Outcome of pregnancies in patients with anti‐SSA/Ro antibodies: A study of 165 pregnancies, with special focus on electrocardiographic variations in the children and comparison with a control group

Costédoat-Chalumeau, Nathalie; Amoura, Zahir; Lupoglazoff, Jean‐Marc; Huong, D. Lê Thi; Denjoy, Isabelle; Vauthier, D.; Sebbouh, Djamel; Fain, Olivier; Georgin‐Lavialle, Sophie; Ghillani, Pascale; Musset, Lucile; Wechsler, B.; Duhaut, P.; Piette, Jean‐Charles

doi:10.1002/art.20554

Cited by 153 publications

(88 citation statements)

References 23 publications

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“…Maternal structural cardiac disease [45][46][47][48] 3-7 (all) 10-14 (AVSD) [13][14][15][16][17][18] …”

Section: Family Historymentioning

confidence: 99%

“…The number of affected pregnancies increases to 11% to 19% for those with a previously affected child with CHB. [13][14][15][16][17] In addition, women with both autoantibodies and hypothyroidism are at a 9-fold increased risk of having an affected fetus or neonate compared with those with SSA or SSB alone. 18 In addition to abnormalities in the conduction system, up to 10% to 15% of SSA-exposed fetuses with conduction system disease may also develop myocardial inflammation, endocardial fibroelastosis, or atrioventricular (AV) valve apparatus dysfunction.…”

Section: Autoimmune Disease and Autoantibody Positivitymentioning

confidence: 99%

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Diagnosis and Treatment of Fetal Cardiac Disease

Donofrio¹,

Moon-Grady²,

Hornberger³

et al. 2014

Circulation

990

543

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Background— The goal of this statement is to review available literature and to put forth a scientific statement on the current practice of fetal cardiac medicine, including the diagnosis and management of fetal cardiovascular disease. Methods and Results— A writing group appointed by the American Heart Association reviewed the available literature pertaining to topics relevant to fetal cardiac medicine, including the diagnosis of congenital heart disease and arrhythmias, assessment of cardiac function and the cardiovascular system, and available treatment options. The American College of Cardiology/American Heart Association classification of recommendations and level of evidence for practice guidelines were applied to the current practice of fetal cardiac medicine. Recommendations relating to the specifics of fetal diagnosis, including the timing of referral for study, indications for referral, and experience suggested for performance and interpretation of studies, are presented. The components of a fetal echocardiogram are described in detail, including descriptions of the assessment of cardiac anatomy, cardiac function, and rhythm. Complementary modalities for fetal cardiac assessment are reviewed, including the use of advanced ultrasound techniques, fetal magnetic resonance imaging, and fetal magnetocardiography and electrocardiography for rhythm assessment. Models for parental counseling and a discussion of parental stress and depression assessments are reviewed. Available fetal therapies, including medical management for arrhythmias or heart failure and closed or open intervention for diseases affecting the cardiovascular system such as twin–twin transfusion syndrome, lung masses, and vascular tumors, are highlighted. Catheter-based intervention strategies to prevent the progression of disease in utero are also discussed. Recommendations for delivery planning strategies for fetuses with congenital heart disease including models based on classification of disease severity and delivery room treatment will be highlighted. Outcome assessment is reviewed to show the benefit of prenatal diagnosis and management as they affect outcome for babies with congenital heart disease. Conclusions— Fetal cardiac medicine has evolved considerably over the past 2 decades, predominantly in response to advances in imaging technology and innovations in therapies. The diagnosis of cardiac disease in the fetus is mostly made with ultrasound; however, new technologies, including 3- and 4-dimensional echocardiography, magnetic resonance imaging, and fetal electrocardiography and magnetocardiography, are available. Medical and interventional treatments for select diseases and strategies for delivery room care enable stabilization of high-risk fetuses and contribute to improved outcomes. This statement highlights what is currently known and recommended on the basis of evidence and experience in the rapidly advancing and highly specialized field of fetal cardiac care.

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“…Maternal structural cardiac disease [45][46][47][48] 3-7 (all) 10-14 (AVSD) [13][14][15][16][17][18] …”

Section: Family Historymentioning

confidence: 99%

Section: Autoimmune Disease and Autoantibody Positivitymentioning

confidence: 99%

Diagnosis and Treatment of Fetal Cardiac Disease

Donofrio¹,

Moon-Grady²,

Hornberger³

et al. 2014

Circulation

990

543

View full text Add to dashboard Cite

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“…Notably, these authors recently replicated their 2005 study in the same but expanded population, and they found similar results [Bourré-Tessier J, Clarke A, Huynh T, Bernatsky S, Joseph L, Bélisle P, Pineau C. Prolongation of the corrected QT interval in Anti-Ro ⁄ SSA positive adults with SLE. 9th International Congress on Systemic Lupus Erythematosus, Vancouver, British Columbia, June [24][25][26][27]2010]. …”

Section: Clinical Findingsmentioning

confidence: 99%

Anti-Ro/SSA Antibodies and Cardiac Arrhythmias in the Adult: Facts and Hypotheses

