The effect of flecainide acetate on fetal heart rate variability: A case report

• Published in: Obstetrics and gynecology (New York. 1953) Vol. 86; no. 4; pp. 667 - 669
• Main Authors: van Gelder-Hasker, M.R., de Jong, C.L.D., de Vries, J.I.P., van Geijn, H.P.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.10.1995; The American College of Obstetricians and Gynecologists; Elsevier Science
• Subjects: Adult; Antiarythmic agents; Biological and medical sciences; Cardiovascular system; Female; Fetal Diseases - drug therapy; Flecainide - pharmacology; Flecainide - therapeutic use; Heart Rate, Fetal - drug effects; Humans; Medical sciences; Pharmacology. Drug treatments; Pregnancy; Tachycardia, Supraventricular - drug therapy; Human; Arrhythmia; Treatment efficiency; Cardiovascular disease; Acetate; Paroxysmal supraventricular tachycardia; Excitability disorder; Case study; Heart rate; Fetal diseases; Chemotherapy; Treatment; Heart disease; Fetus
• DOI: 10.1016/0029-7844(95)00028-P
• ISSN: 0029-7844

Fetal supraventricular tachycardia is most often treated by maternal application of digoxin. A drug used for second-choice therapy is flecainide acetate. For a case in which maternal digoxin therapy failed, flecainide caused a lowering of the fetal heart rate (FHR) but, simultaneously, variability and accelerations nearly disappeared. The fetus demonstrated a normal movement pattern. Fetal well-being during delivery was assessed by regular ultrasound observations of fetal movements. Flecainide was not continued after birth, and digoxin therapy was started when tachycardia reappeared. The heart rate changed into a reactive pattern 5 days after birth. Around that time, flecainide levels in the neonatal serum were below the limit of detection. Flecainide use can cause the absence of accelerations and poor variability in the FHR.