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 < or =1 cardiovascular risk factors and 64 with > or =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 > or =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 > or =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.
BACKGROUND AND PURPOSE: Whether or not combination antiretroviral therapy (CART) alone directly contributes to accelerating atherosclerosis in HIV-infectedpatients 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-infectedpatients with < or =1 cardiovascular risk factors and 64 with > or =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 > or =10%). Thus, 55 (41.7%) of the 132 HIV-infectedpatients 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 > or =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-infectedpatients, regardless of known major cardiovascular risk factors and atherogenic metabolic abnormalities induced by this therapy.
Authors: Morris Schambelan; Peter W F Wilson; Kevin E Yarasheski; W Todd Cade; Victor G Dávila-Román; Ralph B D'Agostino; Tarek A Helmy; Matthew Law; Kristin E Mondy; Sharon Nachman; Linda R Peterson; Signe W Worm Journal: Circulation Date: 2008-06-19 Impact factor: 29.690
Authors: Judith S Currier; Jens D Lundgren; Andrew Carr; Daniel Klein; Caroline A Sabin; Paul E Sax; Jeffrey T Schouten; Marek Smieja Journal: Circulation Date: 2008-06-19 Impact factor: 29.690
Authors: Fred Stephen Sarfo; Ohene Opare-Sem; Martin Agyei; John Akassi; Dorcas Owusu; Mayowa Owolabi; Bruce Ovbiagele Journal: J Neurol Sci Date: 2018-09-20 Impact factor: 3.181
Authors: Paolo Puddu; Giovanni M Puddu; Eleonora Cravero; Susanna De Pascalis; Antonio Muscari Journal: J Biomed Sci Date: 2009-12-09 Impact factor: 8.410
Authors: Robert C Kaplan; Lawrence A Kingsley; Stephen J Gange; Lorie Benning; Lisa P Jacobson; Jason Lazar; Kathryn Anastos; Phyllis C Tien; A Richey Sharrett; Howard N Hodis Journal: AIDS Date: 2008-08-20 Impact factor: 4.177