Mechanisms predisposing HIV-infected patients to increased cardiovascular disease (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.
Forty-one HIV-infected patients on stable antiretroviral therapy without known CVD but with atherosclerotic plaque on coronary CT angiography were evaluated with 18F-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.
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.
These data demonstrate a relationship between arterial inflammation on 18F-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.
*Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA;
†Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, MA; and
‡Cardiovascular Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Correspondence to: Steven Grinspoon, MD, Program in Nutritional Metabolism, Massachusetts General Hospital; 55 Fruit Street, 5 Longfellow Plaza, Suite 207, Boston, MA 02114 (e-mail: email@example.com).
Study design (A.T., J.L., M.V.Z., and S.G.), data collection (A.T., J.L., M.V.Z., E.M., E.J.I., M.M., B.W., U.H., S.A., and S.G.), data interpretation (A.T., J.L., M.V.Z., E.M., B.W., S.A., and S.G.), drafting of article (A.T., M.V.Z., U.H., and S.G.), and critical revision of article (A.T., J.L., M.V.Z., E.M., E.J.I., M.M., B.W., U.H., S.A., and S.G.). All authors have read and approved the text submitted.
Supported by the grants NIH R01 HL095123 to S.G. and NIH K23 HL092792 to J.L.
The authors have no conflicts of interest to disclose.
Received September 26, 2013
Accepted February 20, 2014