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Ann Thorac Surg 2000;70:973
© 2000 The Society of Thoracic Surgeons
a Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia Health System, Box 310, Charlottesville, VA, 22908 USA,
e-mail: ikron{at}virginia.edu
Invited commentary
The issue of whether the anomalous vertical vein (VV) should be ligated during repair of total anomalous pulmonary venous connection (TAPVC) is controversial. Traditionally, most surgeons have emphasized routine interruption of the VV at the time of TAPVC repair to prevent the perceived consequence of a residual left-to-right shunt. However, we recently demonstrated that not only is routine VV ligation unnecessary, but this practice may actually be undesirable for patients with small left heart chambers [1]. Previously, it was shown that the left atrium and ventricle are notoriously small and dysfunctional in TAPVC [2, 3]. We therefore maintain that the unligated VV may serve as a temporary "pop-off valve," allowing the left heart chambers adequate time for growth and functional adaptation. In our series, all long-term survivors in whom the VV was left open demonstrated spontaneous involution of the anomalous venous channel. Only one patient whose VV was not ligated developed a persistent left to right shunt. Interestingly, the basis for persistent VV patency in this child proved to be a stricture at the common pulmonary vein to left atrium anastomosis.
Doctor Shah and colleagues describe two patients who underwent repair of supracardiac-type TAPVC but could not tolerate concomitant VV closure. These individuals developed severe pulmonary hypertension during attempted VV ligation, and as a result this structure was intentionally left open in both children. However, as described, both of these patients developed symptoms of a left-to-right shunt and were found to have persistent VV patency after TAPVC repair. Although delayed surgical closure of the anomalouos VV was successful in both patients, it was attended by extremely high left atrial pressures in one case which proved to be a difficult postoperative management challenge.
The latter situation supports our contention that in order for an unligated VV to undergo spontaneous closure, the left heart chambers must achieve normal size and function. Although Dr Shah and associates do not specifically comment on postoperative left heart dimensions and function in their two patients, the fact that one patient developed severe left atrial hypertension immediately after VV ligation suggests that the left atrium or ventricle had remained small and noncompliant. In the absence of an anastomotic stricture, this may be the primary phenomenon favoring continued shunt flow through the anomalous pathway. In our series [1] as well as the report by Jegier and associates [4], spontaneous closure of an unligated VV was contingent upon normal growth and function of the left heart chambers. As a final comment, we propose that development of a persistent left to right shunt through an unligated VV does not necessarily relegate a patient to a second operation. Such individuals may be candidates for percutaneous angiographic VV embolization, in a manner similar to embolization of portosystemic venous collaterals during creation of a transjugular intrahepatic portosystemic shunt.
References
Related Article
R shunt: a serious consequence of TAPVC repair without ligation of vertical vein
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