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Anti Ro/La antibodies

Fetal heart block

In complete atrioventricular block the atria beat at their own rhythm, and none of their impulses is transmitted to the ventricles which have a slow rate (40-70 beats/min)

In 50% of cases structural anomalies are present (mostly left isomerism and corrected transposition of the great arteries). In the remaining cases, the condition is caused by the presence of maternal autoantibodies anti-Ro (SS-A) or anti-La (SS-B) which cross the placenta and cause irreversible destruction of the fetal myocardium and conduction tissue. Most mothers are asymptomatic but in a few cases connective tissue disease is present (lupus erythematosus, scleroderma, rheumatoid arthritis and Sjogren's syndrome).The prevalence of fetal cardiac damage among women with anti-Ro and anti-La antibodies is 5-10%

The prognosis depends on the presence of cardiac defects, the ventricular rate and the presence of hydrops, which develops when the ventricular rate is less than 50 beats/min

In fetuses with cardiac malformations there is heart block starting from the first trimester and their prognosis is poor

Atrioventricular block secondary to maternal autoantibodies develops slowly throughout gestation. Doppler measurement of the PR-interval allows detection of a first degree heart block (>130 ms). Maternal administration of steroids (Dexamethasone 8 mg/day) at this stage may prevent progression to complete heart block. Once there is complete heart block neither  Dexamethasone nor fetal cardiac pacing have been successful