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J Thorac Cardiovasc Surg 2006;132:340-346
© 2006 The American Association for Thoracic Surgery

Evolving Technology

Evaluation of a novel device for left atrial appendage exclusion: The second-generation atrial exclusion device

Keiji Kamohara, MD a , Kiyotaka Fukamachi, MD, PhD a , * , Yoshio Ootaki, MD, PhD a , Masatoshi Akiyama, MD, PhD a , Faruk Cingoz, MD a , Chiyo Ootaki, MD a , D. Geoffrey Vince, PhD a , Zoran B. Popovic, MD b , Michael W. Kopcak, Jr, BA a , Raymond Dessoffy, AA a , Jenny Liu, BA a , A. Marc Gillinov, MD c

a Department of Biomedical Engineering, Lerner Research Institute, the Cleveland Clinic, Cleveland, Ohio
b Department of Cardiology, the Cleveland Clinic, Cleveland, Ohio
c Department of Thoracic and Cardiovascular Surgery, the Cleveland Clinic, Cleveland, Ohio

Received for publication March 13, 2006; revisions received April 13, 2006; accepted for publication April 18, 2006.

* Address for reprints: Kiyotaka Fukamachi, MD, PhD, Department of Biomedical Engineering/ND20, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195 (Email: fukamak{at}ccf.org).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Discussion
 Conclusions
 References
 
BACKGROUND: The left atrial appendage is a frequent source of thromboemboli in patients with atrial fibrillation. Exclusion of the left atrial appendage may reduce the risk of stroke in patients with atrial fibrillation. The atrial exclusion device, previously developed to perform left atrial appendage exclusion on a beating heart, was modified to accommodate different anatomic patterns of the human left atrial appendage and to ensure uniform pressure and occlusion. The purpose of this study was to evaluate this second-generation atrial exclusion device during a midterm period in a canine model.

METHODS: Ten mongrel dogs (mean weight 28.9 ± 4.6 kg) were used in this study. The atrial exclusion device, constructed from two parallel and rigid titanium tubes and two nitinol springs with a knit-braided polyester fabric, was implanted at the base of the left atrial appendage through a left thoracotomy on a beating heart using a specially designed delivery tool. Dogs were evaluated at 30 days (n = 4) and 90 days (n = 6) by epicardial echocardiography, left atrial and coronary angiography, gross pathology, and histologic inspection.

RESULTS: Device implantation was performed without complications in all dogs. Complete left atrial appendage exclusion without device migration or hemodynamic instability was confirmed, and there was no damage to the left circumflex artery or pulmonary artery. Macroscopic and microscopic assessments revealed favorable biocompatibility during midterm follow-up.

CONCLUSION: The atrial exclusion device enabled rapid, reliable, and safe exclusion of the left atrial appendage. Clinical application may provide a new therapeutic option for reducing the risk of stroke in patients with atrial fibrillation.

Abbreviations and Acronyms AED = atrial exclusion device; AF = atrial fibrillation; 2DEE = 2-dimensional epicardial echocardiography; EDV = end-diastolic volume; ESV = end-systolic volume; LA = left atrial; LAA = left atrial appendage; LCX = left circumflex artery; PA = pulmonary artery


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Discussion
 Conclusions
 References
 
The left atrial appendage (LAA) is a frequent source of thromboemboli in patients with atrial fibrillation (AF), contributing to a 5-fold increase of stroke risk in patients with AF. 1 Go In previous reports, approximately 60% and 91% of left atrial (LA) thrombi occurred in the LAA in rheumatic AF and nonrheumatic AF, respectively. 2,3 Go However, considering that nonrheumatic AF is now more common than rheumatic AF and that compliance with guidelines for anticoagulation therapy for AF is suboptimal, there is interest in investigating the role of LAA exclusion as a therapeutic alternative for reducing stroke risk in AF patients. 4,5 Go Several novel techniques for LAA exclusion using thoracoscopic and percutaneous approaches have been reported. 6-10 Go

A novel device, the atrial exclusion device (AED), has been developed for epicardial LAA exclusion on a beating heart. In a previous study, 11 Go the first-generation AED (first AED) was evaluated, and the validity of the AED concept was confirmed. Subsequently, a second-generation AED was developed with design modifications optimized to ensure uniform compression and occlusion of the anatomically variable human LAA. The purpose of this preclinical study was to determine the safety and effectiveness of the second-generation AED (second AED).


