Anti-Ro-associated sinus bradycardia in newborns.

in Newborns To the Editor: In the study by Mazel et al,1 the authors reported that passive transfer of human anti-Ro/SSA and anti-La/SSB autoantibodies into naive pregnant mice induced bradycardia and first-degree AV block in pups, suggesting a possible sinoatrial node involvement. We have observed similar findings in humans. In the last 4 years, we prospectively followed 21 pregnancies in anti-Ro/SSA–positive mothers, performing ECGs in the newborns in the first days after birth. In 3 cases (14.3%), a significant transient sinus bradycardia was observed (heart rate less than third centile for age). Case 1 was a female newborn, spontaneously delivered at 39 weeks of gestation, weight 2670 g, Apgar score at 1 and 5 minutes of 9/10, and a heart rate of 90 bpm 2 days after birth. Case 2 was a female newborn, spontaneously delivered at 41 weeks of gestation, weight 3200 g, Apgar score at 1 and 5 minutes of 9/10, and a heart rate of 70 bpm 2 days after birth. Case 3 was a male newborn,2 delivered by cesarean section at 38 weeks of gestation because of fetal growth retardation, weight 2340 g, Apgar score at 1 and 5 minutes of 9/10, and a heart rate of 90 bpm 2 days after birth. In the 3 cases, prenatal ultrasound fetal heart rate was normal; no perinatal complications (in particular, no metabolic or thermal problems) were observed, and possible causes of bradycardia in newborns were excluded, eg, electrolyte abnormalities and drug interferences. In all cases, bradycardia disappeared within 10 days after birth, with no sequelae. Two mothers had systemic lupus erythematosus, and 1 had an undifferentiated connective tissue disease. Anti-Ro/SSA antibodies may react with 2 different antigenic components of different molecular weights: 52 and 60 kDa.3 Many observations suggest a prevalent role of anti-Ro/ SSA directed against the 52-kDa component in the pathogenesis of congenital AV block.4 Notably, all the mothers of our 3 cases were anti-Ro/SSA positive, with a fine specificity directed against the 60-kDa component of the Ro antigen in immunoblot. Our observations indicate that sinus bradycardia and sinus node dysfunction occur not only in experimental animals passively transfused with anti-Ro/SSA antibodies but potentially are also detectable in human newborns. In this regard, a possible prevalent role of antibodies directed against the 60-kDa component of the Ro complex is also suggested. It is tempting to speculate that IgG from anti-Ro/SSA–positive mothers could affect calcium channels and/or other physiological mechanisms responsible for the automaticity or action potential genesis at the sinus node.5