Ferran Rius1, Enric Sánchez1, Àngels Betriu2, Juan Antonio Baena-Fustegueras3, Andree Yeramian1, Teresa Vidal2, Marta Hernández1, Carolina López-Cano1, Marta Bueno1, Liliana Gutiérrez-Carrasquilla1, Ferran Herrerías3, Mari Cruz de la Fuente3, Elvira Fernández2, Albert Lecube4,5. 1. Endocrinology and Nutrition Department, University Hospital Arnau de Vilanova, Obesity, Diabetes and Metabolism Research Group (ODIM), IRBLleida, University of Lleida, Av. Rovira Roure 80, 25198, Lleida, Spain. 2. Unit for the Detection and the Treatment of Atherothrombotic Diseases (UDETMAV&R), University Hospital Arnau de Vilanova, Vascular and Renal Translational Research Group, IRBLleida, University of Lleida, Lleida, Spain. 3. Gastrointestinal Surgery Department, University Hospital Arnau de Vilanova, IRBLleida, University of Lleida, Lleida, Spain. 4. Endocrinology and Nutrition Department, University Hospital Arnau de Vilanova, Obesity, Diabetes and Metabolism Research Group (ODIM), IRBLleida, University of Lleida, Av. Rovira Roure 80, 25198, Lleida, Spain. alecube@gmail.com. 5. Centro de Investigación en Red en Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III (ISCIII), Madrid, Spain. alecube@gmail.com.
Abstract
INTRODUCTION/ PURPOSE: Adventitial vasa vasorum (VV) expansion to the avascular intima precedes an increase in carotid intima-media thickness. However, factors involved in the development of the atherosclerotic process and its reversibility remain unclear. We aimed to evaluate the VV signal in both morbid obesity and after bariatric surgery (BS). MATERIALS/ METHODS: We conducted a case-control study to examine the VV signal in the carotid of 40 morbidly obese patients and 40 non-obese controls. The effect of BS was evaluated in 33 patients. Contrast-enhanced carotid ultrasound was used to assess the VV signal. RESULTS: The mean VV density was higher in obese than in non-obese subjects (0.739 ± 0.117 vs. 0.570 ± 0.111, p < 0.001). The VV signal positively correlated with BMI (p < 0.001) and waist circumference (p = 0.001) but was not related to cIMT. The stepwise multivariate regression analysis revealed that waist circumference (beta = 0.507, p < 0.001) together with fasting plasma glucose (beta = 0.229, p = 0.024) were independently associated with the VV signal (R2 = 0.382). Before BS, the median VV signal correlated with soluble intercellular adhesion molecule 1 (p = 0.022). After a 12-month follow-up, a 12.0% decrease in VV (0.731 ± 0.126 vs. 0.643 ± 0.115, p = 0.003) was observed. In the univariate analysis, the decrease in VV was associated with the baseline VV density (p < 0.001), baseline systolic blood pressure (p = 0.019) and a decrease in sICAM (p = 0.005). However, only baseline systolic pressure (beta = 0.417, p = 0.024) independently predicted the absolute change in VV signal (R2 = 0.174). CONCLUSIONS: Morbidly obesity is associated with increased VV density. In addition, BS appears to reduce the earlier expansion of the adventitial vasa vasorum.
INTRODUCTION/ PURPOSE: Adventitial vasa vasorum (VV) expansion to the avascular intima precedes an increase in carotid intima-media thickness. However, factors involved in the development of the atherosclerotic process and its reversibility remain unclear. We aimed to evaluate the VV signal in both morbid obesity and after bariatric surgery (BS). MATERIALS/ METHODS: We conducted a case-control study to examine the VV signal in the carotid of 40 morbidly obese patients and 40 non-obese controls. The effect of BS was evaluated in 33 patients. Contrast-enhanced carotid ultrasound was used to assess the VV signal. RESULTS: The mean VV density was higher in obese than in non-obese subjects (0.739 ± 0.117 vs. 0.570 ± 0.111, p < 0.001). The VV signal positively correlated with BMI (p < 0.001) and waist circumference (p = 0.001) but was not related to cIMT. The stepwise multivariate regression analysis revealed that waist circumference (beta = 0.507, p < 0.001) together with fasting plasma glucose (beta = 0.229, p = 0.024) were independently associated with the VV signal (R2 = 0.382). Before BS, the median VV signal correlated with soluble intercellular adhesion molecule 1 (p = 0.022). After a 12-month follow-up, a 12.0% decrease in VV (0.731 ± 0.126 vs. 0.643 ± 0.115, p = 0.003) was observed. In the univariate analysis, the decrease in VV was associated with the baseline VV density (p < 0.001), baseline systolic blood pressure (p = 0.019) and a decrease in sICAM (p = 0.005). However, only baseline systolic pressure (beta = 0.417, p = 0.024) independently predicted the absolute change in VV signal (R2 = 0.174). CONCLUSIONS: Morbidly obesity is associated with increased VV density. In addition, BS appears to reduce the earlier expansion of the adventitial vasa vasorum.
Entities:
Keywords:
Atherosclerosis; Bariatric surgery; Obesity; Vasa vasorum; Weight loss