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

Abstract Background Inflammation and endothelial dysfunction are associated with morbid obesity (MO) and atherosclerosis. Objective 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). Subjects and methods: Plasma samples from 66 patients with MO were obtained before BS and 6 and 12 months after. Patients were divided into two groups based on the presence of atheromatous plaques (detected by ultrasound imaging). Results Inflammation was increased as demonstrated by changes in the levels of fibroblast growth factor-21, adiponectin, leptin, interleukin-6, tumor growth factor-α, non-esterified 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. Conclusion Endothelial dysfunction and inflammation were detected before the appearance of structural changes in vessel walls on ultrasound 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.