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Ann Thorac Surg 2004;78:2004
© 2004 The Society of Thoracic Surgeons

INVITED COMMENTARY

Markus K. Heinemann, MD, PhD

Department of Cardiac, Thoracic and Vascular Surgery, University Hospital, Langenbeckstr 1, #505Mainz D-55131, Germany

heinemann{at}uni-mainz.de

The theoretical possibility of prenatal intervention to alleviate the sequelae of severe forms of congenital heart disease has fascinated cardiovascular researchers for quite some time. When the technical challenges of placing a fetus on cardiopulmonary bypass in utero had been overcome, it soon became evident that placental dysfunction as a result of an increase in placental vascular resistance was prohibiting success. Consequently, research concentrated on the mechanisms of this placental vasoconstriction and the means to avoid it. By minimizing the circuit, by blocking the cyclooxygenase pathway, and by reducing fetal stress, the first long-term survival well beyond birth could finally be achieved in the ovine model. The group from Fukuoka has now investigated the mechanism of endothelial dysfunction of the umbilical artery in further detail and postulates that impairment of endothelium-derived nitric oxide release is an essential pathophysiologic mechanism, presumably triggered by an inflammatory response to the bypass circuit. This article significantly extends our knowledge of fetal cardiovascular pathophysiology. However, many questions still remain unanswered before responsible clinical application can be considered.

Meanwhile, alternative roads of fetal cardiovascular intervention have also been explored rather successfully following a concept of minimally invasive, fetoscopic catheter techniques, thereby avoiding cardiopulmonary bypass altogether. Although convincing at first sight, these methods still have their own disadvantages (eg, considerable mechanical damage to the vitally important umbilical vessels and their endothelium).

Extrapolating from the experience in the conventional postnatal setting, where catheter interventions in critically ill neonates (eg, with aortic stenosis) only became practicable after the safety net of cardiac surgery had been firmly established, it may be assumed that fetal catheter intervention could be the way to go, but that it is a moral obligation to have something available that can be reverted to in case of failure. Maybe a combination of surgical access for a catheter procedure on a bypass-controlled fetal heart temporarily not supplying its fetus will eventually be the safest strategy for selected highly problematic lesions. All this may sound very complex, but then new challenges have often called for unprecedented solutions and a brand new set of rules.


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Ann. Thorac. Surg. 2004 78: 1999-2003. [Abstract] [Full Text] [PDF]



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