Percutaneous Left Atrial Appendage Closure Ligation and Exclusion as an Alternative Stroke Prevention in Patients with Nonvalvular Atrial Fibrillation

Remo L. Morelli, MD, FACC and Soidjon D. Khodjaev, MD
St. Mary’s Hospital and Medical Center
San Francisco, California

Remo L. Morelli, MD, FACC and Soidjon D. Khodjaev, MD
St. Mary’s Hospital and Medical Center
San Francisco, California

(Editor's note: The following disclosure was not received in time for print publication and is only available in the online version of this article.) Disclosure: Dr. Khodjaev reports no conflicts of interest regarding the content herein. Dr. Morelli reports no financial interests in the company, but that he is a proctor for the procedure, for which he receives per diem compensation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia, and a source of considerable morbidity and mortality. The prevalence of AF is estimated at 1% of the population older than 60 years,1 and it increases with age, affecting 10% of people over the age of 80. Recent studies project that its prevalence will increase to more than 5.6 million by the year 2050, with more than 50% of affected individuals above the age of 80.2 Estimates are that the rate of ischemic stroke among patients with non-rheumatic AF averages >5% per year, which is about 7 times the rate for people without AF. Including transient ischemic attacks (TIA) and clinically silent strokes detected radiographically, the rate of brain ischemia accompanying nonvalvular AF exceeds 7% per year.3 It is well known that the most common source of thrombus and subsequent thromboembolic events in patients with nonvalvular AF is the left atrial appendage (LAA). The efficacy of anticoagulation with warfarin in stroke risk reduction in patients with AF is well understood, yet still underused and often inappropriately discontinued in clinical practice because of difficulty in administration and compliance as well as the risk of bleeding.4 Assuming a baseline risk of 51 ischemic stroke events per 1,000 person-years, it is estimated that adjusted warfarin dose could prevent 28 ischemic strokes at the expense of 11 major or fatal bleeding episodes.5 Gulløv et al showed that after 3 years, the cumulative rate of bleeding events in a group taking adjusted-dose warfarin was 41.1%.6

We report a case of a 79-year-old female with paroxysmal atrial fibrillation whose comorbidities were such that the risk of anticoagulation was felt to be acceptable compared to the expected benefit of stroke prevention with oral anticoagulants. Besides paroxysmal atrial fibrillation, she also suffered from arterial hypertension, type 2 diabetes mellitus, coronary artery disease, temporal arteritis, unilateral renal artery stenosis (status post renal artery stenting), and was recently diagnosed with small cell carcinoma of the lung.

According to CHADS2 stroke risk stratification (Table 1), this patient’s score of 3 put her in the moderate risk group with an annual stroke rate of 5.9% requiring systemic anticoagulation with warfarin. According to the European Society of Cardiology and the CHA2DS2-VASc scoring system (Table 2), this patient’s score of 6 predicts an even higher risk with an annual stroke rate of 9.7%, again requiring systemic anticoagulation.

Given this patient’s significant risk for cerebral vascular accident (CVA), she was started on warfarin. A therapeutic International Normalized Ratio (INR) was maintained for about a year until she was admitted to our hospital with serious GI bleed and required transfusion of seven units of packed red blood cells. Subsequent colonoscopy showed multiple colonic polyps.

This scenario serves as a good example of the challenge in managing anticoagulation in patients with high risk of CVA and risk of bleeding.

The pathophysiology of thrombus formation

Greater than 90% of thromboemboli responsible for strokes in the setting of nonvalvular AF arise in the LAA.7 The absence of organized contraction in the left atrium (LA) creates the substrate of sluggish flow within the LA/LAA, and therefore leads to the spontaneous formation of thrombus and subsequent embolic events.3

Since the 1940s, cardiac surgeons have used a variety of techniques to exclude the LAA in patients who were felt to be at risk of strokes. Suture ligation from the endocardial surface of the left atrium requires the use of cardiopulmonary bypass (CPB) and may be associated with bleeding or injury to the circumflex coronary artery. In addition, endocardial suture ligation may be incomplete in 10–36% of patients, leaving them still predisposed to thromboembolic events.8,9

In contrast, external ligation or excision can be performed without opening the left atrium and without CPB. Such approaches may include suture ligation or use of cutting or non-cutting surgical staplers. These techniques can also lead to bleeding from tearing of the LAA. Despite surgical access, the posterior location of the LAA makes it difficult to identify its anatomic origin on the epicardial surface with the heart beating. This often leads to closure of the appendage distal from the origin of the appendage, resulting in remnant diverticulum that may itself be a nidus for further thrombus formation.

More recently, percutaneous methods of LAA exclusion have been introduced. One such approach includes percutaneous, catheter-based placement of occluding devices within the LAA. For example, in August 2001 the PLAATO (Appriva Medical Inc., Sunnyvale, CA) was the first device used in humans (feasibility studies were completed, nonetheless pivotal investigation was never initiated). A year later, the WATCHMAN LAA closure device (Boston Scientific/Atritech, Inc., Plymouth, MN) was implanted in humans. The subsequent PROTECT AF pivotal clinical study has demonstrated that the WATCHMAN LAA closure device is non-inferior to warfarin therapy in preventing the embolization of thrombi in patients with nonvalvular AF.10 While significantly reducing the risk of hemorrhagic strokes, the relatively high complication rate of 7.7% is a significant limiting factor.11 Furthermore, mainly due to the severity and size of peri-device leakage, 13% of device patients failed to undergo successful withdrawal of warfarin therapy and had to continue anticoagulation beyond the 45th day of follow up. By the twelfth month of follow up, 32.1% of device patients continued to have flow around the device.12,13 Also, the long term fracture or dislodgment rate of a foreign body placed within the heart is unknown. One should realize that as an inclusion criterion for this procedure, all patients must be candidates for use of chronic anticoagulation. In addition, after device implantation is complete, patients have to continue systemic anticoagulation for 45 to 90 days to allow for endothelial overgrowth. During this time, the patients are exposed to both the risks and complications of the implantation procedure itself and the risk of warfarin therapy, without the potential benefit of being off of warfarin.

