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Myocardial injury in fetal aortic stenosis: Insights from amniotic fluid analysis
Kevin G Friedman1,2, Lynn A Sleeper1,2, Raina N Fichorova3,4
1From the Departments of Cardiology, Harvard Medical School, Boston, MA, USA.
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.
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