Abstract
Complete atrioventricular block (CAVB) is the most common cause of persistent fetal bradycardia. In the presence of a structurally normal heart, it develops primarily in anti-Ro and anti-La positive antibody pregnancies after 20 weeks of gestation. There is a significant risk of perinatal demise, particularly in association with fetal hydrops, poor ventricular function, and heart rates < 55 beats/min. Transplacental treatment strategies are aimed at preventing or modulating these risk factors. Maternal administration of dexamethasone to mitigate or prevent concomitant myocardial inflammation, in combination with beta-stimulation for persistent fetal bradycardia < 55 beats/min to increase fetal cardiac output, has resulted in significantly improved fetal and neonatal outcomes without reversing CAVB.
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