Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia in the world, with more than 3 million people affected in the United States and 15 million patients worldwide. AF carries an increase of fivefold incidence of embolic stroke and a threefold risk of mortality.1 AF is responsible for approximately 25% of all ischemic strokes. Cardioembolic stroke as a result of AF is associated with a mortality rate of 30% at 1 year.2,3 The lifetime risk of development of AF is one in four in patients older than 40 years. In patients younger than 80 years, the prevalence increases by 15%. The risk of stroke in AF increases with increasing CHADS2 and CHA2DS2-Vasc scores. At least 50% of patients with AF who are eligible for anticoagulation are not on effective anticoagulation.4

Unfortunately, many patients are unable to tolerate anticoagulation, due to bleeding. In addition, discontinuation of anticoagulation is quite common, varying from 20% to 40% at 1 year.5 Dabigatran, rivaroxaban, and apixaban are new oral anticoagulant therapies that demonstrate noninferiority and/or superiority to warfarin in stroke prevention, but also have risk of serious bleeding complications, as well as higher cost.6-8 As the risk of stroke and major bleeding increases with patient age, potential contraindications to anticoagulation also increase.

The left atrial appendage (LAA) has been identified by echocardiography and CT imaging9 as a source of thrombus development in patients with AF. The LAA is located between the left ventricle and left upper pulmonary vein and usually traverses in the atrioventricular groove anteriorly and inferiorly; however, its orientation is distinctive in each individual.10,11 The LAA may have variable anatomy but usually consists of an elliptical ostial segment that is free of trabeculations. The LAA is often multilobed with trabeculations in the mid and distal segments. Thrombus development in the LAA is often a result of blood stasis due to decreased left atrial flow velocity in AF, often accompanied by decreased left ventricular function and left atrial distention.

SURGICAL CLOSURE OF LAA: A HISTORICAL PERSPECTIVE

Surgical exclusion of the LAA has been performed as a standalone procedure for anticoagulation-intolerant patients, as well as in conjunction with surgery of the mitral or aortic valve, coronary artery bypass, or as part of the maze procedure. The AtriClip device1212 (AtriCure, Inc., West Chester, OH) is a commonly used commercially available device used in these instances. The results of surgical exclusion have been variable. Suture ligation has been fraught with a high propensity for late LAA patency.13 Newer device exclusion has shown promise for permanent exclusion but still requires a surgical incision, and surgical LAA has been associated with postoperative bleeding, perioperative stroke, and LAA laceration related to traction of the LAA.

THE LARIAT DEVICE AND UTILITY OF CTA

The Lariat is a pericardial access closure device that does not leave a permanent LAA implant (Figure 1). The Lariat is approved for soft tissue ligation but not specifically indicated for LAA closure. This technique uses the following equipment: 0.025-inch and 0.035-inch magnet-tipped guidewires (FindrWirz), a 15-mm compliant balloon catheter (EndoCath, SentreHeart, Inc.), and a 12-F suture delivery device (Lariat) (Figure 2).

A preprocedural CTA is helpful and often essential in planning several parts of the procedure, such as assessment of the size of the LAA, positioning of FindrWirz, and pericardial access approach. The CTA can determine in advance that some LAAs will not be able to be approached because of anatomic considerations. LAAs that are hidden behind the pulmonary artery or are severely superior in orientation present unfavorable anatomy for closure. The CTA depicts all lobes in the LAA so the correct lobe for the endocardial wire placement can be chosen (Figure 3). The CTA determines the width of the LAA. Because the width of the Lariat is 40 mm, any diameter measurement > 40 mm may be a relative contraindication for this technique. The CTA aids pericardial access by giving proper orientation from the access site to the tip of the appendage. Threedimensional reconstruction of the LAA with CTA is the most important preprocedural planning tool.

