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Myocardial injury in fetal aortic stenosis: Insights from amniotic fluid analysis
Author(s) -
Friedman Kevin G.,
Sleeper Lynn A.,
Fichorova Rai.,
Weilnau Taylor,
Tworetzky Wayne,
WilkinsHaug Louise E.
Publication year - 2018
Publication title -
prenatal diagnosis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.956
H-Index - 97
eISSN - 1097-0223
pISSN - 0197-3851
DOI - 10.1002/pd.5213
Subject(s) - medicine , fetus , cardiology , troponin t , ventricle , gestational age , amniotic fluid , fetal echocardiography , gestation , stenosis , pregnancy , prenatal diagnosis , myocardial infarction , genetics , biology
Objective Fetal aortic stenosis (AS) imposes pressure load on the developing left ventricle (LV) and leads to derangements in myocardial structure and function via mechanisms that are not well characterized. Methods We compared amniotic fluid NT‐BNP and troponin levels in fetuses with AS prior to fetal valvuloplasty and controls. We estimated correlations between NT‐BNP and fetal echo parameters and identify NT‐BNP cutoff associated with biventricular outcome Results Median NT‐BNP level was higher in fetal AS than controls (3858 vs 1737 pg/mL, P < 0.012). By contrast, troponin levels were lower in fetal AS, with troponin > detectable in 0/25 (0%) AS cases compared with 22/85 (26%) controls ( P = 0.03). Of 25 fetal AS cases, 12 (48%) had biventricular outcome. Fetuses with NT‐BNP < 910 pg/mL were more likely to have biventricular (OR =10) compared with those ≥910 pg/mL ( P = 0.045). Higher NT‐BNP correlated with earlier gestational age and measures of larger left heart size. Conclusion NT‐BNP is elevated in fetal AS, suggesting that LV pressure load and increased wall stress lead to maladaptive stretch‐related myocardial remodeling. Troponin is normal in mid‐gestation fetal AS, suggesting that ischemia is not the primary factor in fetal response to LV pressure load.