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Discussion
 Conclusions
 References
 
Design of the Second AED
The second AED is designed as a self-compensating force distribution clamp, in contrast to the bi-staple clamp design of the first AED. 11 Go The skeleton of the AED is composed of two parallel, curved, rigid titanium tubes and two nitinol springs with a 90° angle at both ends of the titanium tubes (Figure 1, A). The rigid titanium tubes are covered with both a urethane elastomer and a knit-braided polyester sheath (Figure 1, B). These refinements provide the following characteristics: (1) suitable contour to match the LAA anatomy; (2) evenly distributed clamping pressure; (3) rapid promotion of tissue ingrowth to securely anchor the device and prevent damage to surrounding structures, such as the left circumflex artery (LCX) and the pulmonary artery (PA); and (4) circular contour of both ends of the device to minimize contact with the PA. There are two different sizes of the second AED (35 mm and 50 mm in length) to accommodate variability in the patient's LAA orifice size. It is envisioned that intermediate sizes would be made available to allow optimal clip to anatomy relationship.


Figure 1
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  		Figure 1. The second-generation atrial exclusion device (AED) and the specially designed delivery tool. A, The skeleton of the AED, in the closed position, is composed of two titanium rigid tubes and two nitinol springs with a 90° angle at each end of the tubes. B, The AED with a polyester fabric in the open position. The titanium tubes are covered with both a urethane elastomer and a knit-braided polyester sheath. C, The delivery tool has long arms that allow device application to a distant anatomic structure.

 
Figure 1, C shows a specially designed delivery tool with long arms that facilitates device application. The tool has two configurations: open, in which the distance between the members of the attached AED is the greatest (Figure 1, B), and closed, in which the AED is manipulated into a closed position. With the tool in the open position, the AED is placed over the LAA and positioned at its base by closing the delivery tool. If the AED is deployed and the position on the LAA is judged to be suboptimal, the device can be repositioned and reapplied by reattaching the delivery tool to the implanted AED.

Animal Study
A total of 10 mongrel dogs, weighing 28.9 ± 4.6 kg, were used in this study. This study was approved by the Cleveland Clinic's Institutional Animal Care and Use Committee, and all animals received humane care in compliance with the "Guide for the Care and Use of Laboratory Animals" prepared by the Institute of Laboratory Animal Resources, National Research Council, and published by the National Academy Press, revised 1996.

Implant and explant studies
The surgical procedures in the implant and explant studies were similar to the previously reported series of animal study with the exception of the device implant technique.11 In brief, the dogs were placed in the right lateral position with electrocardiogram leads attached under general anesthesia. The left carotid artery was cannulated for continuous monitoring of systemic arterial pressure. After a thoracotomy in the left fourth intercostal space, the pericardium was opened to expose the LAA. A 14-gauge angiocatheter was inserted into the left pulmonary vein to monitor the LA pressure and perform LA angiography. A 35-mm AED was chosen for implantation in 8 animals because of the LAA orifice size in those dogs. In the remaining 2 dogs, an oversized device, a 50-mm AED, was intentionally used to assess the impact of implanting an oversized device. The AED was placed over the end of the LAA and aligned with the base of the LAA using the delivery tool (Figure 2, A). Once in the desired position, the AED was released by gently closing the delivery tool.


Figure 2
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  		Figure 2. Representative intraoperative views at implantation. A, The AED can be precisely positioned and then implanted using the delivery tool. B, The AED was implanted at the base of the LAA. The cranial end of the device was located underneath the main PA. *, LAA, Left atrial appendage; AED, second-generation atrial exclusion device; PA, pulmonary artery; LAD, left anterior descending artery; OM, obtuse marginal artery; LV, left ventricle.

