Objective: To evaluate the evidence for subclinical atherosclerosis among HIV patients.
Design: Systematic review of observational studies.
Data sources: We searched Medline, Cochrane DSR, ACP Journal Club, DARE, CMR, HTA, NHSEED, EMBASE, and the Cochrane Controlled Trials Register for studies published prior to November 2008.
Review methods: Eligible studies were cross-sectional, cohort, or case control studies reporting carotid ultrasound intima media thickness (CIMT), focal plaque incidence, or coronary calcium (CAC), as determined by HIV positivity or protease inhibitor (PI) exposure. Two independent reviewers abstracted data using a standardized form. The primary outcome was weighted mean difference (WMD) for carotid intima media thickness (CIMT) comparing HIV positive versus negative patients. Other outcomes included WMD by PI exposure and the odds ratio (OR) for a focal carotid plaque or CAC.
Data synthesis: Data from six cross-sectional, seven case-control, and 13 cohort studies were included, involving 5,456 HIV positive and 3,600 HIV negative patients. The weighted mean CIMT was 0.04 mm thicker among HIV patients vs. non-HIV (95% CI, 0.02-0.06; p <0.001). HIV positivity was not associated with carotid plaque or CAC. PI exposure did not significantly affect CIMT, carotid plaque, or CAC. There was evidence of publication bias, and stratified analysis and meta-regression showed outcomes were influenced by study design, age, gender, and smoking. However, HIV positivity slightly increased CIMT even after sensitivity analyses.
Conclusions: HIV infection and PI exposure are not strong independent risk factors for subclinical atherosclerosis. Confounding may contribute to over-estimation of the risk associated with HIV and PI exposure.
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