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J Am Coll Cardiol, 2006; 47:1117-1123, doi:10.1016/j.jacc.2005.09.073
(Published online 21 February 2006). © 2006 by the American College of Cardiology Foundation |





* Department of Internal Medicine and Infectious Disease, University Medical Center Utrecht, the Netherlands
Department of Nephrology, Leiden University Medical Center, Leiden, the Netherlands
Department of Internal Medicine, St. Franciscus Gasthuis, Rotterdam, the Netherlands
Centre de Recerca Biomèdica, Hospital Universitari de Sant Joan, Reus, Spain
Manuscript received May 5, 2005; revised manuscript received September 9, 2005, accepted September 20, 2005.
* Reprint requests and correspondence: Dr. Jeroen P. H. van Wijk, Departments of Infectious Disease and Internal Medicine, University Medical Center Utrecht, G02.402, P.O. Box 85500, 3508 GA Utrecht, the Netherlands. (Email: jwijk3{at}hotmail.com).
OBJECTIVES: We investigated functional and structural markers of atherosclerosis in human immunodeficiency virus (HIV)-infected patients in relation to the presence of the metabolic syndrome (MS).
BACKGROUND: Antiretroviral combination therapy in HIV has been associated with cardiovascular risk factors that cluster in the MS.
METHODS: Thirty-seven HIV-infected patients underwent assessment of flow-mediated vasodilation (FMD), aortic pulse-wave velocity (PWV), and carotid intima-media thickness (IMT). Age-matched type 2 diabetic patients (n = 13) and healthy controls (n = 14) served as reference groups.
RESULTS: Fifteen HIV-infected patients (41%) fulfilled the National Cholesterol Education Program criteria of the MS. The FMD was similarly impaired in HIV-infected patients without the MS (MS group) and the diabetic patients (5.1 ± 0.4% and 4.9 ± 0.6%, respectively) compared with controls (8.8 ± 0.7%). The HIV-infected patients with the MS (MS+ group) had even more impaired FMD (2.5 ± 0.3%). Carotid IMT was similarly increased in the MS+ group and the diabetic patients compared with the other groups. Aortic PWV was increased in the diabetic patients only. In HIV-infected patients, FMD was related to metabolic parameters, whereas aortic PWV and IMT were related to parameters of HIV infection, time on antiretroviral combination therapy, inflammatory (C-reactive protein and leukocytes) and metabolic parameters.
CONCLUSIONS: The data of the present study suggest an increased cardiovascular risk in HIV-infected patients, even in the absence of clustering of metabolic risk variables. The presence of the MS in HIV is associated with even more advanced atherosclerotic changes. Presumably, both HIV infection and antiretroviral therapy may promote atherosclerosis through mechanisms involving endothelial cells, either directly or indirectly via metabolic risk factors.
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