 
In addition to hemodynamic parameters, 2-dimensional epicardial echocardiography (2DEE), Doppler echocardiography, and LA angiography in the 60° left anterior oblique and 30° right anterior oblique planes were performed. The LA area was measured by planimetry in the apical 4-chamber view. The LA volume was also assessed by a biplane area-length method from the apical 4- and 2-chamber views. The left ventricular end-diastolic (EDV) and end-systolic volumes (ESV) were measured by the single-plane Simpson rule. Left ventricular ejection fraction was calculated by the equation 100 x (EDV – ESV)/EDV. The left ventricular stroke volume was calculated as the difference of EDV and ESV. Data acquisition was performed as described in our previous report. 11 Go The chest was closed with a chest tube in place. Eight dogs with a 35-mm device were followed up for 30 days (n = 2) and 90 days (n = 6). Two dogs with a 50-mm device were followed up for 30 days.

On the day of the explant study, the pericardium was reopened to expose the implanted AED. Hemodynamic assessment, LA angiography, 2DEE, and Doppler echocardiography were performed in the same manner as at the implant study. Furthermore, in all 90-day dogs, left coronary angiography was conducted to evaluate LCX blood flow in the left anterior oblique 60° and right anterior oblique 30° planes.

To evaluate electrical isolation between the LAA (distal to the AED) and LA body (proximal to the AED), we applied electrical stimulation to two different locations at a pacing rate greater than the native rate during sinus rhythm in three 30-day and four 90-day dogs. Standard epicardial pacing wires were placed on the LA body and LAA remnant. LA body pacing was performed in asynchronous mode to confirm that the heart could be paced. Electrical stimulation at a maximum current of 20 mA was applied to the LAA in the same manner as during LA body pacing. When the LAA pacing was not accomplished at 20 mA, it was determined that the distal LAA was completely electrically isolated. However, when LAA pacing was accomplished at 20 mA, the pacing threshold of the LAA was measured with a stepwise decrease of the pacing current. If the LA body pacing could be established at less than half of the LAA pacing threshold, it was concluded that the LAA was partially electrically isolated.

Gross necropsy and histologic evaluation
After full heparinization, the dogs were humanely killed by rapid intravenous injection of sodium pentobarbital and potassium chloride. The heart was examined to confirm LAA exclusion and to determine tissue response to the polyester fabrics for gross biocompatibility evaluation.

Tissue specimens of the cross section of the entire LAA, including the polyester fabric and a small part of the LA body (adjacent to the orifice of the LAA), were excised and evaluated. The tissues were fixed in 10% formalin for 48 hours and embedded in paraffin. Sections were cut from each block at 4 µm and collected onto glass slides. All sections were then dried for 60 minutes at 60°C and stained with hematoxylin and eosin.

Data Analysis
All values were expressed as mean ± standard deviation. Repeated-measures analysis of variance was used to assess the differences between data at baseline, pre-implantation, and follow-up.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Discussion
 Conclusions
 References
 
Implantation
The AED was implanted on a beating heart in all dogs without any complications or hemodynamic instability. The time required for initial AED application was approximately 15 seconds once the LAA was exposed. Only 1 dog required reapplication. The AED was precisely placed at the base of the LAA without causing acute damage to surrounding structures, such as the LA body, LCX, and PA (Figure 2, B). In the 2 dogs that received an oversized 50-mm AED, no acute compression of the PA was found even though the edge of the device was positioned in direct contact with the main PA. Post-implant 2DEE, Doppler echocardiography, and LA angiography revealed no communication between the LAA and LA body and absence of blood flow in the LAA. All animals survived the procedure without device-related complications and had uneventful postoperative recovery periods.

