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Eur J Cardiothorac Surg 2004;26:1057-1058
© 2004 Elsevier Science NL
Letter to the Editor |
a Department of Surgery, Straub Clinic and Hospital, Honolulu, HI, USA
b Department of Cardiothoracic Surgery, University of Lund, Lund, Sweden
Received 17 June 2004; received in revised form 17 June 2004; accepted 27 July 2004.
* Corresponding author. Tel.: +1-808-522-3234; fax: +1-808-522-4397. (E-mail: mgrattan{at}straub.net).
The studies cited in the Letter to the Editor are indeed important contributions. However, we differ with some of the inferences Dr Fortune makes based on them. The 1988 data in the study by van Renterghem et al. were incomplete due to frequent dislodgment of the coils used to measure strain, greatly reducing the number of valid data. Their measurements of the basal segments indicated that two of three basal segments shortened during ejection. However, more recent studies of Lansac et al. used more sensitive sonometric crystals, and clearly demonstrated an expansion of all three basal segments, such that the aortic base area increased by 29.8% during systole, while the mitral annulus area contracted by 16.1% during systole due to posterior displacement of the intertrigonal area corresponding to the systolic aortic root expansion [1]. The Lansac studies show how the aortomitral apparatus functions as an anatomic unit, and for Dr Fortune to infer from the older van Renterghem study that only one pivot of an aortic valve prosthesis (which is anchored by sutures in the aortic annulus) will be subject to that aortomitral unit's forces is, we believe, unsupported by the current evidence. Normal myocardial forces occurring at the annulus level will be transfigured when a valve prosthesis is inserted, converting aortic annular anatomy from its normal semilunar contour to a more planar, rigid one.
The report by Jaggers cited in our study showed one leaflet of a SJM valve arrested following mitral valve replacement. In Table 1, we reported the consistent finding that, with increasing loads, first one leaflet bound up, followed by the second leaflet at greater loads. Thus, we are not surprised by the Jaggers report, and in fact, would expect that one leaflet would be affected more frequently than both leaflets in clinical situations of beating hearts with varying work loads and pressures.
Finally, Dr Fortune seeks to implicate adjacent tissue as the cause of the SJM valve failures reported. This is a reasonable concern. However, in both cases, we spent considerable time trying to visualize tissue that might have entrapped the leaflets from the aortic side as well as via the left atrium to view the ventricular surface of the prosthesis with a dental mirror placed through the mitral valve. Indeed, when obstructing tissue is a problem, it almost invariably involves just one leaflet of the prosthesis, not two, and the involved leaflet can usually be opened enough to note where the offending tissue resides. In both cases reported in this study, the annulus was resized after the prostheses were explanted, and proper sizing confirmed. Thus, we must dispute Dr Fortune's assertion that proper sizing makes it impossible for a valve prosthesis to malfunction. On the contrary, we believe our case reports prove the opposite to be true, and our experimental model offers an explanation as to why this is so. To this end, we are particularly concerned that SJM is now manufacturing a new valve (Regent) with even less support to its vulnerable pivot guards.
References
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