Fetal Sinus Bradycardia Is Associated with Congenital Hypothyroidism: An Infant with Ectopic Thyroid Tissue

Abstract

Hypothyroidism is rarely included in the differential diagnosis for fetal sinus bradycardia. We report an infant with congenital hypothyroidism caused by ectopic thyroid tissue, who showed antenatal bradycardia. The baseline fetal heart rate was 100-110 bpm at 30 weeks of gestation, and fetal echocardiography revealed sinus bradycardia but no cardiac anomalies. Maternal thyroid function was normal (thyroidstimulating hormone [TSH] 2.03 μIU/ml, free T3 2.65 pg/ml, and free T4 0.99 ng/dl) when measured at 31 weeks of gestation. Her serum anti SS-A and SS-B antibodies, anti-thyroglobulin, and microsomal antibodies were negative. A male infant without cardiac anomalies was delivered at 35 weeks and 4 days of gestation and admitted for prematurity and respiratory distress syndrome. The infant's heart rate was 70-110 bpm (normal: 120-160 bpm) on admission. On 8 days of age, thyroid function tests revealed that the infant had severe hypothyroidism (TSH 903.3 μIU/ml, free T3 1.05 pg/ml, and free T4 0.26 ng/dl). The prolonged jaundice assumed to be due to hypothyroidism. Oral levothyroxine sodium hydrate (10 μg/kg/ day) was immediately started on day 8. After the treatment, the heart rate was gradually increased to 130-140 bpm as the infant's thyroid function was improved (TSH 79.8 μIU/ml, free T3 2.95 pg/dl, and free T4 1.66 ng/dl on day 22). The infant was diagnosed ectopic thyroid tissue because of the high thyroglobulin level (85.9 μ g/l). In conclusion, congenital hypothyroidism should be included in the differential diagnosis in cases of fetal bradycardia without cardiac anomalies or maternal autoimmune diseases.

Isolated Fetal Sinus Bradycardia as a First Sign of Congenital Hypopituitarism

“…Rare cases of fetal bradycardia secondary to hormonal deficiencies have been reported. 3 , 4 To our knowledge, this is the first description of congenital hypopituitarism presenting as isolated fetal sinus bradycardia during an otherwise uneventful pregnancy and term delivery. The case also highlights that the bradycardia was rapidly reversible after neonatal treatment with levothyroxine and GH, suggesting that either or both hormonal deficiencies were responsible for the low heart rate.…”

Early L-T4 intervention improves fetal heart development in pregnant rats with subclinical hypothyroidism rats by activating BMP4/Smad4 signaling pathway

“…It was reported that thyroid hormone deficiency affected the expression profiles of myomiR network in the heart of fetal rats and the expression of downstream targeting genes, which in turn led to increased expression of b-MHC and related cardiac dysfunction in adulthood [22]. An infant with ectopic thyroid tissue was found to have sinus bradycardia associated with congenital hypothyroidism [23]. Another study found that SCH was associated with decreased cardiac output in patients with impaired vascular smooth muscle relaxation and reduced nitric oxide level.…”

Early L-T4 intervention improves fetal heart development in pregnant rats with subclinical hypothyroidism rats by activating BMP4/Smad4 signaling pathway

“…It was reported that thyroid hormone de ciency affected the expression pro les of myomiR network in the heart of fetal rats and the expression of downstream targeting genes, which in turn led to increased expression of b-MHC and related cardiac dysfunction in adulthood [22]. An infant with ectopic thyroid tissue was found to have sinus bradycardia associated with congenital hypothyroidism [23]. Another study found that SCH was associated with decreased cardiac output in patients with impaired vascular smooth muscle relaxation and reduced nitric oxide level.…”