abacavir exposure increased CVE risk.
- HAART, protease inhibitors, indinavir, didanosin, and tenofovir did not significantly impact CVE risk.
Conclusions:
- HIV-infected individuals face a higher risk of CVEs, influenced by IDU, low CD4 count, and abacavir.
- HAART does not appear to increase CVE risk.
- Family risk factors are generally not associated with CVEs, except in parents of IDU HIV-infected individuals.
Objective:
To assess the risk of cerebrovascular events (CVEs) in HIV-infected individuals and evaluate the impact of proven risk factors, injection drug abuse (IDU), immunodeficiency, HAART and family-related risk factors.
Design:
Nationwide, population-based cohort study.
Methods:
The study population included all Danish HIV-infected individuals, a population-based comparison cohort and parents of both cohorts - all with no prior cerebral comorbidity. We computed incidence rate ratios (IRRs) of overall CVEs and CVEs with and without proven risk factors, stratifying the analyses on IDU. Impact of immunodeficiency, HAART, protease inhibitors, indinavir, didanosin, tenofovir and abacavir on risk of CVEs was analyzed using time-dependent Cox regression analyses.
Results:
HIV-infected individuals had an increased risk of CVEs compared with the comparison cohorts [(non-IDU HIV adjusted IRR 1.60; 95% confidence interval [CI] 1.32-1.94), (IDU HIV adjusted IRR 3.94; 95% CI 2.16-7.16)]. The risk was increased with and without proven risk factors. A CD4 cell count of 200 cells/μl or less before the start of HAART and exposure to abacavir increased the risk of CVE [(adjusted IRR 2.26; 95% CI 1.05-4.86) and (adjusted IRR 1.66; 95% CI 1.03-2.68)]. Protease inhibitors, indinavir, didanosin, tenofovir and HAART in general had no impact. Risk of CVEs was only increased in the parents of IDU HIV-infected individuals.
Conclusion:
HIV-infected individuals have an increased risk of CVEs with and without proven risk factors. The risk is associated with IDU, low CD4 cell count and exposure to abacavir, but not with HAART. An association with family-related risk factors seems vague except for parents of IDU individuals.
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