| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 2006;132:207-208
© 2006 The American Association for Thoracic Surgery
Letter to the Editor |
a Krankenanstalt Rudolfstiftung, 2. Medizinische Abteilung, Juchgasse 25, A-1030 Wien, Österreich, Germany
b Klinik für Kardiologie, Städtisches Krankenhaus Süd, Lübeck, Germany
c Krankenanstalt Rudolfstiftung, Wien, Österreich, Germany
(Email: claudia.stoellberger{at}chello.at).
With great interest we read the article by Kamohara and colleagues
1
about a novel device for left atrial appendage (LAA) occlusion. The atrial exclusion device was applied by means of thoracotomy in 8 mongrel dogs and was evaluated between 7 and 90 days by using echocardiography, left atrial angiography, histologic inspection, and gross pathology.
The main criticism regarding the study is the low number of investigated subjects and the lack of a control group. No statistical conclusions can be drawn from such a small series.
The follow-up period was extremely short regarding hemodynamic consequences of LAA occlusion, tolerability of the applied material, and mechanical stability of the device.
It would be of interest to know whether hemodynamic studies were performed during cardiac cathetherization to assess the influence of LAA occlusion on left atrial compliance and cardiac output.
2
It is known that in human subjects LAA size varies extremely and that LAAs tend to be larger in patients with atrial fibrillation than in patients with sinus rhythm.
3
Did the authors also investigate dogs with atrial fibrillation, and what was the size of the occluded LAAs?
The LAA is known as a place of natriuretic peptide secretion.
2
Were serum levels of natriuretic peptides measured during the procedure and follow-up? Did the authors observe weight gain caused by fluid retention after LAA occlusion? Did the dogs show any clinical signs of heart failure, changes in heart rate and blood pressure, and electrocardiographic changes during follow-up after LAA occlusion?
It has been shown in sheep that LAA destruction leads to reduced thirst in hypovolemia.
4
Did the authors observe a similar effect in the investigated dogs?
Were troponin and creatine kinase levels measured after the intervention? Because of the proximity of the circumflex branch of the left coronary artery to the LAA base, the coronary artery might have been affected.
Even though the occlusion rate by the atrial exclusion device seems higher than that in previously reported surgical and interventional procedures, there is still no evidence that this procedure will prevent cardiac thrombus formation outside the LAA and thus prevent stroke in atrial fibrillation. Furthermore, there is evidence that left atrial and appendage thrombi, as detected with transesophageal echocardiography (TEE), are not significant predictors for subsequent stroke or embolism.
5
Additionally, there are no studies that show convincingly that LAA occlusion with any device or surgical technique has prevented strokes.
In conclusion, the value of LAA occlusion to prevent stroke or embolism remains questionable. The LAA, however, plays an important role in regulating hemodynamics, as well as water and sodium hemostasis. As long as the physiologic function of the LAA in human subjects is not completely clarified, it remains unknown whether LAA elimination, by whatever means, is beneficial or harmful.
 |
References |
|---|
 Top References |
|---|
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
