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Ann Thorac Surg 2004;77:2260
© 2004 The Society of Thoracic Surgeons

Correspondence

Shallow stitch close to the rim of the ventricular septal defect after pulmonary artery banding: Reply

Toyoki Fukuda, MD, Ichiro Kashima, MD

Department of Cardiovascular Surgery, Tokyo Metropolitan Kiyose Children's Hospital, 1-3-1 Umezono, Kiyose-shi, Tokyo 204-8567, Japan

e-mail: fukuda{at}chp-kiyose-tokyo.jp

To the Editor:

We thank Sugita and associates for their comments and congratulate them for the excellent results using their suturing technique for repairing perimembranous ventricular septal defects (VSD). In their comments, they argued that pulmonary artery banding (PAB) was a risk factor for postoperative complete right bundle branch block (CRBBB). This view is based on the hypothesis that PAB promotes excessive hypertrophy of the interventricular myocardium so that the third portion of the right bundle branch (RBB) migrates toward the right-sided rim of the VSD where surgical injury tends to occur.

Although their hypothesis is intriguing, we are rather reluctant to accept this view for the following reasons: First, only one of the 8 comparable patients and none of those of group 1 in our series developed CRBBB. Second, the course of RBB in the setting of ventricular hypertrophy is not yet fully determined. This may partly be ascribed to the unsolved questions of whether hypertrophy of the right ventricular wall, including the ventricular septum, is uniform in perimembranous VSD, and whether the morphologic features of the ventricular septum differ between hearts with and without PAB.

Our understanding is that in isolated perimembranous VSD, uniform hypertrophy is the rule irrespective of the presence or absence of PAB. Accordingly, hypertrophy of the septomarginal trabeculation offers more distance between the right surface of the septum and RBB, and thereby reduces the chance of surgical injury. This view formed the theoretical basis of our novel suturing method [1].

Why did patients who previously had PAB develop CRBBB in Sugita's series? Although recognizing the dangers of speculation, we suspect that earlier reports that demonstrated endocardial thickening in the right-sided septum of the hypertrophied ventricle and fibrous degeneration of the conduction tissue beneath the thick endocardium may answer the question [2, 3]. These reports suggest that long-standing PAB precipitates hypertrophy of the ventricular septum and septal endocardial thickening, which accelerates fibrosis and therefore velnerability of the third portion of the RBB to surgical manipulation.

We are aware that the sample size of our clinical experience is not large enough to be conclusive and concede that the issue raised by Sugita and associates deserves further investigation.

References

  1. Fukuda T., Suzuki T., Kashima I., Sato M., Morikawa Y. Shallow stitching close to the rim of the ventricular septal defect eliminates injury to the right bundle branch. Ann Thorac Surg 2002;74:550-555.[Abstract/Free Full Text]
  2. Goor D., Edwards J.E. Friction lesions of the right ventricular endocardium related to tricuspid chordae in cardiac hypertrophy. Arch Path 1969;87:100-109.
  3. Fukuda T., Hawley R.L., Edwards J.E. Lesions of conducting tissue complicating aortic valvular replacement. Chest 1976;69:605-614.[Abstract/Free Full Text]



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