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Letters to the Editor |
Department of Cardiac Surgery, Royal Brompton and Harefield NHS Trust, Harefield Hospital, Hill End Road, Harefield, Middlesex UB9 6JH, United Kingdom
Received 23 October 2008; accepted 24 October 2008.
* Corresponding author. Tel.: +44 1895828665; fax: +44 1895828666. (Email: g.dreyfus{at}rbht.nhs.uk).
Key Words: Tricuspid valve repair • Annuloplasty • Tethering • Functional tricuspid regurgitation
We are grateful to Myers et al. [1] for their appreciation of our innovative technique [2] and more importantly for providing us the opportunity to address key issues relevant to the understanding of this technique as well as the pathophysiology of functional tricuspid regurgitation (FTR).
Septal leaflet lacks a well-defined papillary muscle and is attached to the interventricular septum through chordae, each of which has its own rudimentary papillary muscle. Augmentation of septal leaflet is unlikely to achieve the desired results of elimination of residual/recurrent regurgitation as increase in surface area of the septal leaflet will be negated by its limited excursion due to lack of papillary muscle. Moreover, when tethering is present the septal shift is minimal as opposed to movement of the anterior free wall of the right ventricle (RV) that is the major contributor to this process.
Suspension of the septal leaflet free edge to the native anterior annulus or anterior annuloplasty ring is no doubt a potential strategy but unfortunately not an ideal strategy to tackle severe leaflet tethering. This is for two reasons. Firstly, this technique puts the tissues under increased tension and restricts leaflet motion. Secondly and more importantly it fails to increase the coaptation surface, which is the primary pathology in tethering. On the contrary, our technique is unique amongst existing strategies as it not only avoids these aforementioned drawbacks but also preserves the functional relationship of the tricuspid valve leaflets by ensuring coaptation not at its theoretical level but as deep as needed into the RV cavity.
We acknowledge the comment of Myers et al. [1] regarding the fate of untreated autologous pericardium in the long-term. However, we will take this opportunity to clarify that use of untreated autologous pericardium is not by choice but due to health and safety regulations in United Kingdom that prohibit use of glutaraldehyde in the work place.
As for dynamic right ventricular outflow tract obstruction (RVOTO) after the use of our technique, we will like to mention that RVOTO is impossible due to simple anatomical facts, which differentiate the right ventricle from the left ventricle. Firstly, there is a lack of continuity between the anterior leaflet of tricuspid valve and pulmonary valve annulus unlike the anterior leaflet of mitral valve and its continuity with the aortic valve annulus [3]. Secondly, the inflow tract and outflow tract in the right ventricle are distinct due to the presence of supraventricular crest unlike the left ventricle where no such distinction is present. Thus, due to these anatomical arrangements whereas dynamic left ventricular outflow tract obstruction is a recognised entity dynamic RVOTO is not a possibility.
Finally, we must emphasise that although FTR and functional mitral regurgitation (FMR) are both ventricular diseases the response of the right ventricle to loading conditions is not the same as that of the left ventricle. Hence, strategies to tackle FMR cannot be applied per se to manage FTR.
References
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