Editorial Comment: How could right ventricular outflow tract stenting be made into one of the many small steps on the long road to solid evidence of rehabilitation of pulmonary arteries?

Abstract

In their contribution, Barron et al. [1] draw the conclusion that primary stenting of the right ventricular outflow tract (RVOT) facilitates staged palliation for tetralogy of Fallot in small infants and complex anatomy. The manuscript claims that improved pulmonary arterial blood flow generated by the stent leads to growth of the branch pulmonary arteries and may improve the substrate for subsequent surgical repair [1]. Such a repair is reported to be safe but requiring a transannular patch in a majority[1]. This all sounds fine, but the question can be raised, whether a correct perspective of analysis is being taken. Indeed, small children, complex anatomy or important comorbidity may need preparative treatment before corrective or further palliative treatment may be applied. In this regard, RVOT stenting may be a useful approach in selected cases with obstructed RVOT. RVOT stenting has been shown to be feasible [2–4]; it should, however, be applied based on appropriate indication and should not be used before treatment is indicated. Particularly in the introduction phase of a new approach, this would include strict inclusion criteria, sound methodology, and clear definitions of endpoints and adverse events. Unfortunately, these are missing in the manuscript. The manuscript seems to be regarding a collection of patients in whom an individual decision was made to apply a stent in the RVOT without an apparent departmental strategy in this regard. The manuscript seems to describe only a selection of patients, not the complete experience with RVOT stenting. Of the total experience, a selection of patients is described, and a selection of this selection is further presented in the manuscript with the argument of narrowing the subject down to Fallot-like physiology. However, not all of the described patients have straightforward tetralogy of Fallot. Only a minority of the patients were being treated as a neonate or were <3 kg as a measure of being small. Only a minority of the patients had complex anatomy, and only a minority had important comorbidity. The manuscript is not clear on the indication of putting in the stents or on the selection of the patients. Semi-random selection is not ruled out. No data are provided on whether or not patients had surgical palliation or correction for this indication in this time-frame. It is not clear why most of these patients had no primary surgical correction. In looking at the recruitment of the pulmonary arteries, echocardiography is not the most reliable method of diameter measurement, particularly in small-diameter vessels. Moreover, measurements were not done by independent observers. Only data within a 0.10 mm range were included, but overall data on variability are not reported. The limited number of measurements from before treatment to before surgery suggests a linear development of vessel diameter. As vessel diameter in this setting is dependant, at least in part, on flow, most of the diameter increase takes place directly after the stenting. Unfortunately, no measurements are available from this time point, while these data are available from the stent-implantation procedures. Unfortunately, this does not allow a reliable conclusion on assumed (additional) diameter increase/growth. In analysing a clinical series of patients with an intervention, a formal analysis should be reported of the predefined events. A number of patients in the manuscript were being confronted with major adverse events after stent implantation, but this is not formally analysed in a time dependent way. From a technical point of view, the removal of the stent at the time of surgical repair is an adverse issue of stenting of the RVOT. Stent removal may need to be incomplete, pulmonary valve leaflets are mostly destroyed when the stent covers the annulus as well, and longterm follow-up of the RVOT is mandatory for possible late events. Coming back to the question on how RVOT stenting could be made to one of the many small steps on the long road to solid evidence of rehabilitation of pulmonary arteries, we have to conclude that research in this regard needs thorough defining of the population and anomaly of interest. Further steps are welldefined inclusion criteria and strict definitions of endpoints and adverse events. Adequate imaging at appropriate times is essential. Correct time-related analysis should be applied. A multicentre approach would be logical. Since these aspects are not perfectly executed, the present manuscript is important in sharing the experience and in confirming the feasibility of RVOT stenting, but does not allow making a further step of putting this treatment