Federal State Budgetary Institution, Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo, Russia.
Federal State Budget Educational Institution of Higher Education, Kemerovo State Medical University of the Ministry of Healthcare of the Russian Federation, Kemerovo, Russia.
Cardiovasc Diabetol. 2018 Mar 16;17(1):40. doi: 10.1186/s12933-018-0679-y.
Determination of the impact of visceral obesity and epicardial adipose tissue thickness on stimulating growth factor levels during hospitalization for myocardial infarction is of potential importance for predicting outcomes and assessing the development of cardiofibrotic changes associated with maladaptive myocardial remodeling. In this study, we aimed to investigate the relationships between epicardial adipose tissue thickness, adipokine profiles, and the stimulating growth factor 2/interleukin-33 signaling system during hospitalization for myocardial infarction, and with the cardiac fibrosis extent 1-year post-MI in patients with visceral obesity.
Eighty-eight patients with myocardial infarction were grouped based on their visceral obesity. Serum leptin, adiponectin, stimulating growth factor 2, and interleukin-33 levels were measured on days 1 and 12 and at 1 year. The epicardial adipose tissue widths and the cardiac fibrosis areas were measured on day 12 and at 1 year.
Visceral obesity was associated with epicardial adipose tissue thickness increases, adipokine imbalances, elevated leptin levels, and lower adiponectin levels during early hospitalization, and cardiac fibrosis development. Patients without visceral obesity had higher interleukin-33 and stimulating growth factor 2 levels during early hospitalization and lower cardiac fibrosis rates. Epicardial adipose tissue thickness was positively associated with cardiac fibrosis prevalence and interleukin-33 levels and negatively associated with stimulating growth factor 2 levels. The cardiac fibrosis extent was negatively associated with interleukin-33 levels and positively associated with stimulating growth factor 2 levels.
Increases in epicardial adipose tissue thickness are associated with cardiac fibrosis development 1-year post-myocardial infarction and are higher in patients with visceral obesity. The metabolic activity of the epicardial adipose tissue is associated with elevated interleukin-33 and reduced stimulating growth factor 2 levels.
确定内脏肥胖和心外膜脂肪组织厚度对心肌梗死后住院期间刺激生长因子水平的影响，对于预测结局和评估与适应性心肌重构相关的心肌纤维化变化的发展具有潜在重要性。在这项研究中，我们旨在研究心外膜脂肪组织厚度、脂联素谱与刺激生长因子 2/白细胞介素-33 信号系统之间的关系，以及内脏肥胖患者心肌梗死后 1 年的心脏纤维化程度。
根据内脏肥胖情况将 88 例心肌梗死患者分组。在入院第 1 天和第 12 天以及 1 年后测量血清瘦素、脂联素、刺激生长因子 2 和白细胞介素-33 水平。在入院第 12 天和 1 年后测量心外膜脂肪组织宽度和心脏纤维化面积。
内脏肥胖与心外膜脂肪组织厚度增加、脂联素失衡、早期住院时瘦素水平升高和脂联素水平降低以及心脏纤维化发展相关。无内脏肥胖的患者在早期住院期间白细胞介素-33 和刺激生长因子 2 水平较高，心脏纤维化发生率较低。心外膜脂肪组织厚度与心脏纤维化患病率和白细胞介素-33 水平呈正相关，与刺激生长因子 2 水平呈负相关。心脏纤维化程度与白细胞介素-33 水平呈负相关，与刺激生长因子 2 水平呈正相关。
心外膜脂肪组织厚度的增加与心肌梗死后 1 年的心脏纤维化发展相关，且在伴有内脏肥胖的患者中更高。心外膜脂肪组织的代谢活性与白细胞介素-33 水平升高和刺激生长因子 2 水平降低相关。