Explantation
At explantation, the AED remained positioned at the base of the LAA with no evidence of migration. Structures adjacent to the device, such as the LA body, LCX, and PA, were intact without erosion. The LAA in the 30-day dogs was moderately atrophied. All 6 of the 90-day dogs had dense adhesions surrounding the AED with marked atrophy of the LAA. With respect to the 2 dogs with a 50-mm device, there were no adverse effects on the main PA; we observed neither PA erosion nor compression. Before explantation, Doppler echocardiography and LA angiography confirmed lack of communication between the LAA and LA in all dogs. In addition, coronary angiography in all 90-day dogs demonstrated normal LCX anatomy with no apparent obstruction to blood flow (Figure 3, A and B). Hemodynamic data are summarized in Table 1. There were no statistical changes in hemodynamics throughout the studies. With respect to the LA size, no difference in the LA area (measured in all animals) or LA volume (measured in 6 animals due to unsatisfactory image resolution) was found, which may indicate no device migration. In addition, there were no significant differences in the 2DEE parameters such as EDV, ESV, stroke volume, and ejection fraction. In the three 30-day and four 90-day dogs that were subjected to pacing assessment, either total (n = 4) or partial (n = 3) electrical isolation of the LAA remnant was confirmed.


Figure 3
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  		Figure 3. Representative angiographic findings of the LCX at explantation. A and B, No adverse effects of the implanted AED on the LCX (dotted arrows) were found in LAO 60° or RAO 30° planes. AED, Second-generation atrial exclusion device; LCX, left circumflex artery; LAO, left anterior oblique; RAO, right anterior oblique.

 

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  		TABLE 1. Case information
 
Gross and Histologic Examinations
All dogs had tissue ingrowth that completely covered the entire AED. Examination of the inside of the LA revealed a smooth endocardial surface at the origin of the LAA with no cul-de-sac formation and no evidence of thrombus associated with the AED (Figure 4, A). In the cross section of the occlusion site at 30 and 90 days, the LAA walls underneath the AED were firmly adherent to each other. As illustrated in Figure 4, B (small arrows), the occlusion site was clean and smooth. The internal cavity of the excluded and atrophied LAA was occupied by a well-organized thrombus or dense connective tissue, resulting in elimination of the LAA lumen. The great cardiac vein and LCX were intact without any thrombus formation (Figure 4, B, dotted arrows). In the 2 dogs with an oversized 50-mm AED, the intimal surface where the cranial end of the device was located was inspected, and no damage to the PA intima was observed.


Figure 4
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  		Figure 4. Gross anatomic views of the internal surface of the LAA orifice and the cross section of the occlusion site at 90 days. A, The arrows indicate a smooth, clear, and linear occlusion site. No cul-de-sac formation was found. B, The occlusion line was fully covered with one layer of tissue ingrowth (small arrows). The LAA walls underneath both fabrics were very thin and were firmly adherent to each other. The distal LAA was atrophied, and its lumen was occupied with white connective tissue. The large and small dotted arrows indicate the cross sections of the great cardiac vein and left circumflex artery, respectively. There was no intraluminal thrombus in both vessels. LAA, Left atrial appendage; LA, left atrium; LV, left ventricle.

 
Hematoxylin-and-eosin–stained vertical sections of the entire LAA including the distal LAA, LAA walls at the occlusion site, the polyester fabric with tissue ingrowth, and LA body were inspected. The distal LAA tissues taken from moderately atrophied LAA (30-day dogs) showed myocardium with fatty infiltration, whereas the myocardial tissues from markedly atrophied LAA (90-day dogs) were replaced by fibrous tissue. Figure 5 shows the histologic findings of the cross section of Figure 4, B. There was one layer of endothelium-like cells and underlying layers of connective tissue that expanded on the endocardial surface of the occlusion site (Figure 5, A and C). The polyester fabric was covered by fibrous connective tissue with fibroblast infiltration in 30- and 90-day dogs (Figure 5, B). The LAA walls underneath the AED were replaced by fibrous tissue. The cross section of PA tissue taken from the site where the cranial end of the 50-mm device contacted the PA adventitia revealed no histologic abnormalities.


Figure 5
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  		Figure 5. Histologic findings of the cross section of the occlusion site at 90 days. A, The endocardial surface of the occlusion site was covered with endothelium-like cells without producing irregularity on the endocardial surface (magnification x 20). B, The fibrous connective tissue with fibroblast infiltration was found between both fabrics and around the fabrics (magnification x 200). C, A neoendothelial layer and underlying layers of connective tissue expanding on the endocardial surface of the occlusion site were found (magnification x 200). *, Left atrial musculature; LA, left atrium; LAA, left atrial appendage; LV, left ventricle; LCX, left circumflex artery.

