Levels and clinical implication of serum soluble CD137 in patients with pulmonary hypertension due to left heart disease
-
摘要: 目的:检测左心疾病相关性肺高压(PH-LHD)患者血清可溶性CD137(sCD137)的水平并探讨其临床意义。方法:收集76例左心疾病(LHD)患者的临床资料,以肺动脉收缩压(PASP)≥40 mmHg (1 mmHg=0.133 kPa)作为肺高压(PH)的诊断依据,其中单纯LHD患者40例(LHD组),LHD合并PH患者36例(PH-LHD组),对照组为30例体检健康的成年人。血清sCD137水平采用ELISA法检测。结果:PH-LHD组血清sCD137水平高于LHD组和对照组,3组的血清sCD137水平分别为9.27(7.01,13.71) pg/ml、6.68(4.26,8.26) pg/ml、2.52(1.22,3.22) pg/ml,组间比较差异均有统计学意义(P<0.05)。相关性分析显示PH-LHD组血清sCD137水平与血肌酐、血浆B型尿钠肽(BNP)、左房内径(LAD)、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)及PASP正相关,与左室射血分数(LVEF)呈负相关。Logistic回归分析显示,sCD137为PH-LHD的独立影响因素之一(P<0.05)。sCD137预测PH-LHD的受试者工作特征曲线下面积(AUC)为0.722(95%CI:0.607~0.837,P=0.001),最佳阈值为>8.22 pg/ml,敏感性为0.611,特异性为0.750,当联合BNP及三酰甘油/高密度脂蛋白胆固醇(TG/HDL-C)后预测PH-LHD的AUC为0.910(95%CI:0.841~0.980,P<0.001),最佳阈值为>0.53,敏感性为0.778,特异性为0.950。结论:PH-LHD患者血清sCD137水平较LHD患者升高,提示sCD137可能参与PH-LHD的发生发展。血清sCD137对LHD患者发生PH-LHD有一定预测价值,联合BNP及TG/HDL-C对PH-LHD的预测效果更佳。Abstract: Objective: The aim of the present study was to investigate the levels of serum soluble CD137(sCD137) in patients with pulmonary hypertension due to left heart disease(PH-LHD) and explore it's clinical significance.Method: The clinical data of 76 patients with LHD were collected, and PH was defined by pulmonary artery systolic pressure (PASP) ≥ 40 mmHg, including 40 patients with LHD (LHD group) and 36 patients with PH-LHD (PH-LHD group), 30 healthy adults served as control group. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of sCD137 in serum.Result: The levels of serum sCD137 in PH-LHD group was higher than that in LHD group and healthy control group. Serum sCD137 in three groups were 9.27(7.01, 13.71) pg/ml, 6.68(4.26, 8.26) pg/ml and 2.52(1.22, 3.22) pg/ml, in respectively. The differences were statistically significant (P<0.05) Serum sCD137 levels were positively correlated with serum creatinine, brain natriuretic peptide, left atrial diameter, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and PASP, and negatively correlated with left ventricular ejection fraction. Logistic regression analysis showed that sCD137 was one of the independent influencing factors of PH-LHD (P<0.05).Receiver operating characteristic curves showed that the area under the curve(AUC) of sCD137 was 0.722(95%CI:0.607-0.837, P=0.001) in the prediction of PH-LHD, the cut-off value was >8.22 pg/ml, with the sensitivity at 0.611, specificity at 0.750.When combined with BNP and TG/HDL-C, the AUC of predicting PH-LHD was 0.910(95%CI:0.841-0.980, P<0.001), the cut-off value was >0.53, with the sensitivity at 0.778, specificity at 0.950.Conclusion: The serum sCD137 levels in patients with PH-LHD was higher than that in patients with LHD, suggesting that sCD137 may participate in the occurrence and development of PH-LHD.A certain value was showed in sCD137 of predicting the occurrence of PH-LHD in LHD patients which was better when combined with BNP and TG/HDL-C.
-
Key words:
- soluble CD137 /
- left heart disease /
- pulmonary hypertension
-
[1] Labiano S, Palazón A, Bolaños E, et al.Hypoxia-induced soluble CD137 in malignant cells blocks CD137L-costimulation as an immune escape mechanism[J].Oncoimmunology, 2016, 5(1):e1062967.
[2] 蒋美萍, 陈蕊, 刘培晶, 等.CD137信号通过有氧糖酵解途径促进小鼠肺动脉内皮细胞增殖[J].中国病理生理杂志, 2019, 35(6):968-974.
[3] McLaughlin VV, Archer SL, Badesch DB, et al.ACCF/AHA 2009 expert consensus document on pulmonary hypertension a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association developed in collaboration with the American College of Chest Physicians;American Thoracic Society, Inc.;and the Pulmonary Hypertension Association[J].J Am Coll Cardiol, 2009, 53(17):1573-1619.
[4] Rosenkranz S, Gibbs JS, Wachter R, et al.Left ventricular heart failure and pulmonary hypertension[J].Eur Heart J, 2016, 37(12):942-954.
[5] 王雪芳, 谢萍.肺动脉高压与免疫炎症[J].临床心血管病杂志, 2019, 35(5):12-16.
[6] Zhong W, Li B, Yang P, et al.CD137-CD137L interaction modulates neointima formation and the phenotype transformation of vascular smooth muscle cells via NFATc1 signaling[J].Mol Cell Biochem, 2018, 439(1-2):65-74.
[7] 卢毅, 陈蕊, 马金玉, 等.PDGF-BB通过SIRT3影响糖酵解途径调控肺动脉平滑肌细胞的表型转化[J].中华心血管病杂志, 2019, 47(12):993-999.
[8] Vachiéry JL, Adir Y, Barberà JA, et al.Pulmonary hypertension due to left heart diseases[J].J Am Coll Cardiol, 2013, 62(25 Suppl):D100-108.
[9] Amdani SM, Mian MUM, Thomas RL, et al.NT-pro BNP-A marker for worsening respiratory status and mortality in infants and young children with pulmonary hypertension[J].Congenit Heart Dis, 2018, 13(4):499-505.
[10] Galiè N, Humbert M, Vachiery JL, et al.2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension:The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS):Endorsed by:Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT)[J].Eur Respir J, 2015, 46(4):903-975.
[11] Sharma S, Ruffenach G, Umar S, et al.Role of oxidized lipids in pulmonary arterial hypertension[J].Pulm Circ, 2016, 6(3):261-273.
[12] Sharma S, Umar S, Potus F, et al.Apolipoprotein A-I mimetic peptide 4F rescues pulmonary hypertension by inducing microRNA-193-3p[J].Circulation, 2014, 130(9):776-785.
[13] 钟节雄, 樊红, 杨宏华.原发性高血压患者HDL-C与靶器官损害的相关性分析[J].临床心血管病杂志, 2016, 32(9):890-893.
[14] Jonas K, Waligóra M, Magoń W, et al.Prognostic role of traditional cardiovascular risk factors in patients with idiopathic pulmonary arterial hypertension[J].Arch Med Sci, 2019, 15(6):1397-1406.
[15] Jackson AO, Meng J, Tang H, et al.High-density lipoprotein-mediated cardioprotection in heart failure[J].Heart Fail Rev, 2020.[Epub ahead of print].
计量
- 文章访问数: 43
- PDF下载数: 20
- 施引文献: 0