Fetal and neonatal echocardiographic findings in twin-twin transfusion syndrome

Fesslová, Vlasta; Villa, Laura; Nava, Simon; Mosca, Fabio; Nicolini, Umberto

doi:10.1016/s0002-9378(98)70215-7

Cited by 110 publications

(87 citation statements)

References 13 publications

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“…None of these cases had undergone any form of treatment before laser surgery. The median gestational at diagnosis was 20 (IQR, [18][19][20][21][22] weeks. Quintero Stages I and III cases were the most numerous in our study population, and there were very few Stage IV cases and no Stage V cases.…”

Section: Resultsmentioning

confidence: 99%

Profiling fetal cardiac function in twin–twin transfusion syndrome

Stirnemann

Mougeot

Proulx

et al. 2009

Ultrasound in Obstet & Gyne

104

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Section: Resultsmentioning

confidence: 99%

Profiling fetal cardiac function in twin–twin transfusion syndrome

Stirnemann

Mougeot

Proulx

et al. 2009

Ultrasound in Obstet & Gyne

104

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“…HCM has been documented prenatally and postnatally in the recipient twins of pregnancies complicated by severe TTTS. 20 The pathogenesis of the cardiovascular manifestation remains unclear. The release of growth factors and vasoactive peptides by the placenta to the recipient twin has been implicated in the pathogenesis.…”

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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“…These include ventricular hypertrophy, and pulmonary outflow tract obstruction (Fesslova et al, 1998;Zosmer et al, 1994) A high incidence of other neonatal complications has also been described following TTTS pregnancies in which amnioreduction was the principle intervention (Duncombe et al, 2003;Lopriore et al, 2003). Despite some reports of abnormal brain ultrasonography following the advent of laser ablation of communicating placental vessels for the management of TTTS (Hecher et al, 1999;Quintero et al, 2003;Senat et al, 2004), minimal data are available on neonatal morbidities.…”

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confidence: 99%