2014
DOI: 10.1136/archdischild-2013-305034
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Intertwin cardiac status at 10-year follow-up after intrauterine laser coagulation therapy of severe twin–twin transfusion syndrome: comparison of donor, recipient and normal values

Abstract: Despite severe prenatal cardiac involvement, childhood cardiac function is normal in the majority of surviving donors and recipients after successful LC of severe TTTS. This underlines the favourable impact of intrauterine LC on postnatal cardiovascular performance.

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Cited by 29 publications
(22 citation statements)
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“…5 Some longer term follow-up studies conducted on TTTS survivors beyond the first year of life demonstrate no impact on LV or RV function. 16,17 However, early neonatal data on the post natal adaptation of myocardial performance of the recipient infant, the association with clinical instability after birth, response to therapeutic intervention and long-term outcomes does not exist to date.…”
Section: Discussionmentioning
confidence: 96%
“…5 Some longer term follow-up studies conducted on TTTS survivors beyond the first year of life demonstrate no impact on LV or RV function. 16,17 However, early neonatal data on the post natal adaptation of myocardial performance of the recipient infant, the association with clinical instability after birth, response to therapeutic intervention and long-term outcomes does not exist to date.…”
Section: Discussionmentioning
confidence: 96%
“…Right ventricle hypertrophy may lead to obstruction of the outflow tract and, consequently, to decrease in forward flow across the pulmonary valve, causing decreased growth and PS [21] . Additionally, severe systolic dysfunction of the right ventricle may further decrease the blood flow across the outflow tract and even lead to inability to open the pulmonary valve, thus resulting in a functional PA. Endothelin-1 could play a key role, since it is not only a potent vasoconstrictor but also a mitogenic factor which can induce fetal ventricular myocyte proliferation in vitro [22] .…”
Section: Discussionmentioning
confidence: 99%
“…Several pathways of RVOTO development have been suggested, such as the underdevelopment of the pulmonary valve due to decreased forward flow across the PV, caused by right ventricular hypertrophy, the effect of endothelial damage caused by shear stress, which eventually results in valve dysplasia and damage of the valve due to exposure to abnormal concentrations of vasoactive mediators such as endothelin‐1, renin, and angiotensin II . The decreased flow across the PV may be explained by impaired cardiac function at the time of TTTS .…”
Section: Commentsmentioning
confidence: 99%