Therapeutic Trial of Sympathomimetics in Three Cases of Complete Heart Block in the Fetus

Groves, A.; Allan, Lindsey D.; Rosenthal, Éric

doi:10.1161/01.cir.92.12.3394

Cited by 126 publications

(79 citation statements)

References 8 publications

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“…[8][9][10] Because the atrial and ventricular responses to HR perturbation vary, it appears that terbutaline, by exerting a differential effect on primary and subsidiary pacemakers, acts locally and does not influence neural control of HR. We postulate that the robust increase in the atrial (i.e., primary) pacemaker but not the ventricular (i.e., subsidiary) pacemakers in isoimmune CHB reflect the pathologic findings of disease in the AV node.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6][7] With such morphologic and etiologic heterogeneity, it might be expected that the electrophysiologic characteristics of the atrial and ventricular pacemakers in fetuses with CHB would differ in response to pharmacologic heart rate (HR) augmentation with a β agonist such as terbutaline. [8][9][10] Using the technique of fetal magnetocardiography (fMCG)-the only high-resolution fetal electrocardiography technique with the capacity for beat-to-beat analysis over many hours-we observed patterns of HR accelerations, the atrial and ventricular pacemaker response, and the ventricular rate response to atrial accelerations (i.e., AV correlation) during terbutaline treatment in fetuses with isoimmune and LAI-associated CHB. Our results lead us to postulate a mechanism for the observed difference in acceleration patterns between isoimmune and LAI CHB as it relates to the nature and timing of the conduction system defect.…”

mentioning

confidence: 99%

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Atrial and Ventricular Rate Response and Patterns of Heart Rate Acceleration during Maternal–Fetal Terbutaline Treatment of Fetal Complete Heart Block

Cuneo

Zhao

Strasburger

et al. 2007

The American Journal of Cardiology

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Terbutaline is used to treat fetal bradycardia in the setting of complete heart block (CHB); however, little is known of its effects on atrial and ventricular beat rates or patterns of heart rate (HR) acceleration. Fetal atrial and ventricular beat rates were compared before and after transplacental terbutaline treatment (10 to 30 mg/day) by fetal echocardiography in 17 fetuses with CHB caused by immune-mediated damage to a normal conduction system (isoimmune, n = 8) or a congenitally malformed conduction system associated with left atrial isomerism (LAI, n = 9). While receiving terbutaline, 9 of the 17 fetuses underwent fetal magnetocardiography (fMCG) to assess maternal HR and rhythm, patterns of fetal HR acceleration, and correlation between fetal atrial and ventricular accelerations (i.e., AV correlation). Maternal HR and fetal atrial and ventricular beat rates increased with terbutaline. However, terbutaline's effects were greater on the atrial pacemaker(s) in fetuses with isoimmune CHB and greater on the ventricular pacemaker(s) in those with LAI-associated CHB. Patterns of fetal HR acceleration also differed between isoimmune and LAI CHB. Finally, despite increasing HR, terbutaline did not restore the normal coordinated response between atrial and ventricular accelerations in isoimmune or LAI CHB. In conclusion, the pathophysiologic heterogeneity of CHB is reflected in the differing effect of terbutaline on the atrial and ventricular pacemaker(s) and varying patterns of HR acceleration. However, regardless of the cause of CHB, terbutaline augments HR but not AV correlation, suggesting that its effects are determined by the conduction system defect rather than the autonomic control of the developing heart. Fetal complete heart block (CHB) is a rare condition, occurring in approximately 1 of 15,000 pregnancies. Fetal CHB that occurs in association with maternal immunoglobulin-G Sjögren antibodies (i.e., isoimmune CHB) is believed to be a result of immune-mediated fibrosis disrupting continuity between the atrium and the atrioventricular (AV) bundle relatively late in cardiogenesis, 1-3 whereas CHB associated with congenital cardiac malformations such as left atrial isomerism (LAI) is believed to result from maldevelopment of the conduction system early in cardiogenesis, probably during pattern formation of the specialized versus working myocardium. 4 heterogeneity, it might be expected that the electrophysiologic characteristics of the atrial and ventricular pacemakers in fetuses with CHB would differ in response to pharmacologic heart rate (HR) augmentation with a β agonist such as terbutaline. [8][9][10] Using the technique of fetal magnetocardiography (fMCG)-the only high-resolution fetal electrocardiography technique with the capacity for beat-to-beat analysis over many hours-we observed patterns of HR accelerations, the atrial and ventricular pacemaker response, and the ventricular rate response to atrial accelerations (i.e., AV correlation) during terbutaline treatment in fetuses with isoimmun...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Atrial and Ventricular Rate Response and Patterns of Heart Rate Acceleration during Maternal–Fetal Terbutaline Treatment of Fetal Complete Heart Block

