%0 Journal Article
%T Atrioventricular Conduction Delay in Fetuses Exposed to Anti-SSA/Ro and Anti-SSB/La Antibodies: A Magnetocardiography Study
%A Annette Wacker-Gu£¿mann
%A Henrike Paulsen
%A Isabelle Kiefer-Schmidt
%A Joerg Henes
%A Jana Muenssinger
%A Magdalene Weiss
%A Rangmar Goelz
%A Hubert Preissl
%J Journal of Immunology Research
%D 2012
%R 10.1155/2012/432176
%X Background. The presence of anti-SSA/Ro and anti-SSB/La antibodies during pregnancy is associated with fetal congenital heart block (CHB), which is primarily diagnosed through fetal echocardiography. Conclusive information about the complete electrophysiology of the fetal cardiac conducting system is still lacking. In addition to echocardiography, fetal magnetocardiography (fMCG) can be used. fMCG is the magnetic analogue of the fetal electrocardiogram (ECG). Patients and Methods. Forty-eight pregnant women were enrolled in an observational study; 16 of them tested positive for anti-SSA/Ro and anti-SSB/La antibodies. In addition to routine fetal echocardiography, fMCG was used. Fetal cardiac time intervals (fCTIs) were extracted from the magnetic recordings by predefined procedures. ECGs in the neonates of the study group were performed within the first month after delivery. Results. The PQ segment of the fCTI was significantly prolonged in the study group ( ), representing a delay of the electrical impulse in the atrioventricular (AV) node. Other fCTIs were within normal range. None of the anti-SSA/Ro and/or anti-SSB/La fetuses progressed to a more advanced heart block during pregnancy or after birth. Conclusion. The study identified a low-risk population within antibody positive mothers, where PQ segment prolongation is associated with a lack of progression of the disease. 1. Introduction Fetal exposure to anti-SSA/Ro and anti-SSB/La antibodies is associated with the development of congenital heart block (CHB). The incidence is about 2% in primigravid mothers. The risk is five to tenfold higher in women who previously had an affected child with either CHB or a neonatal lupus rash [1, 2]. Fetuses with CHB carry high rates of mortality (20%) and morbidity (>60% of the surviving children require a permanent pacemaker in adulthood) [3, 4]. Risk factors associated with a poor outcome are gestation <20 weeks, ventricular rate ¡Ü50£¿bpm, hydrops, and impaired left ventricular function [4, 5]. In addition to the expected course of the disease, life-threatening cardiomyopathy is also found in the offspring in 10%¨C15% of cases and can occur in utero or postnatally [6]. The pathogenesis of the disease is presumed to involve transplacental maternal IgG autoantibodies, which cause an atrioventricular (AV) delay. However, the first manifestation may also be sinus node dysfunction, atrial or ventricular ectopies or bundle branch blocks, but also junctional ectopic tachycardia or ventricular tachycardia [7]. Regarding the pathogenesis of these variable expressions of
%U http://www.hindawi.com/journals/jir/2012/432176/