Abstract Body

Coronary atherosclerotic plaque is increased in HIV-infected individuals and associated with subsequent cardiovascular events. Cerebrovascular (CV) events including stroke and transient ischemic attack (TIA) are also increased in HIV; however there are no data characterizing the prevalence, characteristics and prognostic associations of incidental carotid plaque in HIV.  

From a registry, we identified all HIV-infected individuals free of known CV disease who underwent a contrast neck CT from 2005 to 2014. Data collection, including CV and HIV-specific risk factors and image analysis, were performed by blinded independent teams. Image variables included the presence of carotid plaque and non-calcified plaque (NCP). The outcome of interest was a CV event (stroke, TIA) defined by ICD code and independently adjudicated. Association between plaque and events was determined using Cox proportional hazard models and compared with propensity-matched (age, gender, indication for CT, DM, HTN, HLD, smoking) HIV-uninfected controls.

248 HIV-infected individuals free of prior CV disease (43+9 years, 24% female, 10% DM, 10% HTN, 33% smokers, 15% on statins, mean LDL 89+38mg/dl) were compared to 118 matched HIV-uninfected controls. The median duration of HIV was 16 yrs (10-21) and mean nadir CD4 count was 120 cells/mm3. At time of CT, the mean CD4 count was 308 cells/mm3, 79% were on ART, 20% were co-infected with HCV and 51% had an undetectable viral load (VL). On CT, HIV-infected individuals (vs. controls) had a higher prevalence of any carotid plaque (41% vs. 25%, P=0.005) and NCP (56% vs. 29%, P=0.03). Longer duration of HIV and ART were associated with increased plaque, while lower VL was associated with decreased plaque. Over a median follow-up of 3.1 yrs, 28 events occurred in HIV-infected individuals, rate of 4%/yr, as compared to 1%/yr in uninfected controls (P=0.013). Within HIV, the presence of carotid plaque (adjusted HR: 3.5, 1.5-8, P=0.002) and NCP (adjusted HR: 2.7, 1.3-5.8, P=0.01) were associated with an increased risk of subsequent CV events. CV events were compared between HIV-infected individuals with plaque and matched uninfected controls with plaque and HIV infected individuals with plaque were found to be at higher risk (P=0.03, Figure). 

HIV-infected individuals without known CV disease have increased prevalence of carotid plaque and NCP, and both are associated with an increased risk of subsequent CV events.