 

   Discussion
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Discussion
Conclusions
 References
 
The second AED completely excluded the LAA from the systemic circulation and did not migrate or cause damage to adjacent cardiac structures at 30- and 90-day follow-up. No changes in the parameters related to LV volume, such as EDV, ESV, stroke volume, and ejection fraction, were found at follow-up. Macroscopic and microscopic assessments also revealed favorable biocompatibility. In addition, the AED provided partial or total electrical isolation of the LAA in 7 of 7 cases.

AF is epidemiologically the most common cardiac arrhythmia, and its prevalence increases in both genders after 40 years and rises rapidly after 65 years. 1,12 Go Although recent randomized trials have demonstrated that anticoagulation can greatly reduce the stroke rate in patients with AF, 13,14 Go many physicians remain reluctant to prescribe anticoagulant therapy for elderly AF patients because of an increased risk of anticoagulant-related complications with age, the difficulty of warfarin management, and personal preference. 4,5,15 Go

A potential alternative or adjunctive approach to stroke prevention in AF patients is surgical exclusion of the LAA. Various techniques for LAA exclusion either from the exterior of the heart or from inside the LA during cardiac surgery have been introduced; however, several potential disadvantages such as bleeding and late recanalization exist. 16-19 Go Although an epicardial approach to LAA exclusion has the potential advantages of simplicity (no transseptal puncture) and low procedural risk of embolism (no left heart endocardial catheters), there is currently no instrumentation available to facilitate rapid, reliable, and safe epicardial exclusion of the LAA.

This novel device, the AED, has application for epicardial LAA exclusion. The benefit of this type of occlusion device is the simplicity of device application on a beating heart. In our previous preclinical study, we confirmed LAA exclusion in a canine model, validating the AED concept. 11 Go However, we had concluded that refinement of device design would provide improved clinical application. Because there are many anatomic patterns of the LAA (ie, shape, size, and thickness) in humans, a distributed clamping pressure distribution across the width of the device was required so that the device adapts to accommodate the variability of LAA anatomy. Therefore, a design modification of the first AED was made without eliminating the advantages of the AED (namely, the easy device application and reapplication and favorable biocompatibility) resulting in the development of a self-compensating force distribution concept, the second AED. In addition, since a self-compensating force distribution requires physical force to be opened for application, a specially designed delivery tool was also developed to precisely position and apply the second AED on the LAA. This delivery tool permits easy device repositioning and reapplication if initial placement is unsatisfactory.

Thrombus formation on a cul-de-sac or occlusion line formed by the device application at the origin of the LAA is considered one of the most potential and important complications in the chronic phase. In this study, the AED was easily and precisely placed at the base of the LAA, and the resulting occlusion line was smooth and linear without any endocardial furrow or cul-de-sac formation (Figure 5, A). In addition, histologic examination revealed that the endocardial surface of the occlusion site was covered with endothelium-like cells without producing irregularity on the endocardial surface. These findings suggest that the thrombus formation on the occlusion line may be unlikely to occur even in patients with AF. LA and coronary angiography and echocardiography confirmed complete exclusion of the LAA at 30 and 90 days without device migration or damage to the PA, LCX, or other adjacent cardiac structures. As illustrated in Figure 2, B, the cranial end of the second AED was located underneath the main PA without compressing the PA; this lack of compression is attributed to the unique configuration of the 90° nitinol springs at either end of the titanium tubes. The design and physical characteristics of the AED and tissue ingrowth around the polyester covering prevented device migration and damage to adjacent cardiac structures.