Cuneo

Zhao

Strasburger

et al. 2007

The American Journal of Cardiology

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“…When bradyarrhythmias or other arrhythmias are detected perinatally, infants should be monitored closely for progression of conduction abnormalities and cardiomyopathies. Treatment with sympathomimetic agents such as salbutamol and isoprenaline was proved, through case reports, to be effective prenatally in fetuses with congenital heart block [95] but not in postnatal management [96]. Post natal treatment with IVIG or glucocorticoids was found to be ineffective in neonates with CHB [97].…”

Section: Postnatal Treatmentmentioning

confidence: 99%

Neonatal Lupus Erythematosus

Nasef

Hafez²,

Bakr³

2014

NCP

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Neonatal lupus is a passively acquired autoimmune disease that occurs in offspring of mothers with anti-SSA/Ro and/or anti-SSB/La antibodies. The primary clinical features are a photosensitive rash that is usually found on the scalp and periorbital areas, congenital heart block with or without cardiomyopathy, cytopenias, disseminated intravascular coagulation, and neonatal cholestasis with or without elevated transaminases. The diagnosis is usually made in utero by detection of a slow fetal heart rate and subsequent fetal echocardiographic confirmation of heart block and/or cardiomyopathy. Prenatal treatment with fluorinated glucocorticoids beginning as soon after detection has favourable outcome for mothers of fetuses with second degree heart block, is of no value for mothers of fetuses with third degree heart block, and controversial for mothers of fetuses with first degree heart block. Prenatal glucocorticoids can be used also in presence of cardiomyopathy associated with neonatal lupus. Hydroxychloroquine has been used in pregnant women who have anti-SSA/Ro antibodies and who have previously given birth to a child with cardiac manifestations. First and second degree block, detected in utero or at birth, can progress to complete heart block. Infants with complete heart block usually require a pacemaker with an excellent prognosis, although development of heart failure may occur.

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“…Use of maternal corticosteroids, IVIG, and sympathomimetic therapy may ultimately improve the outcome of affected fetuses. 26,27 …”

Section: Extrinsic Causes Of Fetal CMmentioning

confidence: 99%

Fetal Cardiomyopathies

et al. 2002

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Background-Although the prenatal diagnosis of most fetal structural heart defects and dysrhythmias has been described, there is a paucity of information about cardiomyopathies (CMs) in prenatal life. Methods and Results--To determine the pathogenic mechanisms, hemodynamic findings, and outcome of fetal CM, we reviewed the fetal echocardiograms and perinatal histories of 55 affected fetuses. Dilated CM was diagnosed in 22 cases, including 2 with congenital infections, 5 familial cases, 6 with endocardial fibroelastosis related to maternal anti-Ro/La antibodies, and 9 idiopathic cases. Thirty-three had hypertrophic CM, 7 associated with maternal diabetes, 2 with Noonan's syndrome, 2 with ␣-thalassemia, 18 with twin-twin transfusion syndrome, 1 with familial hypertrophy, and 3 with idiopathic hypertrophy. Systolic dysfunction was present in all cases of dilated CM and 15 cases of hypertrophic CM. Diastolic dysfunction was present in 19 of 30 fetuses with assessment of diastolic function parameters. Significant mitral or tricuspid valve regurgitation was seen in 32 cases. Eight fetuses were hydropic and 23 had signs of early hydrops. Seven pregnancies were terminated. Of 46 continued pregnancies with follow-up, 29 (63%) died perinatally. The presence of systolic dysfunction, diastolic dysfunction, and significant atrioventricular valve regurgitation were identified as risk factors for mortality. By multiple logistic regression, diastolic dysfunction was associated with an 8-fold increased risk relative to the other parameters. Conclusions-Fetal CM has a broad spectrum of intrinsic and extrinsic causes. A poor outcome is observed in many affected fetuses. Diastolic dysfunction in fetal CM is associated with the highest risk of mortality. (Circulation. 2002; 106:585-591.)

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Therapeutic Trial of Sympathomimetics in Three Cases of Complete Heart Block in the Fetus

Abstract: We conclude that salbutamol can be effective in the treatment of fetal complete heart block and should be considered in patients with this condition where there is evidence of deteriorating cardiac function.

Cited by 126 publications

References 8 publications

Atrial and Ventricular Rate Response and Patterns of Heart Rate Acceleration during Maternal–Fetal Terbutaline Treatment of Fetal Complete Heart Block

Atrial and Ventricular Rate Response and Patterns of Heart Rate Acceleration during Maternal–Fetal Terbutaline Treatment of Fetal Complete Heart Block

Neonatal Lupus Erythematosus

Fetal Cardiomyopathies

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