Department of Biochemistry and Molecular Biomedicine, Biology Faculty, University of Barcelona, Barcelona, Spain.
Gastrointestinal Surgery Department, Arnau de Vilanova University Hospital, IRB Lleida, University of Lleida, Lleida, Spain.
Surg Obes Relat Dis. 2020 Oct;16(10):1419-1428. doi: 10.1016/j.soard.2020.05.035. Epub 2020 Jun 10.
The main cause of death in obese individuals is cardiovascular disease precipitated by atherosclerosis. Endothelial dysfunction and inflammation are considered early events in the development of the disease.
The aim of this study was to identify biomarkers of subclinical atherosclerosis in patients with morbid obesity by comparing clinical, vascular, and biochemical parameters indicative of endothelial dysfunction in patients with and without atheromatous plaque and monitoring changes after bariatric surgery.
Multicenter collaboration between Biochemistry and Biomedicine Department in Barcelona University and University Hospital Arnau de Vilanova in Lleida.
Plasma samples from 66 patients with morbid obesity were obtained before bariatric surgery and at 6 and 12 months after. Patients were divided into 2 groups based on the presence of atheromatous plaque. We used contrast-enhanced carotid ultrasound, enzyme-linked immunosorbent assay, Griess, and EndoPAT-2000 methods.
Patients with plaque showed the worst profile of cardiovascular risk factors. Carotid intima-media thickness and plasminogen activator inhibitor-1 were higher in plaque group (P < .0001). After bariatric surgery, vasa vasorum, oxidized low-density lipoprotein, and plasminogen activator inhibitor-1 decreased (P < .0001 in all cases).
Obesity promotes atherogenesis, leading to vascular endothelial damage. Bariatric surgery reduces cardiovascular risk and the prognosis is better for patients without plaque. The increase in plasminogen activator inhibitor-1, carotid intima-media thickness, and vasa vasorum proliferation might be the first alterations in the atheromatous process in obesity and could serve as good biomarkers of subclinical atherosclerosis.
肥胖个体的主要死亡原因是由动脉粥样硬化引起的心血管疾病。内皮功能障碍和炎症被认为是疾病发展的早期事件。
本研究旨在通过比较有和无动脉粥样斑块患者的内皮功能障碍的临床、血管和生化参数，来确定病态肥胖患者亚临床动脉粥样硬化的生物标志物，并监测减重手术后的变化。
巴塞罗那大学生物化学与生物医学系与莱里达大学医院阿努尔·德·维拉诺瓦大学之间的多中心合作。
在减重手术前和手术后 6 个月和 12 个月，从 66 例病态肥胖患者中获得血浆样本。根据是否存在动脉粥样斑块，将患者分为两组。我们使用了对比增强颈动脉超声、酶联免疫吸附试验、Griess 和 EndoPAT-2000 方法。
有斑块的患者心血管危险因素的最差。斑块组颈动脉内膜中层厚度和纤溶酶原激活物抑制剂-1较高（P<0.0001）。减重手术后，血管生成、氧化型低密度脂蛋白和纤溶酶原激活物抑制剂-1降低（所有情况均 P<0.0001）。
肥胖促进动脉粥样硬化形成，导致血管内皮损伤。减重手术降低了心血管风险，无斑块的患者预后更好。纤溶酶原激活物抑制剂-1、颈动脉内膜中层厚度和血管生成的增加可能是肥胖症中动脉粥样硬化过程的最初改变，并可作为亚临床动脉粥样硬化的良好生物标志物。
