Abstract Objective To preliminarily investigate the relationship between serum apelin level and pulmonary artery pressure in children with congenital heart disease. Methods One hundred and twenty-six children with congenital heart disease undergoing surgical treatment were enrolled as subjects. The serum level of apelin was determined before surgery and at 7 days after surgery. The ratio of pulmonary artery systolic pressure to aortic systolic pressure (Pp/Ps) was calculated before extracorporeal circulation. According to the Pp/Ps value, patients were classified into non-pulmonary arterial hypertension (PAH) group, mild PAH group, moderate PAH group, and severe PAH group. Pulmonary artery mean pressure was estimated by echocardiography at 7 days after surgery. Results The non-PAH group had the highest serum level of apelin before and after surgery, followed by the mild PAH group, moderate PAH group, and severe PAH group (PPr=-0.51, Pr=-0.54, PConclusions The decrease in serum apelin level is associated with the development of pulmonary hypertension in children with congenital heart disease. The significance of serum apelin in predicting the development and degree of pulmonary hypertension in children with congenital heart disease deserves further studies.
MA Chao,SHEN Ding-Rong,ZHANG Qing et al. A preliminary investigation of relationship between serum apelin level and pulmonary artery pressure in children with congenital heart disease[J]. CJCP, 2016, 18(4): 340-344.
MA Chao,SHEN Ding-Rong,ZHANG Qing et al. A preliminary investigation of relationship between serum apelin level and pulmonary artery pressure in children with congenital heart disease[J]. CJCP, 2016, 18(4): 340-344.
Tabib A, Khorgami MR, Meraji M, et al. Accuracy of Dopplerderived indices in predicting pulmonary vascular resistance in children with pulmonary hypertension secondary to congenital heart disease with left-to-right shunting[J]. Pediatr Cardiol, 2014, 35(3): 521-529.
Myers PO, Tissot C, Beghetti M. Assessment of operability of patients with pulmonary arterial hypertension associated with congenital heart disease[J]. Circ J, 2013, 78(1): 4-11.
Betkier-Lipińska K, Ryczek R, Kwasiborski P, et al. Pulmonary arterial hypertension: modern diagnostics and therapy--Part 1[J]. Pol Merkur Lekarski, 2013, 34(204): 355-359.
[7]
Farkas L, Gauldie J, Voelkel N F, et al. Pulmonary hypertension and idiopathic pulmonary fibrosis, a tale of angiogenesis, apoptosis, and growth factors[J]. Am J Respir Cell Mol Biol, 2011, 45(1): 1-15.
[8]
Abman SH, Hansmann G, Archer SL, et al. Pediatric Pulmonary Hypertension: Guidelines From the American Heart Association and American Thoracic Society[J]. Circulation, 2015, 132(21): 2037-2099.
[9]
Lau EM, Manes A, Celermajer DS, et al. Early detection of pulmonary vascular disease in pulmonary Arterial hypertension: time to move forward[J]. Eur Heart J, 2011, 32(20): 2489-2498.
[10]
Bossone E, Ferrara F, Grünig E. Echocardiography in pulmonary hypertension[J]. Curr Opin Cardiol, 2015, 30(6): 574-586.
[11]
Dai HL, Guo Y, Guang XF, et al. The changes of serum angiotensin-converting enzyme 2 in patients with pulmonary arterial hypertension due to congenital heart disease[J]. Cardiology, 2013, 124(4): 208-212.
[12]
Giannakoulas G, Mouratoglou SA, Gatzoulis MA, et al. Blood biomarkers and their potential role in pulmonary arterial hypertension associated with congenital heart disease. a systematic review. Int J Cardiol, 2014, 174(3): 618-623.
[13]
Schuuring MJ, van Riel AC, Vis JC, et al. New predictors of mortality in adults with congenital heart disease and pulmonary hypertension: Midterm outcome of a prospective study.Int J Cardiol, 2015, 181C(2014): 270-276.
[14]
Bertrand C, Valet P, Castan-Laurell I. Apelin and energy metabolism[J]. Front Physiol, 2015, 6(115): 1-5.
[15]
Yang P, Maguire JJ, Davenport AP. Apelin, Elabela/Toddler, and biased agonists as novel therapeutic agents in the cardiovascular system[J]. Trends Pharmacol Sci, 2015, 36(9): 560-567.
Zhang J, Liu Q, Hu X, et al. Apelin/APJ signaling promotes hypoxia-induced proliferation of endothelial progenitor cells via phosphoinositide-3 kinase/Akt signaling[J]. Mol Med Rep, 2015, 12(3): 3829-3834.
[18]
Fan XF, Xue F, Zhang YQ, et al. The Apelin-APJ axis is an endogenous counterinjury mechanism in experimental acute lung injury[J]. Chest, 2015, 147(4): 969-978.
[19]
Cao J, Li H, Chen L.Targeting drugs to APJ receptor: the prospect of treatment of hypertension and other cardiovascular diseases[J]. Curr Drug Targets, 2015, 16(2): 148-155.
Blok IM, van Riel AC, Mulder BJ, et al. Management of patients with pulmonary arterial hypertension due to congenital heart disease: recent advances and future directions[J]. Expert Rev Cardiovasc Ther, 2015, 13(12): 1377-1392.
Chandra SM, Razavi H, Kim J, et al. Disruption of the apelin-APJ system worsens hypoxia-induced pulmonary hypertension[J]. Arterioscler Thromb Vasc Biol, 2011, 31(4): 814-820.
[26]
Alastalo TP, Li M, Perez JP, et al. Disruption of PPARγ/β-cateninmediated regulation of apelin impairs BMP-induced mouse and human pulmonary arterial EC survival[J]. J Clin Invest, 2011, 121(9): 3735-3746.
[27]
Zeng X, Yu SP, Taylor T, et al. Protective effect of apelin on cultured rat bone marrow mesenchymal stem cells against apoptosis[J]. Stem Cell Res, 2012, 8(3): 357-367.
