Fetal tachyarrhythmia with atrial flutter in obstetric cholestasis

Inizi, Shamma Al; Gupta, Richa; Gale, Alan

doi:10.1016/j.ijgo.2005.12.030

Cited by 50 publications

(43 citation statements)

References 3 publications

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“…Some studies have reported an high incidence of caesarean section [52,53,55,57], and foetal arrhythmias [53,54,60]. In a primarily Latina population in Los Angeles, ICP was found to be associated with chorioamnionitis [23].…”

Section: Foetal Morbidity and Mortalitymentioning

confidence: 99%

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Zecca¹,

Luca²,

Marras³

et al. 2007

CPR

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Intrahepatic cholestasis of pregnancy (ICP) is a clinical syndrome of unknown pathophysiology, occurring during the second half of pregnancy and persisting until delivery. The incidence of ICP varies from 0.1% to 1.5% of pregnancies in Europe, North America and Australia and from 9.2% to 15.6% in South American countries such as Bolivia and Chile. This syndrome has been associated with increased foetal distress, intrauterine death, premature delivery, perinatal mortality and, more recently, with the occurrence of respiratory distress syndrome in the newborn infant. Bile acids (BA) are supposed to be the main mediators for these complications because ICP seriously impairs the placental clearance of foetal BA leading to a dangerous accumulation of these compounds within the foetus and the newborn. Cholestatic pregnancies have to be considered high risk ones, recent reports showing that BA can interfere with surfactant metabolism and are particularly harmful for the developing lung.This review summarizes existing literature data on this topic with particular emphasis on bile acids-induced lung injury. The authors discuss possible mechanisms of lung damage and highlight future research perspectives in this field.

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Section: Foetal Morbidity and Mortalitymentioning

confidence: 99%

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Zecca¹,

Luca²,

Marras³

et al. 2007

CPR

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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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Fetal tachyarrhythmia with atrial flutter in obstetric cholestasis

Cited by 50 publications

References 3 publications

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

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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