Our patient was offered an altogether different approach of excluding LAA from the systemic circulation, Percutaneous Left Atrial Appendage Closure Ligation and Exclusion (PLACE) utilizing the LARIAT® suture delivery device (SentreHEART, Inc., Redwood City, CA).

PLACE Method

After a transesophageal echocardiogram (TEE) is performed to verify that the LAA is free of thrombi, the patient is anesthetized (Figure 1A). The TEE is retained for intraprocedural monitoring and to aid in the transseptal catheterization and ligation of the LAA. Access into the anterior pericardial space is then achieved and a 14 Fr soft-tipped guide cannula (SentreHEART) is placed. A transseptal catheterization is then performed and an 8 Fr sheath is placed within the LA (Figure 1B). The patient is then fully anticoagulated. A magnet-tipped  guide wire (SentreHEART) is directed into the LAA over which a balloon-tipped catheter is advanced, location verified both by TEE and by injection of contrast into the LA (Figure 2). A second magnet-tipped wire is introduced into the pericardium and is mated with the corresponding wire within the LAA (Figure 3). The LARIAT suture delivery device is then advanced over the pericardial wire and the LAA appendage is ensnared (Figure 4). After verifying appropriated placement of the snare by TEE, the permanent suture is delivered, and absence of leakage is confirmed by both fluorography and echocardiogram (Figure 5). Protamine is given and a 5 Fr pericardial catheter is left in place to monitor for possible bleeding, removed a few hours later once hemostasis is confirmed.

Our patient was discharged home within 24 hours off of anticoagulation. She continues to do well throughout 15 months of follow up, and completed her course of chemotherapy for small cell lung cancer.

While this method has yet to be proven effective at stroke prevention, experience with the first 450 patients has shown the procedure to be safer (1.9% vs. 7.7% complication rate) and highly successful (96% successful complete ligation of the LAA compared to 86% for the WATCHMAN device). In all our patients thus far, anticoagulation has been discontinued immediately upon completion of the procedure.


While no claims can be made for stroke prevention, our experience with the first 450 patients has shown that the PLACE procedure can achieve successful closure of the LAA, and rates highly with the WATCHMAN, a procedure which has been shown to be non-inferior to warfarin anticoagulation for stroke prevention.

We propose the use of this procedure in those patients with nonvalvular atrial fibrillation presently deemed high risk for anticoagulation.

Editor’s Note: This article underwent peer review by one or more members of EP Lab Digest®’s editorial board.


  1. Libby P. Bonow RO, Mann DL, Zipes DP. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: Saunders Elsevier, 2008, p.869–870.
  2. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: National implications for rhythm management and stroke prevention: The AnTicoagulation and Risk Factors In Atrial Fibrillation (ATRIA) Study. JAMA 2001;285:2370–2375.
  3. Fuster V, Rydén LE, Asinger RW, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation. Circulation 2001;104:2118–2150.
  4. Stafford RS, Singer DE. Recent national patterns of warfarin use in atrial fibrillation. Circulation 1998;97:1231–1233.
  5. Cooper NJ, Sutton AJ, Lu G, Khunti K. Mixed comparison of stroke prevention treatments in individuals with nonrheumatic atrial fibrillation. Arch Intern Med 2006;166:1269–1275.
  6. Gulløv AL, Koefoed BG, Petersen P. Bleeding during warfarin and aspirin therapy in patients with atrial fibrillation: The AFASAK 2 study. Atrial Fibrillation Aspirin and Anticoagulation. Arch Intern Med 1999;159:1322–1328.
  7. Blackshear JL, Odell JA. Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation. Ann Thorac Surg 1996;61:755–759.
  8. Katz ES, Tsiamtsiouris T, Applebaum RM, et al. Surgical left atrial appendage ligation is frequently incomplete: A transesophageal echocardiographic study. J Am Coll Cardiol 2000;36:468–471.
  9. Rosenzweig BP, Katz E, Kort S, et al. Thromboembolus from a ligated left atrial appendage. J Am Soc Echocardiogr 2001;14:396–398.
  10. The WATCHMAN® PROTECT AF Pivotal Clinical Report.
  11. Reddy VY, Holmes D, Doshi SK, et al. Safety of percutaneous left atrial appendage closure: Results from the Watchman Left Atrial Appendage System for Embolic Protection in Patients with AF (PROTECT AF) clinical trial and the Continued Access Registry. Circulation 2011;123:417–424.
  12. Holmes DR, Reddy VY, Turi ZG, et al. Percutaneous closure of the left atrial appendage versus warfarin therapy for prevention of stroke in patients with atrial fibrillation: A randomized non-inferiority trial. Lancet 2009;374:534–542.
  13. Viles-Gonzalez JF, Kar S, Douglas P, et al. The clinical impact of incomplete Left Atrial Appendage Closure with the Watchman device in patients with Atrial Fibrillation. J Am Coll Cardiol  2012;59:923–929.

This article was originally published in EP Lab Digest, August 2012, pages 20-22. Reprinted with permission.