Klin Padiatr 2010; 222 - GNPI_PO_171
DOI: 10.1055/s-0030-1261638

Not only bradycardia of prematurity – transitory sinus node dysfunction in a preterm infant

A Wörner 1, JP Pfammatter 2, J McDougall 1
  • 1Neonatology, Children's University Hospital, Bern, Schweiz
  • 2Pediatric Cardiology, Children's University Hospital, Bern, Schweiz

Aims: Sinus node dysfunction is rare in neonates, but can occur secondary to congenital heart disease, surgical interventions or endovascular manipulations. In addition, cardiac conduction disorders affecting the atrioventricular node are associated with maternal collagen vascular disorders. Here, we present the case of a hypotrophic preterm infant with transitory sinus node dysfunction in the context of maternal antiphospholipid antibody syndrome. Case report: Marked intrauterine growth restriction with oligohydramnios were diagnosed at 29 weeks of gestation in a 32 year old second gravida. A hypotrophic female infant was delivered via cesarean section with a birth weight of 430g (P<3, -3.3 SDS) and normal Apgar scores and umbilical pH. Respiratory complications included respiratory distress syndrome requiring CPAP therapy for 5 days and a mild bronchopulmonary dysplasia, requiring supplemental oxygen until 36 weeks of gestation. Further diagnostic measures revealed an asymptomatic antiphospholipid antibody syndrome in the mother with severe placental insufficiency as the probable cause of hypotrophy. Echocardiography on day 1 was normal. The baby developed mild apnea of prematurity treated with caffeine citrate until 34 weeks of gestation. At 36 weeks, repeated self-limiting episodes of severe bradycardia with asystolic phases lasting 5 seconds were noted. During these episodes the baby was asymptomatic, with absence of gastroesophageal reflux or neurologic events. Holter ECG confirmed a sinus arrhythmia with sinus pauses up to 4.5 seconds and initiation of an ectopic atrial or junctional rhythm, consistent with sinus node dysfunction. The infant showed persistence of sinus arrhythmia until 40 weeks of gestation. Monitor surveillance was discontinued shortly before discharge at 4 weeks of corrected age as the baby was stable. A follow-up Holter ECG at 46 weeks of gestation was normal. Discussion: Cardiac conduction disorders associated with maternal collagen vascular disease are a well-known entity, e.g. congenital heart block in neonatal lupus. However, neonatal sinus node dysfunction in the context of maternal antiphospholipid antibody syndrome has not yet been described and the association in our case is speculative. There are case reports describing maternal conduction disturbances associated with anti-phospholipid antibody syndrome. In addition, as has been previously described, transient sinus node dysfunction could be associated with immature autonomic nervous sytem activity in preterm infants.

Conclusion: Neonatal sinus node dysfunction in absence of congenital heart disease could be associated with antiphospholipid antibody syndrome and should be investigated in mothers of affected infants.