We identified three segments of the carotid arteries on which to conduct the measurements, the common carotid artery (1 cm proximal to the bifurcation), the carotid bulb (in the bifurcation) and the internal carotid artery (1 cm distal to the bifurcation). Far wall CIMT images were obtained and digitalized for each patient [31]. The median value of the measurements obtained in the three segments BAY 80-6946 nmr was used in the

statistical analyses. The presence of subclinical atherosclerosis was defined as a median CIMT >0.8 mm or the presence of a plaque. A plaque was defined as a thickness >1.5 mm or a focal structure that encroaches into the arterial lumen by at least 0.5 mm, or 50% of the surrounding CIMT value [32]. We used the χ2 test or Fisher’s exact Protease Inhibitor Library mouse test to evaluate the associations between categorical variables. The κ coefficient was used as

a measure of the agreement between the presence of subclinical atherosclerosis and the CVD risk calculated by the FRS. Means for variables with a normal distribution were compared using analysis of variance (anova) and the Kruskall–Wallis test was used for variables with nonnormal (skewed) distributions. When significant differences among CVD risk groups were found, pair-wise comparisons were performed between the groups representing the three levels of CVD risk. Post hoc analyses included the Bonferroni test. Logistic regression analysis was used to study the variables associated with the presence of subclinical atherosclerosis (as a binary variable) in the group of patients with low CVD risk as stratified by FRS (i.e. risk <10%). Variables included in the multivariate

analyses were age, gender, smoking status, systolic blood pressure (SBP), diastolic blood pressure (DBP), glucose, LDL cholesterol, HDL cholesterol, triglycerides, GNA12 BMI, HIV-1 basal viral load, basal CD4 cell count, lipodystrophy, exposure time to nucleoside reverse transcriptase inhibitor (NRTI), nonnucleoside reverse transcriptase inhibitor (NNRTI) and protease inhibitor (PI) treatments, inflammatory markers, and oxidative markers. Statistical analyses were performed with the spss 17.0 statistical package (SPSS, Chicago, IL, USA). A significant difference was defined as two-tailed P<0.05. We observed a low level of agreement between the stratification of CVD risk measured using the FRS and the presence of subclinical atherosclerosis measured using CIMT (Table 1). Of note is the finding that a high number of patients who did have subclinical atherosclerosis were classified as having a low CVD risk using the FRS score (n=66; 56.4%). Table 2 summarizes the data on the patients stratified into three groups according to the presence of atherosclerosis, but with a low or high CVD risk according to the FRS. The group of patients with a high CVD risk according to the FRS and with atherosclerosis were older (P<0.