Compared with epicardial stapling devices, 18,19 Go the AED offers two advantages: (1) easy reapplication and (2) elimination of the risk of bleeding that may occur along or beneath the staple line. Other occlusion devices currently available, such as a surgical stapler or clip applier, permanently deform the occlusion apparatus, thereby delivering a permanent implant. The promotion of distal LAA atrophy by the AED may eliminate the possibility of late recanalization of the LAA lumen, one of the potential problems of noncutting stapling devices. 16,17 Go

Although not assessed specifically in this study, the specially designed delivery tool may enable a minimally invasive thoracoscopic approach for LAA exclusion in lone AF patients, providing a possible therapy for stroke prevention. In addition, several reports have indicated that the LAA may be one source of thrombus in patients in sinus rhythm with congestive heart failure. 20,21 Go The AED and its delivery tool may be beneficial for these high-risk patients in sinus rhythm to prevent embolic events resulting from LAA thrombi. However, it is likely that in patients with LAA thrombi that extend to the orifice of the LAA, epicardial approaches should be avoided.

There are limitations to this preclinical study. The study series was small (n = 10), and the follow-up duration was only a maximum of 90 days. In addition, the application of a normal canine model in this study provided us with idealized implant situations (ie, narrow LAA base, absence of increased LA wall tension or pressure resulting from LA enlargement, absence of LAA fragility caused by advanced age, malnutrition, or other etiology). It is possible that there may be device failures and/or complications of deployment with longer follow-up or with application in patients who do not have tissues as resilient as those of a healthy dog. Furthermore, the possibility of LA thrombus formation after AED application in an AF setting cannot be excluded in this study. Although a very smooth and linear endocardial surface of the occlusion line was found with no cul-de-sac formation in this study, this finding does not alone indicate that the AED can completely eliminate the risk of thrombus formation on the occlusion line in the long-term phase. Therefore, future evaluations using an AF animal model may be required to confirm the long-term stability, durability, and biocompatibility of the device as well as the existence of thrombus formation.

Although LAA exclusion may cause potential adverse effects because of reduced production of serum natriuretic peptide, 22,23 Go we did not analyze biochemistry levels such as serum natriuretic peptide, troponin, and creatine kinase. In this series, however, no clinical signs of heart failure (general fatigue or significant changes in the weights and heart rates of dogs) were observed. In preparation for clinical AED application, further study will also be required to understand the neurohumoral effects of LAA exclusion.


   Conclusions
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Discussion
 Conclusions
References
 
The second-generation AED provides a potential new therapeutic option for stroke prevention in patients with AF. The device has been redesigned to enhance its performance, and preclinical safety and effectiveness studies are encouraging. Further animal studies in an AF model are warranted to better simulate clinical conditions.


   Footnotes
 
This study was supported financially by the Atrial Fibrillation Innovation Center, an Ohio Wright Center of Innovation, and by AtriCure, Inc. A. Marc Gillinov reports consulting fees from Atricure. Faruk Cingoz and Kiyotaka Fukamachi report grant support from Atricure. The Cleveland Clinic holds equity interests in Atricure.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Discussion
 Conclusions
 References
 