PERICARDIAL ACCESS

First, percutaneous pericardial access is attained, using a midline approach with a 17-gauge beveled needle (Pajunk Medical Systems, Norcross, GA). A micropuncture pericardial needle is also a useful device, especially if there is concern of accessing the right ventricle. The direction of access is toward the left shoulder of the patient (which is usually the direction of the tip of the LAA), with the access site on the anterior surface of the heart. The needle access must be kept anteriorly for sheath placement and ultimately wire attachment; posposterior access or midline access to the pericardial space will not allow proper engagement of the FindrWirz. The ideal location for pericardial access is several centimeters superior to the right ventricular apex on the anterior surface of the heart. A pigtail catheter is often placed in the right ventricular apex to mark it, allowing better direction for the pericardial needle. If a right ventricular pacing lead is in place at the apex, it can also serve as an excellent marker.

Tenting of the pericardium prior to puncture is seen using small amounts of contrast injection through the needle. Excessive use of contrast with staining of the subcutaneous tissue may make visualization a challenge. Verification of pericardial access is made by a characteristic appearance of a small amount of contrast in the pericardial space.

Once access is achieved, a 0.035-inch guidewire is generously fed into the pericardial space for confirmation. This guidewire should be able to move freely across the midline to ensure there are no significant adhesions present, which could complicate passage of the Lariat. A series of dilators, starting with 8 F and working up to 12 F or 14 F, are used prior to placement of a 14-F, soft-tipped epicardial sheath. The right ventricle is observed on transesophageal echocardiography (TEE) as the sheath is placed to make sure compression of the right ventricle does not occur. A “buddy” wire is placed alongside the 14-F sheath so that in case a pericardial effusion should develop, a drain may quickly be placed.

TRANSSEPTAL ACCESS AND DEVICE PLACEMENT

An inferior and posterior position is desirable for transseptal access, using an 8.5-F SL1 transseptal catheter (St. Jude Medical, Inc., St. Paul, MN). TEE is very useful to ensure the proper site of puncture. It is also helpful throughout the remainder of the procedure to assess the LAA site of closure, completeness of closure, presence or absence of thrombus, and development of pericardial effusion. A left atriagram is obtained in a right anterior oblique caudal projection to visualize the LAA body and lobes (Figure 4).

The SL1 sheath is often atraumatically advanced to the ostium of the LAA over a pigtail catheter placed in the LAA. The 0.025-inch endocardial wire is advanced through the balloon catheter to the apex of the LAA. The balloon catheter is placed at the ostium of the LAA for identifying the proper landing zone of closure and for support during LARIAT placement. If needed, the endocardial wire is steered into the desired lobe of the LAA, which is usually superior and anterior. Proper wire positioning is enhanced by making a gentle curve in the wire, advancing the guide catheter to the ostium of the LAA, and making use of the balloon for support.

The 0.035-inch epicardial wire is placed through the epicardial sheath, creating a magnetic union with the endocardial wire. The union is visualized fluoroscopically in the anteroposterior and lateral projections to ensure the Lariat device will travel anteriorly and superiorly. The Lariat device is then advanced over the epicardial wire and closed at the site of the LAA opening. The balloon is inflated in the LAA and is used as a marker for proper location of Lariat closure. This location is approximately 1 to 2 mm distal to the LAA ostium and near the circumflex artery, as visualized by TEE. Once satisfactory closure is confirmed by TEE and LAA angiography, the endocardial wire and balloon are removed, and final tightening of the suture is performed. The Lariat device is removed, and the suture is cut near the LAA ostium using a Lariat suture cutter. A pericardial drain is left in place overnight after the pericardial sheath is removed.

CLINICAL RESULTS

Suture ligation for LAA closure has been evaluated in animals,14 a feasibility registry (PLACE II), and single-center experiences. There have been no randomized clinical trials for stroke reduction.

In the single-center, PLACE II registry,15 85 of 89 patients had successful LAA ligation, with 81 patients having complete closure immediately. The mean CHADS2 score was 1.9 ± 0.95. Three patients had a small residual leak (< 2 mm), and onehad a leak > 3 mm. There was one pericardial-access– related complication and two transseptal-access– related complications. Other complications included pericarditis, late pericardial effusion, and two late unexplained sudden deaths and late nonembolic strokes. At follow-up, 95% of patients had complete closure by TEE at 6 months (77 of 81) and 98% closure at 1 year (63 of 65). The Lariat device demonstrated highly effective rates of LAA closure, with limited complications.

