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International Children's Heart Foundation, Villa Loreto, Casa No. 6A, En Frente del Asilo de Ancianos, Las Colinas, Managua, Nicaragua
(Email: kathleennf{at}msn.com).
The advent of fetal echocardiography rapidly confirmed what cardiac morphologists had long hypothesized in that some developing hearts start out normal in early gestation, and due to an intrauterine event that results in changed blood flow patterns, develop severe and uncorrectable defects develop by the time the child is born. As evidence for this has accumulated, it has brought a new challenge for congenital heart surgeons to address the problem of restoring normal blood flow pattern and hopefully normal growth in the fetus.
Early attempts at fetal bypass were technically successful but fatal (ie, the fetus died from respiratory acidosis due to placental dysfunction). This was subsequently found to result from placental vasoconstriction, and is at least partially related to the fetal stress response. Fetal gas exchange, of course, depends on placental perfusion from both the maternal side and the fetal side. In the case of fetal cardiac bypass, the problem essentially seems to be entirely on the fetal side. Most obstetric research in general has been approached from the maternal side, so little is known about what affects the fetal contribution to gas exchange.
The article by Heeb and associates [1] represented a further step in elucidating the mechanism of the placental vasoconstriction caused by fetal cardiac bypass. This study was organized with some animals getting a sternotomy and others not, as this group has previously done, to try to eliminate the confounding variable of surgical stress and focus solely on the effects of bypass. As the authors acknowledge, the clinical usefulness is somewhat limited by the fact that their technique is really one of partial bypass, as the heart was not completely empty and thus contributed, probably substantially, to cardiac output. They used a flow rate that represents approximately 30% to 50% of the normal fetal combined ventricular output. Given the fact that the production of natriuretic peptides is closely related to the volume status of the heart, this could make a significant difference in the results and their clinical applicability. Obtaining adequate venous drainage is always a challenge in fetal cardiac bypass. Placental blood flow was also probably affected significantly by the placement of the umbilical flow probe. Any manipulation of the umbilical vessels generally causes severe vasospasm. It is difficult to predict how this may have affected natriuretic peptides and cGMP, but one might, at the very least, speculate that it affected the analysis of the placenta. Certainly the suggestion that the fetus is experiencing occult myocardial damage during fetal bypass is concerning and will require further clarification. The technique of bypass is important here as well, as is the technique of anesthesia, because various anesthetic agents are known to be poorly tolerated by the fetal heart.
In summary, this well-designed study adds new key information to the understanding of why fetal bypass causes placental dysfunction, and at the same time raises a number of important new questions. Trying to sort out what "goes wrong" with fetal gas exchange during and after cardiac bypass has essentially opened up "Pandora's box" of what controls the placental perfusion from the fetal side. Sorting out this seemingly obscure problem has implications far beyond fetal cardiac surgery and even fetal general surgery, and may one day shed some light on much more common problems, such as intrauterine growth retardation.
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