Increased arterial inflammation relates to high-risk coronary plaque morphology in HIV-infected patients.
Increased arterial inflammation relates to high-risk coronary plaque morphology in HIV-infected patients.
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DOI:
10.1097/qai.0000000000000138
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发表时间:
2014-06-01
期刊:
影响因子:
--
通讯作者:
Grinspoon S
中科院分区:
文献类型:
--
作者:
Tawakol A;Lo J;Zanni MV;Marmarelis E;Ihenachor EJ;MacNabb M;Wai B;Hoffmann U;Abbara S;Grinspoon S
Mechanisms predisposing HIV-infected patients to increased CVD risk remain unclear. To determine the interrelationship between arterial inflammation and high-risk coronary plaque morphology in HIV-infected patients with subclinical coronary atherosclerosis. 41 HIV-infected patients on stable ART without known CVD but with atherosclerotic plaque on coronary CT angiography were evaluated with 18F-FDG-PET. Patients were stratified into two groups based on relative degree of arterial inflammation (aortic target-to-background-ratio, or TBR). High-risk coronary atherosclerotic plaque morphology features were compared between groups. HIV-infected patients with higher and lower TBR’s were similar with respect to traditional CVD risk parameters. Among HIV-infected patients with higher TBR, an increased percentage of patients demonstrated at least one low attenuation coronary atherosclerotic plaque (40% vs. 10%, p = 0.02) and at least one 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 (LAP’s) 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 LAP’s/subject (β=0.35, p = 0.004), controlling for age, gender, LDL, duration HIV, and CD4. These data demonstrate a relationship between arterial inflammation on 18F-FDG-PET and high-risk coronary atherosclerotic plaque features among HIV-infected patients with sublclinical 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.