Carotid artery remodelling in relation to body fat distribution, inflammation and sustained weight loss in obesity

BACKGROUND: Obesity is known to be associated with carotid artery remodelling, but less is known about how body fat distribution, inflammation and weight loss may affect this relation. METHODS: Ultrasonography, dual-energy X-ray absorptiometry and computed tomography were performed to evaluate carotid artery intima-media thickness (IMT), body composition and fat distribution, respectively. Participants were divided into three matched study groups (n = 44 per group): obese patients with sustained weight loss 10 years after bariatric surgery [surgery group, body mass index (BMI) 31.5 kg m(-2)]; obese patients who maintained stable weight during the same time period (obese group, BMI 42.5 kg m(-2)); and normal weight subjects (lean group, BMI 24.4 kg m(-2)). RESULTS: Patients in the surgery group, compared with those in the obese group, had slightly lower common carotid artery (CCA) IMT (0.75 ± 0.18 vs. 0.78 ± 0.17 mm) and common carotid bulb (CCB) IMT (0.92 ± 0.32 vs. 0.97 ± 0.32 mm); however, these differences were not statistically significant. Lean individuals, compared with those in the surgery group, had significantly lower CCA and CCB IMT values (P < 0.001). In forward stepwise multiple regression analyses including all subjects (n = 132), CCA IMT was predicted mainly by visceral adipose tissue, but was also related to blood pressure and levels of triglycerides and high-sensitivity C-reactive protein. Carotid lumen diameter was primarily influenced by lean body mass. CONCLUSION: Visceral adiposity was the main determinant of premature carotid artery atherosclerosis, possibly through elevated blood pressure, dyslipidaemia and inflammation. Lean body mass predicted carotid artery lumen diameter. Obese patients with long-term sustained weight loss did not have thinner carotid artery walls compared with their weight-stable obese counterparts.