To the Editor,
We have read with great interest the study published by León et al.,1 in which the authors report the reduction in paravalvular regurgitations and in left ventricular hypertrophy, according to echocardiography, one month after percutaneous implantation of the CoreValve prosthesis in a group of 22 patients. The former effect is attributed to the self-expandability of the prosthesis and the latter to its excellent hemodynamic profile.
We would like to make a few observations on the basis of our own experience. In our center, between April 2008 and December 2010, 144 prostheses were implanted in patients with severe aortic valve disease—mean age, 79.6±6 years; logistic EuroSCORE, 20±14%—who underwent Doppler echocardiography prior to implantation, on the third day and 6 and 12 months postimplantation. After a mean follow-up of 11.6±8 months, we could confirm the excellent hemodynamic profile of the prosthesis, with peak and mean gradients of 15.9±6mmHg and 8.8±4mmHg, respectively, as well as an improvement in the ejection fraction (from 62±14% to 67±10%; P=.01), which was detected in the majority of the patients with dysfunction prior to implantation. There was also an improvement in the functional class and quality of life questionnaires.
However, during follow-up we have not observed a significant reduction in paravalvular regurgitations (moderate in 23.4%, mild or trivial in 39.7% and absent in 36.9% on the third day after implantation versus moderate in 18.9%, mild or trivial in 46.8% and absent in 34.2% in the sixth month), with good agreement (κ=0.724).
These data are similar to those published in other series,2, 3 and we should point out the fact that in no case did the regurgitation affect hemolysis and that, in our series, it was not related to functional class or medium-term mortality. Its presence in trivial or mild cases could be considered to be of no greater clinical importance than the so-called “physiological” regurgitations observed in mechanical prostheses. In contrast, in a recently published multicenter study,4 moderate or higher grade regurgitation has been found to be a predictor of mortality between 30 days and 1 year after the procedure.
These paravalvular regurgitations could develop because of a poor choice of the prosthesis size, insufficient expansion of the prosthesis, too low a placement site or perhaps a nonuniform distribution of the valve calcium when, upon expansion of the prosthesis, it remains pressed between the device and the aortic wall. If the late reduction in aortic regurgitation observed in the series of León et al., can be attributed to the adaptability and self-expandability of the prosthesis, it should also be detected in the other series. These differences could be due to the bias associated with the selection of a small cohort or to other mechanisms related to patient characteristics or to postimplantation treatment. The formation of a periprosthetic thrombus or intimal proliferation may have sealed small periprosthetic leaks in the series of León et al., and the difference with respect to other series could lie in the postimplantation treatment. It will be interesting to follow the course of these patients in case a hypothetical leak-sealing intimal proliferation should lead to the development of pannus and an increase in the transprosthetic gradient.
On the other hand, assessment of the changes in left ventricle following implantation in our patients revealed an improvement in the ejection fraction, especially in cases of nonischemic ventricular dysfunction, but there was no evidence of a significant reduction in hypertrophy during follow-up (the interventricular septal thickness decreased from 13.2±2mm to 12.4±2mm, P=.3; and that of posterior wall from 12.5±2mm to 12.2±2mm, P=.78). These findings coincide with those reported by De Jaegere et al.,3 who detected no differences in left ventricular mass or diastolic function 30 days after implantation, and are in accordance with the fact that these are cases of nonphysiological hypertrophy (in contrast to that observed in athletes), secondary to a chronic pressure overload (aortic stenosis, sometimes accompanied by hypertension) with varying degrees of fibrosis and, thus, with slow and limited reversibility. This circumstance, however, does not appear to impede the short-term and medium-term improvement in functional class in these patients.
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Corresponding author: irodriguezbailon@gmail.com