Maternity care and therapeutic approaches for fetal bradyarrhythmia

Aim. To investigate the causes of and therapeutic approaches for different types of fetal bradyarrhythmia. Materials and methods. We examined 15 women with fetal bradycardia at 18-36 weeks of gestation. Group I included nine pregnant women with moderate bradycardia (fetal heart rate 86-110 bpm). Six women with severe bradycardia (fetal heart rate 45-78 bpm) made up group II. The study methods included special laboratory examination and statistical analysis. Therapeutic approaches were based on indications and comprised hydroxychloroquine, therapeutic plasmapheresis, immunoglobulin therapy, and pulse corticosteroid therapy. Results. Group II patients were statistically significantly more likely to have autoimmune diseases and higher titers of autoantibodies to SSA (Ro) and antinuclear antibodies. In the setting of specific therapy, 33.3% of patients showed regression of bradyarrhythmia to grade 1-2 AVblock. In 66.7% of patients, there was no heart failure progression or the development of non-immune fetal hydrops. In group I, 88.8% of patients required no specific therapy. The gestational age at delivery in both groups was 38.4 (1.1) weeks. Thirty-three percent of the neonates in group I had multiple cardiovascular and pulmonary malformations. Transient cardiac arrhythmias were observed in 44% of group I neonates. Four out of 6 newborns in group II required pacemaker implantation. Conclusion. Early diagnosis (up to 19-20 weeks of gestation) of fetal heart rate abnormalities, timely and comprehensive examination of the pregnant woman contributes to the early initiation of therapy and the prevention of irreversible damage to the fetal cardiac conduction system.

fetal bradyarrhythmia, congenital atrioventricular heart block, anti-Ro antibodies, anti-La antibodies, antinuclear antibodies