Key result
Protease inhibitor exposure and HIV infection were not associated with increased carotid intima-media thickness (median 0.690 mm for PI users vs 0.712 mm for PI-naive and 0.698 mm for uninfected).
Why the study?
Does protease inhibitor exposure or HIV infection increase carotid artery intima-media thickness compared to unexposed or uninfected matched subjects?
Population
134 individuals matched by age, sex, race/ethnicity, smoking status, blood pressure, and menopausal status…
Comparison
Continuous use of protease inhibitor therapy for… vs HIV-infected subjects without prior PI use, and…
Design
Cohort
Authors
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Traditional CV risks overshadow HIV/PI effects on carotid IMT; leaves open independent contributions in lower-risk cohorts.
Cohort (n=134)
Yes
Does protease inhibitor exposure or HIV infection increase carotid artery intima-media thickness compared to unexposed or uninfected matched subjects?
Absolute Event Rate: 0.69% vs 0.712%
Traditional cardiovascular risk factors, rather than HIV infection or protease inhibitor exposure, are the primary predictors of subclinical atherosclerosis as measured by carotid intima-media thickness.
Currier et al. (2005) conducted a cohort in HIV infection (n=134). Protease inhibitor (PI) therapy vs. HIV-infected without prior PI use and HIV-uninfected subjects was evaluated on Intima-media thickness (IMT) of the carotid artery. Protease inhibitor exposure and HIV infection were not associated with increased carotid intima-media thickness (median 0.690 mm for PI users vs 0.712 mm for PI-naive and 0.698 mm for uninfected).
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