Refractory Fetal Supraventricular Tachycardia and Obstetric Cholestasis

Shand, Antonia; Dickinson, Jan E.; D’Orsogna, Lloyd

doi:10.1159/000151676

Cited by 21 publications

(23 citation statements)

References 35 publications

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“…Bile acids have been shown to cause cardiac arrhythmias in an in vitro model of the fetal heart, and this effect is ameliorated by the addition of UDCA to the culture medium . Although human data are lacking, there are three case reports of antenatal fetal cardiac arrhythmia in the literature, including drug‐resistant supraventricular tachycardia (SVT), refractory SVT and atrial flutter . It should be noted that the outcome in all three of these pregnancies was good.…”

Section: Associated Adverse Perinatal Outcomesmentioning

confidence: 99%

Intrahepatic cholestasis of pregnancy

Geenes

Williamson

Chappell

2016

The Obstetric & Gynaecologis

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Key content Obstetric cholestasis is also known as intrahepatic cholestasis of pregnancy (ICP). ICP affects approximately 0.7% of pregnant women in the UK, equating to approximately 6000 women per year. Pruritus, elevated liver enzymes and raised serum bile acids are key to the diagnosis of ICP. There is an increased risk of adverse perinatal outcomes associated with severe ICP, including spontaneous preterm birth, meconium staining of the amniotic fluid and stillbirth. ICP may be treated with ursodeoxycholic acid (UDCA), with some improvement in serum biochemistry and pruritus; however, the impact on the fetus is uncertain. Learning objectives To understand the presentation, investigation and management options for women with ICP. To appreciate the perinatal implications of ICP. To be aware of the differential diagnoses for antenatal and postnatal abnormal liver function tests. Ethical issues Use of unlicensed drugs in pregnancy. Uncertain feto‐protective benefits of UDCA. Implications of the adoption of early elective delivery on the development of children born to women with ICP.

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Section: Associated Adverse Perinatal Outcomesmentioning

confidence: 99%

Intrahepatic cholestasis of pregnancy

Geenes

Williamson

Chappell

2016

The Obstetric & Gynaecologis

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“…A few studies have reported abnormal fetal heart rates (≤ 100 or ≥ 180 beats per minute (bpm)) as well as reduced heart rate variability in ICP (Gorelik et al, 2003;Inizi et al, 2006;Laatikainen, 1975;Reid et al, 1976;Shand et al, 2008). Therefore, spontaneous beating rate was assessed in neonatal rat cardiomyocytes cultured with fibroblasts.…”

Section: Counteracting the Effect Of Taurocholic Acidmentioning

confidence: 99%

The protective effect of ursodeoxycholic acid in an in vitro model of the human fetal heart occurs via targeting cardiac fibroblasts

Schultz

Hasan

Alvarez-Laviada

et al. 2016

Progress in Biophysics and Molecular Biology

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“…Fetal tachycardia and bradycardia have been reported in ICP [7,18]. More recently, there have been reports of fetal atrial flutter and supraventricular tachycardia in ICP pregnancies [19,20]. …”

Section: Bile Acid Signaling and The Fetal Heartmentioning

confidence: 99%

Bile Acid Signaling in Fetal Tissues: Implications for Intrahepatic Cholestasis of Pregnancy

Williamson¹,

Miragoli

Kadir

et al. 2011

Dig Dis

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Background/Aims: Intrahepatic cholestasis of pregnancy (ICP) is complicated by spontaneous preterm labor, fetal anoxia and unexplained fetal death. We aim to evaluate the mechanisms by which raised fetal bile acids cause placental abnormalities and fetal cardiac pathology. Methods: The study was performed using placental samples taken from ICP pregnancies, placental explant culture, neonatal and adult cardiomyocytes, and murine and human embryonic stem cell-derived cardiomyocytes. Results: Maternal cholestasis causes a placental phenotype with histological abnormalities. This can be evaluated using placental explant cultures. Taurocholate, the principal bile acid raised in the fetal compartment in ICP, causes abnormal cardiomyocyte contraction, rhythm and desynchronization of calcium dynamics. To extend our observations that the muscarinic M2 receptor plays a role in bile acid-induced arrhythmia in cardiomyocytes, we are developing a model containing mixed cell populations to represent the fetal and maternal hearts. This will be used to evaluate the underlying mechanisms to explain fetal arrhythmia in the presence of cholestasis. Conclusion: Bile acids signal via a spectrum of pathways in the placenta and the fetal heart.

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Refractory Fetal Supraventricular Tachycardia and Obstetric Cholestasis

Cited by 21 publications

References 35 publications

Intrahepatic cholestasis of pregnancy

Intrahepatic cholestasis of pregnancy

The protective effect of ursodeoxycholic acid in an in vitro model of the human fetal heart occurs via targeting cardiac fibroblasts

Bile Acid Signaling in Fetal Tissues: Implications for Intrahepatic Cholestasis of Pregnancy

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