Kozakova M.,University of Pisa |
Palombo C.,University of Pisa |
Morizzo C.,University of Pisa |
Hojlund K.,University of Southern Denmark |
And 133 more authors.
Nutrition and Diabetes | Year: 2015
BACKGROUND/OBJECTIVE: The present study tested the hypothesis that obesity-related changes in carotid intima-media thickness (IMT) might represent not only preclinical atherosclerosis but an adaptive remodeling meant to preserve circumferential wall stress (CWS) in altered hemodynamic conditions characterized by body size-dependent increase in stroke volume (SV) and blood pressure (BP). SUBJECTS/METHODS: Common carotid artery (CCA) luminal diameter (LD), IMT and CWS were measured in three different populations in order to study: (A) cross-sectional associations between SV, BP, anthropometric parameters and CCA LD (266 healthy subjects with wide range of body weight (24-159 kg)); (B) longitudinal associations between CCA LD and 3-year IMT progression rate (δIMT; 571 healthy non-obese subjects without increased cardiovascular (CV) risk); (C) the impact of obesity on CCA geometry and CWS (88 obese subjects without CV complications and 88 non-obese subjects matched for gender and age). RESULTS: CCA LD was independently associated with SV that was determined by body size. In the longitudinal study, baseline LD was an independent determinant of δIMT, and δIMT of subjects in the highest LD quartile was significantly higher (28 ± 3 μm) as compared with those in the lower quartiles (8 ± 3, 16 ± 4 and 16 ± 3 μm, P = 0.001, Po0.05 and P = 0.01, respectively). In addition, CCA CWS decreased during the observational period in the highest LD quartile (from 54.2 ± 8.6 to 51.6 ± 7.4 kPa, Po0.0001). As compared with gender- and age-matched lean individuals, obese subjects had highly increased CCA LD and BP (Po0.0001 for both), but only slightly higher CWS (P = 0.05) due to a significant increase in IMT (P = 0.005 after adjustment for confounders). CONCLUSIONS: Our findings suggest that in obese subjects, the CCA wall thickens to compensate the luminal enlargement caused by body size-induced increase in SV, and therefore, to normalize the wall stress. CCA diameter in obesity could represent an additional biomarker, depicting the impact of altered hemodynamics on arterial wall.
Del Rincon I.,University of Texas Health Science Center at San Antonio |
Polak J.F.,Ultrasound Reading Center |
O'Leary D.H.,Ultrasound Reading Center |
Battafarano D.F.,U.S. Army |
And 4 more authors.
Annals of the Rheumatic Diseases | Year: 2015
Objective To estimate atherosclerosis progression and identify influencing factors in rheumatoid arthritis (RA). Methods We used carotid ultrasound to measure intima-media thickness (IMT) in RA patients, and ascertained cardiovascular (CV) risk factors, inflammation markers and medications. A second ultrasound was performed approximately 3 years later. We calculated the progression rate by subtracting the baseline from the follow-up IMT, divided by the time between the two scans. We used logistic regression to identify baseline factors predictive of rapid progression. We tested for interactions of erythrocyte sedimentation rate (ESR) with CV risk factors and medication use. Results Results were available for 487 RA patients. The mean (SD) common carotid IMT at baseline was 0.571 mm (0.151). After a mean of 2.8 years, the IMT increased by 0.050 mm (0.055), p≤0.001, a progression rate of 0.018 mm/year (95% CI 0.016 to 0.020). Baseline factors associated with rapid progression included the number of CV risk factors (OR 1.27 per risk factor, 95% CI 1.01 to 1.61), and the ESR (OR 1.12 per 10 mm/h, 95% CI 1.02 to 1.23). The ESR×CV risk factor and ESR×medication product terms were significant, suggesting these variables modify the association between the ESR and IMT progression. Conclusions Systemic inflammation and CV risk factors were associated with rapid IMT progression. CV risk factors may modify the role of systemic inflammation in determining IMT progression over time. Methotrexate and antitumour necrosis factor agents may influence IMT progression by reducing the effect of the systemic inflammation on the IMT.
Polak J.F.,Ultrasound Reading Center |
Tracy R.,University of Vermont |
Harrington A.,Ultrasound Reading Center |
Zavodni A.E.H.,University of Toronto |
O'Leary D.H.,Saint Elizabeths Medical Center
Journal of the American Society of Echocardiography | Year: 2013
Background: Carotid and coronary atherosclerosis are associated with each other in imaging and autopsy studies. The aim of this study was to evaluate whether carotid artery plaque seen on carotid ultrasound can predict incident coronary artery calcification (CAC). Methods: Agatston calcium score measurements were repeated in 5,445 participants of the Multi-Ethnic Study of Atherosclerosis (MESA; mean age, 57.9 years; 62.9% women). Internal carotid artery lesions were graded as 0%, 1% to 24%, or >25% diameter narrowing, and intima-media thickness (IMT) was measured. Plaque was present for any stenosis >0%. CAC progression was evaluated with multivariate relative risk regression for CAC scores of 0 at baseline and with multivariate linear regression for CAC score > 0, adjusting for cardiovascular risk factors, body mass index, ethnicity, and common carotid IMT. Results: CAC was positive at baseline in 2,708 of 5,445 participants (49.7%) and became positive in 458 of 2,837 (16.1%) at a mean interval of 2.4 years between repeat examinations. Plaque and internal carotid artery IMT were both strongly associated with the presence of CAC. After statistical adjustment, the presence of carotid artery plaque significantly predicted incident CAC with a relative risk of 1.37 (95% confidence interval, 1.12-1.67). Incident CAC was associated with internal carotid artery IMT, with a relative risk of 1.13 (95% confidence interval, 1.03-1.25) for each 1-mm increase. Progression of CAC was also significantly associated (P <.001) with plaque and internal carotid artery IMT. Conclusions: In individuals free of cardiovascular disease, subjective and quantitative measures of carotid artery plaques by ultrasound imaging are associated with CAC incidence and progression. © 2013 by the American Society of Echocardiography.