Lazzerini

Capecchi

Laghi-Pasini

2010

Scandinavian Journal of Immunology

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It is well established that the passive trans‐placental passage of anti‐Ro/SSA antibodies from mother to foetus is associated with the risk to develop an uncommon syndrome named neonatal lupus (NLE), where the congenital heart block represents the most severe clinical feature. Recent evidence demonstrated that also adult heart, classically considered invulnerable to the anti‐Ro/SSA antibodies, may represent a target of the arrhythmogenicity of these autoantibodies. In particular, the prolongation of the QTc interval appears the most frequent abnormality observed in adults with circulating anti‐Ro/SSA antibodies, with some data suggesting an association with an increased risk of ventricular arrhythmias, also life threatening. Moreover, even though the association between anti‐Ro/SSA antibodies and conduction disturbances is undoubtedly less evident in adults than in infants, from the accurate dissection of the literature data the possibility arises that sometimes also the adult cardiac conduction tissue may be affected by such antibodies. The exact arrhythmogenic mechanisms involved in foetus/newborns and adults, respectively, have not been completely clarified as yet. However, increasing evidence suggests that anti‐Ro/SSA antibodies may trigger rhythm disturbances through an inhibiting cross‐reaction with several cardiac ionic channels, particularly the calcium channels (L‐type and T‐type), but also the potassium channel hERG, whose different expression and involvement in the cardiac electrophysiology during lifespan might account for the occurrence of age‐related differences.

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“…No sudden infant death or symptomatic arrhythmia occurred during the first year of life. The authors concluded that the ECG findings in children of anti-SSA-positive and anti-SSA-negative mothers were not significantly different [37]. However, this study was mainly retrospective.…”

Section: Qt Interval Prolongationmentioning

confidence: 82%

“…The French group studied 165 consecutive pregnancies in 106 anti-SSA-positive women with connective tissue diseases (CTDs) [37]. ECGs obtained on 58 children of this group were compared with those obtained on 85 infants born to mothers with CTDs who were negative for both anti-SSA and anti-SSB.…”

Section: Qt Interval Prolongationmentioning

confidence: 99%

Arrhythmias Presenting in Neonatal Lupus

Brucato

Previtali

Ramoni

et al. 2010

Scandinavian Journal of Immunology

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Arrhythmogenicity and electrophysiological effects of anti-Ro ⁄ SSA antibodiesBased on the facts that there is no convincing evidence that maternal antibodies can cross the sarcolemma of a normal cardiac myocyte, essentially two major categories of mechanisms for congenital complete heart block (CHB) can be identified. The first is abnormal surface expression of intracellular SSA ⁄ Ro and SSB ⁄ La antigens, eventually induced by apoptosis [1, 2], viral infection [3], UV light and IFNc treatment [4]. The other mechanism is the cross-reactivity of maternal antibodies with targets other than SSA ⁄ Ro and SSB ⁄ La antigens. Maternal antibodies were reported to cross-react with laminin and with human cardiac myosin heavy chain at a critical stage during foetal cardiac development [5,6], but the L-type calcium channels seem particularly important in this hypothesis [7][8][9][10].After preliminary reports, [11,12] Boutjdir in an outstanding paper [7] showed that IgG-enriched fractions and anti-52-kD SSA ⁄ Ro antibodies affinity-purified from the sera of mothers whose children have CHB reversibly induce complete atrioventricular (AV) block in the human foetal heart perfused by the Langendorff technique. At 33 min of perfusion, complete AV block was observed with the presence of only P waves and missing QRS complexes. Reperfusion of the heart with antibodyfree Tyrode's solution for 48 min resulted in partial and slow recovery. Superfusion of hearts with IgG fractions from mothers with affected children also induced bradycardia and AV dissociation. In contrast, IgG from control mothers did not have any measurable effect on AV conduction. In the same paper, the authors showed that anti-Ro ⁄ SSA antibodies inhibit L-type Ca 2+ currents at the whole-cell and single-channel level. Immunization of female BALB ⁄ c mice with recombinant 52-kD SSA ⁄ Ro protein generated high-titre antibodies that crossed the placenta during pregnancy and were associated with varying degrees of AV conduction abnormalities, including complete AV block, in the pups. These findings suggest that anti-52-kD SSA ⁄ Ro antibodies are causally related to the development of CHB.The same group reported that the passive transfer of human anti-Ro/SSA into pregnant mice induced AbstractPerfusion of human foetal heart with anti-Ro ⁄ SSA antibodies induces transient heart block. Anti-Ro ⁄ SSA antibodies may cross-react with T-and L-type calcium channels, and anti-p200 antibodies may cause calcium to accumulate in rat heart cells. These actions may explain a direct electrophysiological effect of these antibodies. Congenital complete heart block is the more severe manifestation of so-called ''Neonatal Lupus''. In clinical practice, it is important to distinguish in utero complete versus incomplete atrioventricular (AV) block, as complete AV block to date is irreversible, while incomplete AV block has been shown to be potentially reversible after fluorinated steroid therapy. Another issue is the definition of congenital AV block, as cardiologists have considered co...

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Outcome of pregnancies in patients with anti‐SSA/Ro antibodies: A study of 165 pregnancies, with special focus on electrocardiographic variations in the children and comparison with a control group

Cited by 153 publications

References 23 publications

Diagnosis and Treatment of Fetal Cardiac Disease

Diagnosis and Treatment of Fetal Cardiac Disease

Anti-Ro/SSA Antibodies and Cardiac Arrhythmias in the Adult: Facts and Hypotheses

Arrhythmias Presenting in Neonatal Lupus

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