Influence of Morbid Obesity and Bariatric Surgery Impact on the Carotid Adventitial Vasa Vasorum Signal View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-12

AUTHORS

Ferran Rius, Enric Sánchez, Àngels Betriu, Juan Antonio Baena-Fustegueras, Andree Yeramian, Teresa Vidal, Marta Hernández, Carolina López-Cano, Marta Bueno, Liliana Gutiérrez-Carrasquilla, Ferran Herrerías, Mari Cruz de la Fuente, Elvira Fernández, Albert Lecube

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. More... »

PAGES

3935-3942

References to SciGraph publications

Journal

TITLE

Obesity Surgery

ISSUE

12

VOLUME

28

Author Affiliations

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11695-018-3410-x

DOI

http://dx.doi.org/10.1007/s11695-018-3410-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1105734398

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30030728


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    "description": "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).\nMATERIALS/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.\nRESULTS: The mean VV density was higher in obese than in non-obese subjects (0.739\u2009\u00b1\u20090.117 vs. 0.570\u2009\u00b1\u20090.111, p\u2009<\u20090.001). The VV signal positively correlated with BMI (p\u2009<\u20090.001) and waist circumference (p\u2009=\u20090.001) but was not related to cIMT. The stepwise multivariate regression analysis revealed that waist circumference (beta\u2009=\u20090.507, p\u2009<\u20090.001) together with fasting plasma glucose (beta\u2009=\u20090.229, p\u2009=\u20090.024) were independently associated with the VV signal (R2\u2009=\u20090.382). Before BS, the median VV signal correlated with soluble intercellular adhesion molecule 1 (p\u2009=\u20090.022). After a 12-month follow-up, a 12.0% decrease in VV (0.731\u2009\u00b1\u20090.126 vs. 0.643\u2009\u00b1\u20090.115, p\u2009=\u20090.003) was observed. In the univariate analysis, the decrease in VV was associated with the baseline VV density (p\u2009<\u20090.001), baseline systolic blood pressure (p\u2009=\u20090.019) and a decrease in sICAM (p\u2009=\u20090.005). However, only baseline systolic pressure (beta\u2009=\u20090.417, p\u2009=\u20090.024) independently predicted the absolute change in VV signal (R2\u2009=\u20090.174).\nCONCLUSIONS: Morbidly obesity is associated with increased VV density. In addition, BS appears to reduce the earlier expansion of the adventitial vasa vasorum.", 
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41 schema:description 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.
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