Abstract Objective To study the change and significance of serum pentraxin-3 (PTX-3) and syndecan-4 in children with chronic heart failure (CHF). Methods A total of 40 children with CHF who were admitted to the Department of Pediatrics of the First Affiliated Hospital of Zhengzhou University were enrolled as the heart failure group, and 30 children who underwent physical examination in the outpatient service during the same period of time were enrolled as the control group. The serum levels of PTX-3, syndecan-4, and N-terminal pro-brain natriuretic peptide (NT-proBNP) were compared between the two groups. Results The children with CHF had significant reductions in the serum levels of PTX-3, syndecan-4, and NT-proBNP after treatment. The levels of these markers in children with CHF were significantly higher than the control group before and after treatment (P < 0.05). The CHF children with grade II/III/IV cardiac function had significantly higher serum levels of PTX-3 and syndecan-4 than the control group (P < 0.05). The levels of PTX-3 and syndecan-4 were related to the severity of cardiac function. Compared with the grade II cardiac function group, the grade IV cardiac function group had significant increases in the serum levels of PTX-3 and syndecan-4 (P < 0.05). The serum level of PTX-3 was positively correlated with that of syndecan-4 in children with CHF (rs=0.999, P < 0.05); the serum level of PTX-3 was positively correlated with NT-proBNP, left ventricular mass index (LVMI), and cardiac function grade (rs=0.726, 0.736, and 0.934 respectively, P < 0.05) and was negatively correlated with left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) (rs=-0.852 and -0.767 respectively, P < 0.05); the serum level of syndecan-4 was positively correlated with NT-proBNP, LVMI, and cardiac function grade (rs=0.733, 0.743, and 0.934 respectively, P < 0.05) and was negatively correlated with LVEF and LVFS (rs=-0.856 and -0.771 respectively, P < 0.05). Conclusions Serum PTX-3 and syndecan-4 may be involved in the development and progression of ventricular remodeling in children with CHF and may be used as markers for the diagnosis, cardiac function grading, and treatment outcome evaluation of children with heart failure.
ZHANG Feng-Hua,ZHAO Xiao-Lin,FENG Song et al. Change of serum levels of pentraxin-3 and syndecan-4 in children with chronic heart failure[J]. CJCP, 2021, 23(5): 513-518.
ZHANG Feng-Hua,ZHAO Xiao-Lin,FENG Song et al. Change of serum levels of pentraxin-3 and syndecan-4 in children with chronic heart failure[J]. CJCP, 2021, 23(5): 513-518.
Ueland T, Gullestad L, Nymo SH, et al. Inflammatory cytokines as biomarkers in heart failure[J]. Clin Chim Acta, 2015, 443:71-77.
[5]
Liu BH, Li YG, Liu JX, et al. Assessing inflammation in Chinese subjects with subtypes of heart failure:an observational study of the Chinese PLA Hospital Heart Failure Registry[J]. J Geriatr Cardiol, 2019, 16(4):313-319.
[6]
Herum KM, Lunde IG, Skrbic B, et al. Syndecan-4 is a key determinant of collagen cross-linking and passive myocardial stiffness in the pressure-overloaded heart[J]. Cardiovasc Res, 2015, 106(2):217-226.
Matsubara J, Sugiyama S, Nozaki T, et al. Incremental prognostic significance of the elevated levels of pentraxin 3 in patients with heart failure with normal left ventricular ejection fraction[J]. J Am Heart Assoc, 2014, 3(4):e000928.
[15]
Michel JB. Anoikis in the cardiovascular system:known and unknown extracellular mediators[J]. Arterioscler Thromb Vasc Biol, 2003, 23(12):2146-2154.
[16]
Russo I, Cavalera M, Huang SB, et al. Protective effects of activated myofibroblasts in the pressure-overloaded myocardium are mediated through smad-dependent activation of a matrix-preserving program[J]. Circ Res, 2019, 124(8):1214-1227.
[17]
Lunde IG, Herum KM, Carlson CC, et al. Syndecans in heart fibrosis[J]. Cell Tissue Res, 2016, 365(3):539-552.
[18]
Lipphardt M, Dihazi H, Maas JH, et al. Syndecan-4 as a marker of endothelial dysfunction in patients with resistant hypertension[J]. J Clin Med, 2020, 9(9):3051.
[19]
Herum KM, Romaine A, Wang A, et al. Syndecan-4 protects the heart from the profibrotic effects of thrombin-cleaved osteopontin[J]. J Am Heart Assoc, 2020, 9(3):e013518.
[20]
Linssen PBC, Brunner-La Rocca HP, Schalkwijk CG, et al. Serum matrix metalloproteinases and left atrial remodeling-the hoorn study[J]. Int J Mol Sci, 2020, 21(14):4944.
[21]
Takahashi R, Negishi K, Watanabe A, et al. Serum syndecan-4 is a novel biomarker for patients with chronic heart failure[J]. J Cardiol, 2011, 57(3):325-332.
