This Article Full Text Full Text (PDF) All Versions of this Article: 37/3/812    most recent 01.STR.0000204037.26797.7fv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jericó, C. Articles by Pedro-Botet, J. Search for Related Content PubMed PubMed Citation Articles by Jericó, C. Articles by Pedro-Botet, J. Related Collections Risk Factors Other arteriosclerosis Doppler ultrasound, Transcranial Doppler etc. Risk Factors for Stroke

(Stroke. 2006;37:812.)
© 2006 American Heart Association, Inc.

Original Contributions

Subclinical Carotid Atherosclerosis in HIV-Infected Patients

Role of Combination Antiretroviral Therapy

Carlos Jericó, MD; Hernando Knobel, MD; Nahum Calvo, MD; María L. Sorli, MD; Ana Guelar, MD; Juan L. Gimeno-Bayón, MD; Pere Saballs, MD; José L. López-Colomés, MD Juan Pedro-Botet, MD

From the Departments of Medicine (C.J., H.K., M.L.S., A.G., J.L.G.-B., P.S., J.L.L.-C., J.P.-B.) and Radiology IDIMAS-CRC Mar (N.C.), Hospital del Mar, Barcelona, Spain; and the Universidad Autónoma de Barcelona (C.J., H.K., J.L.G.-B., P.S., J.L.L.-C., J.P.-B.), Spain.

Correspondence to Professor J. Pedro-Botet, Department of Medicine, Paseo Marítimo, 25-29, 08003 Barcelona, Spain. E-mail 86620{at}imas.imim.es

Background and Purpose— Whether or not combination antiretroviral therapy (CART) alone directly contributes to accelerating atherosclerosis in HIV-infected patients has not been studied in depth. This study aimed to ascertain the relationship between this therapy and subclinical carotid atherosclerosis according to cardiovascular risk.

Methods— Sixty-eight HIV-infected patients with 1 cardiovascular risk factors and 64 with 2 risk factors completed the study protocol consisting of clinical, laboratory, and vascular evaluation by carotid high-resolution B-mode ultrasonography. Univariate and multivariate logistic regression analyses were performed with the presence of subclinical carotid atherosclerosis, defined by carotid intima-media thickness >0.8 mm or the presence of plaque being the dependent variable.

Results— Among the 132 enrolled patients, 93 (70.5%) were on CART and 39 (29.5%) had never been on antiretroviral therapy. In accordance with cardiovascular risk stratification, subclinical carotid atherosclerosis was found in 26.6% (17 of 64 patients) of the very low–risk group (10-year coronary risk <5%), 35.3% (12 of 34 patients) of the low-risk group (10-year coronary risk between 5% and 9%) and 76.5% (26 of 34 patients) of the moderate/high-risk group (10-year coronary risk 10%). Thus, 55 (41.7%) of the 132 HIV-infected patients had subclinical carotid atherosclerosis, and independent variables associated with carotid atherosclerosis (odds ratio; 95% CI) were: CART exposure (10.5; 2.8 to 39) and 10-year coronary risk 10% (4.2; 1.5 to 12). In very low coronary risk patients (<5%), age (per 10-year increment: 4.01; 1.12 to 14.38), systolic blood pressure (per unit mm Hg 1.07; 1.01 to 1.14), and CART exposure (8.65; 1.54 to 48.54) were independently associated with subclinical carotid atherosclerosis.

Conclusions— CART should be considered a strong, independent predictor for the development of subclinical atherosclerosis in HIV-infected patients, regardless of known major cardiovascular risk factors and atherogenic metabolic abnormalities induced by this therapy.

Key Words: arteriosclerosis • carotid arteries • HIV • risk factors • ultrasonography

This article has been cited by other articles:

				J. Pou, A. Rebollo, N. Roglans, R. M. Sanchez, M. Vazquez-Carrera, J. C. Laguna, J. Pedro-Botet, and M. Alegret Ritonavir Increases CD36, ABCA1 and CYP27 Expression in THP-1 Macrophages Experimental Biology and Medicine, December 1, 2008; 233(12): 1572 - 1582. [Abstract] [Full Text] [PDF]

				J. S. Currier, J. D. Lundgren, A. Carr, D. Klein, C. A. Sabin, P. E. Sax, J. T. Schouten, M. Smieja, and for Working Group 2 Epidemiological Evidence for Cardiovascular Disease in HIV-Infected Patients and Relationship to Highly Active Antiretroviral Therapy Circulation, July 8, 2008; 118(2): e29 - e35. [Full Text] [PDF]

				P. Y. Hsue, K. Squires, A. F. Bolger, B. Capili, G. A. Mensah, Z. Temesgen, C. A. Wanke, D. A. Wohl, and for Working Group 4 Screening and Assessment of Coronary Heart Disease in HIV-Infected Patients Circulation, July 8, 2008; 118(2): e41 - e47. [Full Text] [PDF]

				M. Schambelan, P. W.F. Wilson, K. E. Yarasheski, W. T. Cade, V. G. Davila-Roman, R. B. D'Agostino Sr, T. A. Helmy, M. Law, K. E. Mondy, S. Nachman, et al. Development of Appropriate Coronary Heart Disease Risk Prediction Models in HIV-Infected Patients Circulation, July 8, 2008; 118(2): e48 - e53. [Full Text] [PDF]

				B. Coll, S. Parra, C. Alonso-Villaverde, G. Aragones, M. Montero, J. Camps, J. Joven, and L. Masana The Role of Immunity and Inflammation in the Progression of Atherosclerosis in Patients With HIV Infection Stroke, September 1, 2007; 38(9): 2477 - 2484. [Abstract] [Full Text] [PDF]

				G. Ortiz, S. Koch, J. G. Romano, A. M. Forteza, and A. A. Rabinstein Mechanisms of ischemic stroke in HIV-infected patients Neurology, April 17, 2007; 68(16): 1257 - 1261. [Abstract] [Full Text] [PDF]

				N. R. Madamanchi and M. S. Runge Mitochondrial Dysfunction in Atherosclerosis Circ. Res., March 2, 2007; 100(4): 460 - 473. [Abstract] [Full Text] [PDF]