Atrial Fibrillation

Atrial fibrillation (AF) is a type of heart rhythm where the heart beats irregularly. It occurs when one or both of the upper chambers, called atria, beat very quickly and not in a steady rhythm. The blood pools in the atria and does not pump completely into the lower chambers, called the ventricles. This increases the risk of clotting and if the clot breaks off, it increases stroke risk. This is the reason why AF patients are put on blood-thinners. AF can also lead to heart failure, decreased quality of life, and other heart-related complications.

  • AF affects 1%–2% of the population and its prevalence increases with age.1
  • AF is different than the normal sinus rhythm (SR). In SR, the heart contracts as it follows an electrical signal in the heart. The electrical signal starts in a group of cells called the sinoatrial node (SA node) and then to the atrioventricular (AV) node. The AV node is located between the atria and the ventricle. The AV node slows the electrical signal to allow the ventricles to fill with blood before it pumps the blood to the rest of the body. In AF, the electrical signal does not start in the SA node, but from the pulmonary veins (PVs). The left atrial appendage (LAA) or other spots in the heart can also contribute.2 As AF progresses, it is more common for the electrical signals to come from other sections of the heart. The electrical signal travels directly to the ventricle, not going through the AV node, and is not slowed. This is why there is an irregular heartbeat in AF.
  • AF is classified by the duration of the episodes1
    • Paroxysmal AF – Self-terminating, usually within 48 hours. The AF episode may continue up to 7 days.
    • Persistent AF – AF episode that lasts longer than 7 days or requires termination by cardioversion, either with drugs or by direct current cardioversion.
    • Longstanding persistent AF – AF episode that has lasted ≥1 year when it is decided to adopt a rhythm control strategy.
    • Permanent AF – Presence of arrhythmia is accepted by patient and physician.
    • Paroxysmal (HRS3) – AF episode that terminates spontaneously or with intervention within 7 days of onset. The episodes may recur with variable frequency.
    • Persistent AF – Continuous AF that is sustained >7 days.
    • Longstanding persistent AF – Continuous AF of >12 month duration.
    • Permanent AF – Joint decision by patient and clinician to cease further attempts to restore and/or maintain sinus rhythm. Acceptance of AF represents a therapeutic attitude on the part of the patient and clinician, rather than an inherent pathophysiological attribute of the AF. Acceptance of the AF may change as symptoms, the efficacy of therapeutic interventions, and patient and clinical preferences evolve.
  • AF is treated either with medication or with a procedure.
    • Physicians will prescribe blood-thinning drugs to prevent blood clot formation. There are several types of blood-thinning drugs (eg, aspirin, warfarin, heparin, apixaban) that work differently and have different risks, benefits, and interactions. These blood-thinning medications need to be carefully monitored.
    • Physicians can also prescribe medications (antiarrhythmic drugs, AADs) to control the heart rate or to restore sinus rhythm. Rate control is preferred, since many of the symptoms can be alleviated with a controlled heart rate.
    • Physicians will tailor the medication type and dose to the patient, particularly since the side effects of some of the medications may cause a different type of heart rhythm or tissue damage. These AADs have a modest effect and usually just reduce the frequency or duration of the arrhythmia.
    • AF is treated either surgically with the Cox-MAZE procedure or percutaneously to restore sinus rhythm. Both procedures aim to prevent the non-SA node electrical signals from traveling to the ventricles.
    • The Cox-MAZE procedure includes pulmonary vein isolation, LAA exclusion, and other lines in the right and left atrium. The idea was to create conduction barriers and prevent sustained AF. The Cox-MAZE procedure became the standard therapy for surgical AF treatment. Surgical treatment of AF is more effective, but includes more procedural risks than the catheter ablation. Since it is more risky, AF is usually treated while doing another cardiac surgery and not typically done alone. Catheter ablation is the recommended procedural treatment for AF.
    • The AF catheter procedure was developed to mimic the surgical procedure in a less invasive manner. Wires are inserted though veins in the leg and threaded to the heart and similar lines of conduction block are created.
    • Paroxysmal AF ablation has success rates >70%.4 The efficacy rates for persistent or longstanding AF after one ablation procedure is low (average 20%) and only increases to 45% despite multiple ablation procedures.5 These success rates do not reflect all of the same Cox-MAZE conduction barriers created in the surgical procedure.
    • A close-chested Cox-MAZE procedure may be emulated by performing LAA exclusion with percutaneous AF ablation.


