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Ann Thorac Surg 2004;78:1515
© 2004 The Society of Thoracic Surgeons


Correspondence

Cause of Degenerative Disease of the Trileaflet Aortic Valve

Zsolt L. Nagy, MD, PhD, Kevin G. Watterson, FRACS

Yorkshire Heart Centre, Calverley St, Leeds LS1 3EX, UK

kevin.watterson{at}leedsth.nhs.uk

To the Editor:

We have read with great interest the new theory of Robicsek and associates about the pathogenesis of degenerative aortic valve disease [1]. The authors designed an interesting experimental model to demonstrate that the loss of functional elasticity of the aortic wall in elderly people results in abnormal strain on normal aortic valve leaflets. In their model the aortic root was distended with a pressure of 40 mm Hg and then stiffened. However, the dilation of the native aortic root is linear in the pressure range of 0 to 120 mm Hg, as was shown in one of our previous models [2]. Therefore the diameter of the distended aortic roots at 40 mm Hg must have been smaller than the minimum diameter during the cardiac cycle (normal diastolic pressure is 80 mm Hg), which might have resulted in redundant valve leaflets. It would therefore be rather interesting to repeat the experiments with aortic roots distended with pressures of 80 to 100 mm Hg.

The authors preferred the subcoronary implantation of the pulmonary autograft to the root replacement technique. They also mentioned that despite the best surgical technique, perfect matching of the pulmonary valve leaflets with the aortic sinuses is impossible because of the anatomic differences. Previously we have extensively investigated the hydrodynamic characteristics and leaflet motion of the native aortic and pulmonary roots, as well as the pulmonary autograft, under pulmonary and systemic pressures [2, 3]. Our results showed that the pulmonary valve under low pressures has some redundant leaflet, which can compensate for the increase in root diameter under systemic pressures. Also as the pressure increases, the coaptation surface of the pulmonary leaflets is transferred to the edge of the leaflets, providing perfect valve opening and closing even at systemic pressures. Preserving the anatomic integrity of the autograft root and sinuses may result in smoother leaflet closure and less strain on the leaflets despite the increase in root diameter and the reduction of functional elasticity. We have more concerns about the occasional cases of early autograft dilation and failure than about the leaflet deformation. Currently we are trying to identify the preoperative factors responsible for early autograft dilation.

References

  1. Robicsek F, Thubrikar MJ, Fokin AA. Cause of degenerative disease of the trileaflet aortic valve: review of subject and presentation of a new theory. Ann Thorac Surg. 2002;73:1346–1354[Abstract/Free Full Text]
  2. Nagy ZL, Fisher J, Walker PG, Watterson KG. The influence of size mismatch on the hemodynamic performance of the pulmonary autograft in vitro. Eur J Cardiothorac Surg. 1999;15:294–301[Abstract/Free Full Text]
  3. Nagy ZL, Fisher J, Walker PG, Watterson KG. The in vitro hydrodynamic characteristics of the porcine pulmonary valve and root with regard to the Ross procedure. J Thorac Cardiovasc Surg. 2000;120:284–289[Abstract/Free Full Text]

Related Article

Reply
Francis Robicsek, Mano J. Thubrikar, and Alexander A. Fokin
Ann. Thorac. Surg. 2004 78: 1515. [Extract] [Full Text] [PDF]




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