EHRA/EAPCI expert consensus statement on catheter-based left atrial appendage occlusion

Abstract

Atrial fibrillation (AF) is the most common clinically relevant cardiac arrhythmia. The estimated prevalence in the general population is 1–2% and increases with age.1–8 Patients with AF are at increased risk of thromboembolism, in particular ischaemic stroke. The risk of stroke in patients with non-valvular (essentially non-rheumatic) AF is ∼5% per year.9 Moreover, strokes related to AF are associated with a higher mortality and morbidity when compared with non-AF strokes, emphasizing the need for more effective stroke prevention in these patients.10 The CHADS2 score (cardiac failure, hypertension, age, diabetes, stroke counted double) was established to assess the risk of thrombo-embolic events in patients with AF of non-valvular origin.11 Although there is a clear relationship between the CHADS2 score and stroke rate, the CHA2DS2-VASc score has recently been introduced and adopted by the European Society of Cardiology (ESC) as well as by American Heart Association, American College of Cardiology, and Heart Rhythm Society and other national bodies’ guidelines for AF in an attempt to improve risk stratification in the low-risk group by considering additional stroke risk factors (gender, vascular disease) in addition to old factors including cardiac failure, hypertension, age (divided to two risk classes) diabetes, and stroke that may influence a decision for anticoagulation therapy.12 Prospective and randomized studies show that oral anticoagulation (OAC) significantly reduces the risk of thromboembolism.13 However, this treatment is underutilized in patients with AF due to poor patient compliance, contraindications, and potential bleeding complications.14–18 The pathogenesis of thrombogenesis in AF is multifactorial and includes the Virchow triad of events leading to thrombus formation, i.e. endothelial or endocardial damage or dysfunction, abnormal blood stasis, and altered haemostasis, platelet function, and fibrinolysis.19 There is evidence for endothelial damage, as well as intense fibrosis and inflammation in the left atrium (LA) in patients with AF.20 These changes are especially prominent in the left atrial appendage (LAA), a particularly low flow area, and may enhance to thrombus formation by their effect on the endocardial surface.21,22 There is also strong evidence for the presence of a prothrombotic and hypercoagulable state in AF, as manifested by increased blood levels of markers reflecting coagulation activity (prothrombin fragments 1 and 2, fibrinopeptide A, thrombin–antithrombin complexes, and D dimer).23,24 The LAA is the remnant of the embryonic LA. The LAA is a tubular blind-ended structure with different lobes and variable morphology. Its complex structure with areas of relative low flow predisposes to stasis, especially during AF when blood flow velocity decreases, as can be visualized on transoesophageal echocardiography (TOE) examination with spontaneous contrast (smoke) or on pulsed-wave Doppler during paroxysms of AF.25–28 It has been shown that in patients with non-valvular AF, 90% of thrombi are located in the LAA.29 Thrombi detected in the LAA as well as a reduced LAA peak flow velocity were identified as independent predictors of an increased thrombo-embolic risk,30,31 and also for recurrence of stroke among non-valvular AF patients recovering from ischaemic stroke.32 Moreover, patients with certain LAA morphologies have been shown to have different levels of thrombo-embolic risk further supporting the role of LAA in embolization.33 Left atrial appendage occlusion or exclusion in AF34–50 is based on the concept that only ∼10% of clinically relevant emboli in non-valvular AF do not originate in the LAA.51–61 The rationale is that, after excluding the LAA as an embolic source, the remaining small risk does not longer warrant OAC with its inherent risk for major bleeds. The risk of embolism from the LAA or the LA increases with age, but so does the risk of bleeding under OAC. Various surgical and catheter-based methods have been developed to exclude the LAA and the success of catheter-based methods attests to the validity of this concept.62 This document reviews the catheter-based methods and their results. Incidental surgical LAA exclusions during heart surgery have been performed for decades.63 A first report by Madden dates back to 1949.34 The popularity of this procedure remained low as it did prolong the surgical procedure and required some specific techniques. Moreover, follow-up TOE often detected residual flow in the LAA in case of a simple suture64 and in a large number of these patients the need for lifelong OAC with a vitamin K antagonist (VKA) remained due to indications unrelated to AF, most commonly mechanical valve prostheses in the mitral position. An electrocardiographically guided thoracoscopic technique for isolated surgical LAA occlusion65 and a percutaneous endocardial/epicardial approach (Lariat, SentreHeart)46,47,50 where an epicardial sling suture is guide