Author + information
- Robert Schueler, MD and
- Christoph Hammerstingl, MD∗ ()
- ↵∗Medizinische Klinik und Poliklinik II, Universitätsklinikum Bonn, Siegmund-Freud-Strasse 25, 53105 Bonn, Germany
We thank Drs. Rogers and Smith for their comments on our paper (1).
Drs. Rogers and Smith state that they were able to publish data from the roll-in phase of the EVEREST II (A Study of the Evalve Cardiovascular Valve Repair [MitraClip] System Endovascular Valve Edge-to-Edge Repair Study EVEREST II High Risk Registry) in 2012 reporting on markedly lower incidence rates of iatrogenic septal defect (iASD) after MitraClip use (27%) (2). This group reported a correlation of detectable iASD with cardiac remodeling (2), which was in part confirmed by our findings (1). Consequently, Drs. Rogers and Smith question the novelty of our data. Before we started our study program, we read their paper with great interest and acknowledge this early work. We want to point out that we did not deem ourselves to be the first group investigating incidence rates of iASD after percutaneous mitral valve repair. To the best of our knowledge we performed the first study in this field “with serial TEE examinations” (1).
Furthermore, several important differences between the 2 studies must be stressed, which makes a head-to-head comparison impossible.
First, Smith et al. (2) reported transthoracic echocardiographic findings, which has important limitations in this setting. Current guidelines define TEE the gold standard for the evaluation of interatrial shunt defects (3), and several studies were able to show significant differences in detectable iASD rates if determined with transthoracic echocardiographic findings or transesophageal echocardiography (TEE) (4). Second, the main focus of our research was to evaluate the correlation of iASD persistence with the treated patients’ clinical outcomes, which was not addressed by Smith et al. (2).
Third, we included nonsurgical, highest-risk patients, including 73% of subjects with functional mitral valve regurgitation, which is in contrast to Smith et al. (2) reporting on degenerative valve disease in patients suitable for MV replacement. The persistence rate of iASD and its clinical consequences might differ relevantly between high-risk heart failure patients and the early EVEREST II population (5). As we discussed in our paper (1), we agree with Smith and Rogers that the “true” significance of iASD after percutaneous mitral valve repair remains unknown. Our results— in context with available data—showed a noticeable correlation of iASD persistence with patients’ functional outcomes and survival. As we clearly stated (1), the underlying pathomechanisms for iASD persistence are not fully understood, and we emphasize the need for prospective trials addressing this topic. Currently, interventional closure of an iASD after percutaneous mitral valve repair must be planned based on a careful, individual case-by-case decision.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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