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J Thorac Cardiovasc Surg 2003;126:1254-1256
© 2003 The American Association for Thoracic Surgery

Editorials

Fetal cardiac surgery: Simplicity versus success in a new frontier

^a Division of Pediatric Cardiovascular Surgery, University of Texas, Houston/Memorial Hermann Children’s Hospital, Houston, Tex, USA

Received for publication January 7, 2003; accepted for publication March 4, 2003.

^* Address for reprints: Bradley S. Allen, MD, University of Texas, 6431 Fannin St, MSB 1.214, Houston, TX 77030, USA
bradley.allen@uth.tmc.edu

The first 20% of the full text of this article appears below.

See related article in 2003;125: 1276-82.

 

The current status of fetal cardiac surgery is similar to the field of infant heart surgery 50 years ago, when it was clear that correction of certain congenital defects would provide great benefit, but there was no safe and effective method to gain access to the heart. However, with the development of cardiopulmonary bypass (CPB) equipment and techniques, intraoperative access to the heart became possible. Moreover, surgeons developed an understanding of the pathophysiologic responses of the child to these techniques and learned how to protect the myocardium, as well as the patient, during open cardiac repair.^1,2 This allowed postnatal cardiac surgery to be done safely and effectively. If similar "low-risk" techniques, understanding, and equipment existed for the fetus, there would be little argument that fetal cardiac surgery would be preferable for certain congenital lesions. However, little is known about the pathophysiologic effect of surgical intervention or CPB on the developing fetus. As a consequence, many of the surgical techniques developed over the past 50 years for patients with cardiac disease, including those of extracorporeal circulation and myocardial protection, must be redeveloped before application to the fetus.

Early experimental work on fetal cardiovascular interventions demonstrated it was technically possible to place the fetal lamb on and separate from CPB.^3,4 Nevertheless, most animals died within hours as a result of placental dysfunction after a marked increase in placental vascular resistance. Moreover, even when placental dysfunction was prevented, the post-CPB fetus routinely had progressive metabolic acidosis as a result of decreased cardiac output, leading to late death.^3,5,6 These studies clearly establish that the major limitation to successful clinical fetal cardiac surgery would not be technical but related . . . [Full Text of this Article]

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