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J Am Coll Cardiol, 2005; 45:635, doi:10.1016/j.jacc.2004.11.020
© 2005 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTERS TO THE EDITOR

Effects of percutaneous left atrial appendage transcatheter occlusion (PLAATO) on left atrial structure and function: Reply

Ibrahim R. Hanna, MD and Peter C. Block, MD*

* Department of Cardiology, Emory University Hospital, F606, 1364 Clifton Road, Atlanta, GA 30322 (Email: Peter_block{at}emoryhealthcare.org).


We thank Dr. Schneider and colleagues for their interest in our study evaluating the effect of percutaneous left atrial appendage transcatheter occlusion (PLAATO) on left atrial (LA) structure and function (1). They list "several points of criticism" deserving of comment.

Our study population is part of the cohort of patients in the PLAATO feasibility trial. The report was based on all but one of the U.S. patients who had completed six-month follow-up. Measurements were available on a majority of patients (>70% at six months) (1). Data analysis showed no statistically significant change in pulmonary venous flow or diastolic transmitral flow following PLAATO. As described in our methods, LA size was carefully measured at each time point. Though not included in the final report, no significant change occurred compared to baseline.

Interesting endocrine functions of the left atrial appendage (LAA) have been detailed by Stöllberger et al. (2). Human data on atrial appendectomy are limited. To our knowledge no data suggest detrimental clinical effects of LAA occlusion attributable to a decrease in atrial natriuretic peptide. Yoshihara and colleagues have indicated that exclusion of the LAA without exclusion of the right atrial appendage has even less effect (3,4). Data concerning endocrine LAA function were not part of the PLAATO trial and remains an interesting area for research.

The circumflex coronary artery is variable in its relation to the LAA. The artery runs in the atrioventricular groove and is separated from the base of the LAA by atrial tissue. Oversizing of an occlusion device could theoretically result in arterial compression. We used careful angiographic and echocardiographic sizing. This and postimplant residual flow around PLAATO make compromise of circumflex flow unlikely. Clinical data so far support this.

Finally, Dr. Schneider and colleagues re-emphasize the point that we made in our Discussion section. The impact of minimal residual flow around the device on the occurrence of stroke has to be assessed when the clinical follow-up is reported.

The aim of our study was to show no detrimental effect of PLAATO on pulmonary vein flow and diastolic transmitral flow in our patient population. Clinical follow-up data will be reported for the entire PLAATO cohort. We agree that long-term data will help answer many questions about the efficacy of PLAATO, but we believe that percutaneous LAA occlusion will offer an important option for selected patients with atrial fibrillation.


    References
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 References
 
1. Hanna IR, Kolm P, Martin R, et al. Left atrial structure and function after percutaneous left atrial appendage transcatheter occlusion (PLAATO) J Am Coll Cardiol 2004;43:1868-1872.[Abstract/Free Full Text]

2. Stöllberger C, Schneider B, Finsterer J. Elimination of the left atrial appendage to prevent stroke or embolism? Anatomic, physiologic, and pathophysiologic considerations Chest 2003;124:2356-2362.[Abstract/Free Full Text]

3. Yoshihara F, Nishikimi T, Kosakai Y, et al. Atrial natriuretic peptide secretion and body fluid balance after bilateral atrial appendectomy by the Maze procedure J Thorac Cardiovasc Surg 1998;116:213-219.[Abstract/Free Full Text]

4. Yoshihara F, Nishikimi T, Sasako Y, et al. Preservation of the right atrial appendage improves reduced plasma atrial natriuretic peptide levels after the Maze procedure J Thorac Cardiovasc Surg 2000;119:790-794.[Abstract/Free Full Text]


Related Article

Effects of percutaneous left atrial appendage transcatheter occlusion (PLAATO) on left atrial structure and function
Birke Schneider, Josef Finsterer, and Claudia Stöllberger
J. Am. Coll. Cardiol. 2005 45: 634-635. [Full Text] [PDF]




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