Key result
Low cord blood sFlt1 and elevated NT-proBNP track with poor outcomes in left-sided CHD.
Why the study?
Fetal echocardiography has limited prognostic ability in left-sided congenital heart defects, and cord blood cardiovascular biomarkers could improve prognostic evaluation.
Do cord blood cardiovascular biomarkers correlate with clinical outcomes in fetuses with left-sided congenital heart defects?
Cohort (n=80)
Yes
Do cord blood cardiovascular biomarkers correlate with clinical outcomes in fetuses with left-sided congenital heart defects?
Effect estimate: AUC 0.848 (95% CI 0.706-0.991)
Absolute Event Rate: 259% vs 1848.3%
p-value: p=<0.001
Distinct cord blood biomarker profiles, primarily characterized by reduced sFlt1 and elevated NT-proBNP, could help improve prognostic evaluation and stratify clinical risk for fetuses with left-sided congenital heart defects.
Cord blood sFlt1 and NT-proBNP differences may support fetal left-heart defect risk stratification; leaves open need for prospective validation before clinical use.
Fetal echocardiography has limited prognostic ability in the evaluation of left-sided congenital heart defects (left heart defects). Cord blood cardiovascular biomarkers could improve the prognostic evaluation of left heart defects. A multicenter prospective cohort (2013−2019) including fetuses with left heart defects (aortic coarctation, aortic stenosis, hypoplastic left heart, and multilevel obstruction (complex left heart defects) subdivided according to their outcome (favorable vs. poor), and control fetuses were evaluated in the third trimester of pregnancy at three referral centers in Spain. Poor outcome was defined as univentricular palliation, heart transplant, or death. Cord blood concentrations of N-terminal precursor of B-type natriuretic peptide, Troponin I, transforming growth factor β, placental growth factor, and soluble fms-like tyrosine kinase-1 were determined. A total of 45 fetuses with left heart defects (29 favorable and 16 poor outcomes) and 35 normal fetuses were included, with a median follow-up of 3.1 years (interquartile range 1.4−3.9). Left heart defects with favorable outcome showed markedly increased cord blood transforming growth factor β (normal heart median 15.5 ng/mL (6.8−21.4) vs. favorable outcome 51.7 ng/mL (13.8−73.9) vs. poor outcome 25.1 ng/mL (6.9−39.0), p = 0.001) and decreased placental growth factor concentrations (normal heart 17.9 pg/mL (13.8−23.9) vs. favorable outcome 12.8 pg/mL (11.7−13.6) vs. poor outcome 11.0 pg/mL (8.8−15.4), p < 0.001). Poor outcome left heart defects had higher N-terminal precursor of B-type natriuretic peptide (normal heart 508.0 pg/mL (287.5−776.3) vs. favorable outcome 617.0 pg/mL (389.8−1087.8) vs. poor outcome 1450.0 pg/mL (919.0−1645.0), p = 0.001) and drastically reduced soluble fms-like tyrosine kinase-1 concentrations (normal heart 1929.7 pg/mL (1364.3−2715.8) vs. favorable outcome (1848.3 pg/mL (646.9−2313.6) vs. poor outcome 259.0 pg/mL (182.0−606.0), p < 0.001). Results showed that fetuses with left heart defects present a distinct cord blood biomarker profile according to their outcome.
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Soveral et al. (2022) conducted a cohort in Left-sided congenital heart defects (n=80). Left-sided congenital heart defects vs. Structurally normal hearts (healthy controls) and favorable outcome Left-CHD was evaluated on Cord blood soluble fms-like tyrosine kinase-1 (sFlt1) concentration in poor outcome vs favorable outcome Left-CHD (AUC 0.848, 95% CI 0.706-0.991, p=<0.001). Fetuses with left-sided congenital heart defects and poor outcomes presented drastically reduced cord blood sFlt1 concentrations and higher NT-proBNP compared to favorable outcome cases.
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