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Ann Thorac Surg 1999;67:300
© 1999 The Society of Thoracic Surgeons


Correspondence

Reply

Michael D. Black, MDa

a Department of Cardiac Surgery, Lucile Packard Children’s Hospital, Stanford University School of Medicine, Stanford, CA 94305-5407 USA

To the Editor

We previously hypothesized, as others, that nodular truncal valve thickening and fibrosis might be the result rather than the cause of chronic valvular regurgitation. We assumed that over time it might be possible that progressive remodeling of the dysmorphic truncal valve may take place with the eventual delay in truncal valve replacement [1]. We unfortunately lack both critical intermediate and long-term follow-up substantiating neonatal truncal valvuloplasty as a superior method of palliation for severe truncal valve regurgitation. Doctors Komai and Naito thus provide an important piece of the puzzle for the ongoing endorsement of neonatal truncal valvuloplasty [2].

Despite advances in the surgical repair of those afflicted with a common arterial trunk, truncal valve regurgitation remains a challenging lesion. Alternatives to truncal valve repair (ie, allograft or mechanical prosthesis implantation) are fraught with excessive mortality rates. In the latter subgroup the 12-month mortality rate continues to remain exorbitant. Stabilization of the actuarial survival curve beyond 1 year after operation suggests that "the 1-year survival may be a more precise and appropriate indicator of successful repair" [3]. Thus, if truncal valve replacement can be avoided or at least delayed past the first year, the neonatal and overall survival must improve.

From our limited experience, we believe that the probability of successful truncal valvuloplasty remains intimately related to the morphology of the valve, ie, the number of valve leaflets. Thickening and unequal size of valve cusps are recurring characteristics of incompetent truncal valves. Successful truncal valvuloplasty is most likely to occur with quadracuspid valves, because successful conversion to a trileaflet valve is possible without significant postoperative stenosis unlike the reciprocal conversion for instance of a trileaflet to a bicuspid valve. Furthermore, quadracuspid valves are more likely to be initially dysplastic and thus have the greatest incidence of significant preoperative regurgitation, ie, they are the valves that require repair [1].

Our fifth and most recent truncal valvuloplasty success, a 2.3-kg neonate diagnosed with truncus arteriosus, interrupted aortic arch, and severe truncal valve regurgitation is illustrated in Figure 1. Note the similarity of reparative strategies to those depicted by Komai and Naito [2]. Their patient, although recently deceased, provides indispensable necropsy information. Even though preliminary, truncal valve repair holds much promise for those neonates afflicted with severe truncal valve regurgitation.



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Fig 1. (A) View of a quadracuspid truncal valve through a 4-mm 0° cardioscope. Note the lack of central coaptation of the poorly formed gelatinous and dysplastic truncal leaflets. (B) View of the same valve after resuspension of two of the commissures, annuloplasty, and conversion of the quadracuspid truncal valve into a trileaflet structure.

 
References

  1. Black M.D., Adatia I., Freedom R.M. Truncal valve repair: initial experience in neonates. Ann Thorac Surg 1998;65:1737-1740.[Abstract/Free Full Text]
  2. Komai H., Naito Y. Truncal valve repair in the neonate: fate of the valve. Ann Thorac Surg 1999;67:299.[Free Full Text]
  3. McElhinney D.B., et al. Trends in the management of truncal valve insufficiency. Ann Thorac Surg 1998;65:517-524.[Abstract/Free Full Text]

Related Article

Truncal valve repair in the neonate: fate of the valve
Hiroyoshi Komai and Yasuaki Naito
Ann. Thorac. Surg. 1999 67: 299. [Extract] [Full Text] [PDF]




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