Effect of bariatric surgery on inflammation and endothelial dysfunction as processes underlying subclinical atherosclerosis in morbid obesity

• Published in: Surgery for obesity and related diseases Vol. 16; no. 12; pp. 1961 - 1970
• Main Authors: Carmona-Maurici, Júlia, Cuello, Elena, Ricart-Jané, David, Miñarro, Antonio, Baena-Fustegueras, Juan Antonio, Peinado-Onsurbe, Julia, Pardina, Eva
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2020
• Subjects: Atheromatous plaque; Atherosclerosis - etiology; Bariatric Surgery; Biomarkers; C-Reactive Protein; Endothelial dysfunction; Humans; Inflammation; Morbid obesity; Obesity, Morbid - surgery; Atheromatous plaque; Endothelial dysfunction; Inflammation; Morbid obesity; Bariatric surgery
• ISSN: 1550-7289; 1878-7533
• DOI: 10.1016/j.soard.2020.07.036

Inflammation and endothelial dysfunction are associated with morbid obesity (MO) and atherosclerosis. To evaluate inflammation and endothelial function as the initial mechanisms underlying subclinical atherosclerosis in patients with MO, with and without atheromas, and their evolution after bariatric surgery (BS). Arnau de Vilanova University Hospital and University of Barcelona. Plasma samples from 66 patients with MO were obtained before BS and 6 and 12 months after BS. Patients were divided into 2 groups based on the presence of atheromatous plaques (detected by ultrasound imaging). Inflammation was increased as demonstrated by changes in the levels of fibroblast growth factor 21, adiponectin, leptin, interleukin 6, tumor growth factor α, nonesterified free fatty acids, lipoprotein(a) and C-reactive protein (CRP). Endothelial dysfunction was characterized by impaired angiogenesis (measured through angiopoietin 1 and 2 and brain-derived neurotrophic factor), vascular function (changes in endothelin 1 and thrombomodulin levels), and diapedesis (changes in intercellular and vascular cell adhesion molecules, and E- and P-selectins). Both mechanisms occurred regardless of the presence of atheromas. BS ameliorated both processes even in patients who already had subclinical atherosclerosis. However, CRP, thrombomodulin, and P-selectin levels were higher in patients with atheromas. Endothelial dysfunction and inflammation were detected before the appearance of structural changes in vessel walls on ultrasonography images. BS might prevent or slow atherogenesis in the early stages by breaking the vicious circle between inflammation and endothelial dysfunction. CRP, thrombomodulin, and P-selectin may have a critical role in plaque development and, together with the study of endothelial dysfunction, might be useful in assessing early atherosclerosis and its evolution after BS.