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We read with great interest and surprise the article published by Therrien et al. in the November issue of the Journal(1). These results are extremely disappointing. All the physicians familiar with the treatment of patients with repaired tetralogy of Fallot share the idea that one should not wait too long before implanting a valve in the right ventricular outflow tract of patients presenting with dilated right ventricle. Extremely dilated right ventricles might not benefit from valvulation as much as moderately dilated ones. However, it is extremely surprising that all patients operated on in a major center like Toronto showed neither clinical improvement nor regression of ventricular volumes after reoperation.
Although their patients were operated on quite late, we wonder whether their unexpectedly bad results might not be related to another reason than the delay for reoperation. The Toronto team has the peculiarity of implanting bioprosthetic material in the right ventricular outflow tract of these patients. Almost all patients received a stented bioprosthesis varying in size between 25 and 33 mm in diameter. It is noteworthy that true diameters of the outer rings are even larger than these measurements. The only way to implant these rather bulky bioprostheses at the level of the pulmonary annulus is to cover them with a patch extending from the main pulmonary artery to the infundibulum of the right ventricle. The immediate effect of this patching is to further increase the size of the right ventricular cavity, which may at least partly explain the fact that no decrease was observed in end-systolic and end-diastolic volumes of these patients after reoperation. We have recently shown that pulmonary insufficiency might not be the leading factor causing right ventricular dilation after repair of tetralogy of Fallot, and we suspect that the contractile function of the pulmonary infundibulum may play a role in the preservation of right ventricular function (2). Adding a patch to this already weakened area might further contribute to the deterioration of this function.
Like others, we believe that homografts are the ideal valve substitute for the right ventricular outflow tract because they offer a better effective orifice area, and they do not necessitate a patch enlargement. Although 40% of the patients presented in this series had an aneurysm resection, it is not clear whether the researchers believe that they effectively reduced right ventricular size at the time of the procedure.
In conclusion, we wonder whether the extremely poor results presented by Therrien et al. (1)might not be at least partially explained by their surgical technique rather than by the delay in the reoperation. The insertion of a patch in the already dilated area of the pulmonary infundibulum might further impede right ventricular function and as such increase rather than decrease right ventricular volumes.
- American College of Cardiology