Higher arterial inflammation on F-FDG-PET in HIV-infected patients was associated with an increased prevalence of at least one low-attenuation coronary plaque (40% vs 10%, P=0.02).
Cross-Sectional (n=41)
Does higher arterial inflammation relate to high-risk coronary plaque morphology in HIV-infected patients with subclinical coronary atherosclerosis?
Increased arterial inflammation on F-FDG-PET is significantly associated with high-risk coronary plaque features in HIV-infected patients with subclinical atherosclerosis.
Tasa de eventos absoluta: 40% vs 10%
valor p: p=0.02
BACKGROUND: Mechanisms predisposing HIV-infected patients to increased cardiovascular disease (CVD) risk remain unclear. OBJECTIVE: To determine the interrelationship between arterial inflammation and high-risk coronary plaque morphology in HIV-infected patients with subclinical coronary atherosclerosis. METHODS: Forty-one HIV-infected patients on stable antiretroviral therapy without known CVD but with atherosclerotic plaque on coronary CT angiography were evaluated with F-FDG-PET. Patients were stratified into 2 groups based on relative degree of arterial inflammation aortic target-to-background ratio (TBR). High-risk coronary atherosclerotic plaque morphology features were compared between groups. RESULTS: HIV-infected patients with higher and lower TBRs were similar with respect to traditional CVD risk parameters. Among HIV-infected patients with higher TBR, an increased percentage of patients demonstrated at least 1 low-attenuation coronary atherosclerotic plaque (40% vs. 10%, P = 0.02) and at least 1 coronary atherosclerotic plaque with both low attenuation and positive remodeling (35% vs. 10%, P = 0.04). Moreover, in the higher TBR group, both the number of low-attenuation plaques per patient (P = 0.02) and the number of vulnerability features in the most vulnerable plaque (P = 0.02) were increased. TBR grouping remained significantly related to the number of low-attenuation plaques/subject (β = 0.35, P = 0.004), controlling for age, gender, low-density lipoprotein, duration of HIV, and CD4. CONCLUSIONS: These data demonstrate a relationship between arterial inflammation on F-FDG-PET and high-risk coronary atherosclerotic plaque features among HIV-infected patients with subclinical coronary atherosclerosis. Further studies are needed to determine whether arterial inflammation and related high-risk coronary morphology increase the risk of clinical CVD events in the HIV population.
Tawakol et al. (Thu,) conducted a cross-sectional in HIV infection with subclinical coronary atherosclerosis (n=41). Higher arterial inflammation (higher aortic target-to-background ratio) vs. Lower arterial inflammation was evaluated on Presence of at least 1 low-attenuation coronary atherosclerotic plaque (p=0.02). Higher arterial inflammation on F-FDG-PET in HIV-infected patients was associated with an increased prevalence of at least one low-attenuation coronary plaque (40% vs 10%, P=0.02).
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