Author + information
- Birke Schneider, MD* (, )
- Josef Finsterer, MD and
- Claudia Stöllberger, MD
- ↵*Klinik für Kardiologie, Sana Kliniken Lübeck, Kronsforder Allee 71/73, D-23560 Lübeck, Germany
With great interest we read the study by Hanna et al. (1) on left atrial (LA) structure and function after percutaneous left atrial appendage transcatheter occlusion (PLAATO). In 11 patients, adequate seal of the left atrial appendage (LAA) is reported without affecting LA function or the left upper pulmonary vein. The PLAATO had first been performed in 25 dogs in sinus rhythm. This study by Nakai et al. (2) has been the scientific basis for implanting the device in humans (1,3,4). Although this technique appears very attractive, there are several points of criticism concerning study design, data collection, and interpretation of the results.
1. The LA diameter is reported only at baseline. Furthermore, peak mitral E-wave velocity and diameter, peak systolic, and diastolic velocities of the left upper pulmonary vein were not registered in every patient at baseline, 1, and 6 months. Overall, only 3 of the 11 patients (cases 1, 2, and 5) had all measurements completed. Thus, conclusions based on fragmentary data in this small patient population are limited.
2. Concerning the importance of the LAA as a hormone-releasing site, the study lacks information about levels of natriuretic peptides before and after PLAATO.
3. The investigators state that PLAATO does not interfere with LA function because there was no significant change in transmitral or pulmonary venous flow. However, no LA pressure measurements are reported. Because LAA occlusion may result in reduced atrial compliance, data on LA diameter and volume during follow-up would be of interest.
4. Hanna et al. conclude that the PLAATO device does not result in any detrimental anatomic or physiologic changes to adjacent structures. Besides left upper pulmonary vein and mitral valve, however, the circumflex branch of the left coronary artery lies adjacent to the LAA base. Therefore, information on the development of anginal chest pain after PLAATO is of importance.
5. The finding of minimal flow around the PLAATO device in every patient immediately after implantation and at follow-up is in contrast to complete LAA occlusion found at necropsy in dogs of the initial study by Nakai et al. (2). In that study, stability of the device and completeness of LAA occlusion was assessed in formalin-fixed hearts. Formalin fixation, however, results in tissue-shrinkage (5). Thus, complete LAA closure and device stability may have been due to an artificial decrease of the LAA size. Moreover, the mode of conservation may explain the discrepancy between complete LAA occlusion in all dogs at the postmortem study and the small leaks around the device in living dogs immediately after the procedure and during follow-up.
6. Residual flow around the PLAATO device does not preclude thrombus formation in the LAA. However, residual leaks in case of thrombosis may be a new potential mechanism for embolic events as in patients with incomplete surgical LAA ligation (6). Therefore, it would be of great interest whether patients with residual leaks experienced embolic events during follow-up.
Before recommending PLAATO as a therapeutic option in atrial fibrillation patients, more evidence about the long-term effects of this procedure is required.
- American College of Cardiology Foundation
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