  1. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke. the Framingham Study. Stroke 1991;22:983-988.[Abstract/Free Full Text]
  2. Blackshear JL, Odell JA. Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation. Ann Thorac Surg 1996;61:755-759.[Abstract/Free Full Text]
  3. Al-Saady NM, Obel OA, Camm AJ. Left atrial appendage. structure, function, and role in thromboembolism. Heart 1999;82:547-554.[Abstract/Free Full Text]
  4. Stafford RS, Singer DE. National pattern of warfarin use in atrial fibrillation. Arch Intern Med 1996;156:2537-2541.[Abstract/Free Full Text]
  5. Stafford RS, Singer DE. Recent national pattern of warfarin use in atrial fibrillation. Circulation 1998;97:1231-1233.[Abstract/Free Full Text]
  6. Nakai T, Lesh, MD, Gerstenfeld EP, Virmani R, Jones R, Lee RJ. Percutaneous left atrial appendage occlusion (PLAATO) for preventing cardioembolism. first experience in canine model. Circulation 2002;105:2217-2222.[Abstract/Free Full Text]
  7. Sievert H, Lesh, MD, Trepels T, Omran H, Bartorelli A, Bella PD, et al. Percutaneous left atrial appendage transcatheter occlusion to prevent stroke in high-risk patients with atrial fibrillation. early clinical experience. Circulation 2002;105:1887-1889.[Abstract/Free Full Text]
  8. Hanna IR, Kolm P, Martin R, Reisman M, Gray W, Block PC. Left atrial structure and function after percutaneous left atrial appendage transcatheter occlusion (PLAATO). six-month echocardiographic follow-up. J Am Coll Cardiol 2004;43:1868-1872.[Abstract/Free Full Text]
  9. Meier B, Palacios I, Windecker S, Rotter M, Cao QL, Keane D, et al. Transcatheter left atrial appendage occlusion with Amplatzer devices to obviate anticoagulation in patients with atrial fibrillation. Catheter Cardiovasc Interv 2003;60:417-422.[Medline]
  10. Odell JA, Blackshear JL, Davies E, Byrne WJ, Kollmorgen CF, Edward WD, et al. Thoracoscopic obliteration of the left atrial appendage. potential for stroke reduction?. Ann Thorac Surg 1996;61:565-569.[Abstract/Free Full Text]
  11. Kamohara K, Fukamachi K, Ootaki Y, Akiyama M, Zahr F, Kopcak Jr MW, et al. A novel device for left atrial appendage exclusion. J Thorac Cardiovasc Surg 2005;130:1639-1644.[Abstract/Free Full Text]
  12. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke. results from the National Registry of Atrial Fibrillation. JAMA 2001;285:2864-2870.[Abstract/Free Full Text]
  13. Albers GW, Dalen JE, Laupacis A, Manning WJ, Petersen P, Singer DE. Antithrombotic therapy in atrial fibrillation. Chest 2001;119:194S-206S.[Free Full Text]
  14. Munschauer FE, Priore RL, Hens M, Castilone A. Thromboembolism prophylaxis in chronic atrial fibrillation. practice patterns in community and tertiary-care hospitals. Stroke 1997;28:72-76.[Abstract/Free Full Text]
  15. Levine MN, Raskob G, Beyth RJ, Kearon C, Schulman S. Hemorrhagic complications of anticoagulant treatment. the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:287S-310S.[Abstract/Free Full Text]
  16. Katz ES, Tsiamtsiouris T, Applebaum RM, Schwartzbard A, Tunick PA, Kronzon I, et al. Surgical left atrial appendage ligation is frequently incomplete. a transesophageal echocardiographic study. J Am Coll Cardiol 2000;36:468-471.[Abstract/Free Full Text]
  17. Rosenzweig BP, Katz E, Kort S, Schloss M, Kronzon I. Thromboembolus from a ligated left atrial appendage. J Am Soc Echocardiogr 2001;14:396-398.[Medline]
  18. DiSesa V, Tam S, Cohn LH. Ligation of left atrial appendage using an automatic surgical stapler. Ann Thorac Surg 1988;46:652-653.[Abstract]
  19. Gillinov AM, Pettersson G, Cosgrove DM. Stapled excision of the left atrial appendage. J Thorac Cardiovasc Surg 2005;129:679-680.[Free Full Text]
  20. Vigna C, Russo A, De Rito V, Perna G, Villella A, Testa M, et al. Frequency of left atrial thrombi by transesophageal echocardiography in idiopathic and in ischemic dilated cardiomyopathy. Am J Cardiol 1992;70:1500-1501.[Medline]
  21. Siostrzonek P, Koppensteiner R, Gössinger H, Zangeneh M, Heinz G, Kreiner G, et al. Hemodynamic and hemorrheologic determinants of left atrial spontaneous echo contrast and thrombus formation in patients with idiopathic dilated cardiomyopathy. Am Heart J 1993;125:430-434.[Medline]
  22. Zimmerman MB, Blaine EH, Stricker EM. Water intake in hypovolemic sheep. effects of crushing the left atrial appendage. Science 1981;211;:489-491.[Abstract/Free Full Text]
  23. 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]



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K. Kamohara, Z. B. Popovic, M. Daimon, M. Martin, Y. Ootaki, M. Akiyama, F. Zahr, F. Cingoz, C. Ootaki, M. W. Kopcak Jr, et al.
Impact of left atrial appendage exclusion on left atrial function
J. Thorac. Cardiovasc. Surg., January 1, 2007; 133(1): 174 - 181.
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