Stone et al16 have reported their experience evaluating early outcomes in 27 patients who were at high risk or ineligible to take anticoagulant therapy. The mean CHADS2 score was 3.5 ± 1.6, CHA2DS2-Vasc score was 5.1 ± 1.5, and the HAS-BLED score was 4.6 ± 0.9. The procedural success rate was 92.6%, and TEE at 4 months confirmed complete closure in 22 of 25 patients. One patient developed a procedural perforation of the LAA that was managed conservatively, ultimately undergoing a surgical atrial fibrillation ablation and LAA ligation 1 day later. Three patients developed pericarditis, and one patient developed a remote cerebrovascular accident thought to be due to aortic atheroembolism.

Massumi et al17 reported their initial clinical experience in 21 patients at high risk or ineligible for oral anticoagulation. The mean CHADS2 score was 3.2 ± 1.2, the CHA2DS2-Vasc score was 4.8 ± 1.3, and the HASBLED score was 3.5 ± 1. Twenty patients maintained complete closure at 90-day follow-up, and there were no stroke events reported. There was one right ventricular perforation resulting in pericardial tamponade and requiring surgery. There were two prolonged hospitalizations: one due to pericarditis requiring pericardiocentesis and the other for noncardiac comorbidities. Three patients had pericarditis within 1 month of the procedure.

Han et al18 investigated electrical activity in the LAA before and after Lariat deployment in 30 patients. All patients had complete electrical isolation of the LAA after complete closure of the LAA.

MANAGEMENT OF PROCEDURAL COMPLICATIONS

Procedural complications include pericardial effusion and tamponade, right ventricular perforation, and LAA perforation. Many of these same complications are well known when performing transseptal puncture and/or pericardial access for ventricular tachycardia ablation. LAA perforation has occurred with intracardiac device placement for LAA closure.

Pericardial effusions most commonly occur from puncture or irritation of the right ventricle during pericardial access. Catheter drainage for fluid removal and reversal of anticoagulation are often necessary. Occasionally, surgical drainage or repair of the puncture site may be necessary. Pericardial effusions occurring late (after the pericardial drain is removed) are treated medically in the usual fashion with NSAIDS or colchicine. Occasionally, drainage of fluid is necessary.

LAA perforation is a very rare, but potentially lifethreatening, complication. Once the FindrWirz are connected for Lariat delivery, excessive tension on the epicardial wire can pull the endocardial wire through the LAA. If the wires are still connected, the best solution is to quickly close the Lariat on the LAA to prevent further bleeding. Otherwise, closing the LAA may be attempted with an intracardiac device, such as a Watchman (Boston Scientific Corporation, Natick, MA) or Amplatzer cardiac plug (St. Jude Medical, Inc.) device, or surgical closure may be necessary.

FUTURE CONSIDERATIONS

Because the Lariat device is not approved specifically for LAA closure by the FDA, it is used only for anticoagulation- ineligible patients at high risk of stroke from atrial fibrillation. Furthermore, future clinical trials should be focused on the safety and efficacy of this procedure using the Lariat in this patient population. As newer anticoagulants with greater safety and efficacy profiles than warfarin have been approved for use, there is need to compare interventional strategies as standalone procedures or adjunctive therapy. The greatest need may be in patients in whom anticoagulation is contraindicated. Further studies to determine best clinical practice are needed in warfarin-ineligible patients. Interruption of anticoagulation is an increasing problem, especially when switching from warfarin.

The use of closure devices in conjunction with AF ablation may enhance ablation success because nearly 25% of AF recurrence is near the LAA ostium. Devices that may interrupt those AF signals, such as the Lariat, may be helpful. New techniques to enhance device placement, such as better guiding catheters, safer ways to access the pericardial space, and enhanced imaging are being developed. Finally, improvements and innovation of all devices will make these procedures less complicated, with decreased procedural times and enhanced safety.

Portions of this article were previously published in the January/February 2013 issue of Cardiac Interventions Today. The author thanks Connor B. Yakubov for his editorial assistance in preparing this manuscript.

Steven J. Yakubov, MD, FACC, FSCAI, is with OhioHealth Research Institute, Riverside Methodist Hospital in Columbus, Ohio. He has disclosed that he has served as a consultant to SentreHeart. Dr. Yakubov may be reached at steven.yakubov@gmail.com.

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