AF increases a patient’s risk of ischemic (or embolic) stroke 5-fold.6,7 In fact, AF is responsible for up to 20% of all strokes, with a mean annualized stroke rate of 4.0% per year.8-10 The left atrial appendage (LAA) has been implicated in propagating AF and the source of thrombus formation.11 Ninety percent of the LA thrombi found in non-valvular AF patients occurred in the LAA, while only 57% of valvular AF subjects’ LA thrombi were located there.12

There are 2 main types of stroke, ischemic and hemorrhagic. Ischemic stroke occurs when blood flow to the brain is blocked. This blockage is typically a blood clot. The brain cells are deprived of oxygen and die. Brain bleeding may cause a hemorrhagic stroke if the brain cells are damaged.

Stroke treatment

Physicians will prescribe blood-thinning drugs to prevent blood clot formation. There are several types of blood-thinning drugs (eg, aspirin, warfarin, heparin, apixaban) that work differently and have different risks, benefits, and interactions. These blood-thinning medications need to be carefully monitored or the patient will have bleeding complications.


The LAA is a pouch connected to the left atrium (LA) of the heart. Unlike the rest of the LA, the tissue is not smooth, but has many grooves (or trabeculation). During SR, all of the blood is squeezed out of the LAA into the LA. If the blood is stagnant, patient is in AF, clot may form in this trabeculation. The LAA is not the same in everyone and has different shapes and sizes. The LAA does not have a known function in the developed heart.

  • The LAA was excluded during mitral valve surgeries as early as the 1940s.13-15
  • Guidelines
    • Guidelines recommend LAA occlusion if anticoagulation is contraindicated or not well tolerated.16
    • Guidelines recommend amputation of the LAA in surgical procedures.17
  • Surgical exclusion
    • The basis for this is well established with its integral part in the Cox-MAZE procedure for AF treatment. Over the years, methods of LAA exclusion have included surgical resections, suture ligation, cutting and non-cutting staples, percutaneous implants, and surgical clips. Previously surgical LAA exclusion has shown inconsistent closure results. This is usually done surgically with another surgical cardiac procedure.
  • Percutaneous exclusion
    • LAA occlusion has developed in percutaneous implants and the LARIAT device.


1 Camm AJ, Kirchhof P, Lip GY, et al. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Eur Heart J. 2010;31(19):2369-2429.
2 Di Biase L, Burkhardt JD, Mohanty P, et al. Left atrial appendage: an underrecognized trigger site of atrial fibrillation. Circulation. 2010;122(2):109-118.
3 January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014;130(23):2017-2104.
4 Cappato R, Calkins H, Chen SA, et al. Updated worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circ Arrhythm Electrophysiol. 2010;3(1):32-38.
5 Tilz RR, Rillig A, Thum AM, et al. Catheter ablation of long-standing persistent atrial fibrillation: 5-year outcomes of the Hamburg sequential ablation strategy. J Am Coll Cardiol. 2012;60(19):1921-1929.
6 Lip GY, Tse HF. Management of atrial fibrillation. Lancet. 2007;370(9587):604-618.
7 Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke. 1991;22(8):983-988.
8 Hart RG, Halperin JL. Atrial fibrillation and stroke: concepts and controversies. Stroke. 2001;32(3):803-808.
9 Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics–2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2008;117(4):e25-e146.
10 Assiri A, Al-Majzoub O, Kanaan AO, Donovan JL, Silva M. Mixed treatment comparison meta-analysis of aspirin, warfarin, and new anticoagulants for stroke prevention in patients with nonvalvular atrial fibrillation. Clin Ther. 2013;35(7):967-984 e962.
11 Blackshear JL, Odell JA. Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation. Ann Thorac Surg. 1996;61(2):755-759.
12 Onalan O, Crystal E. Left atrial appendage exclusion for stroke prevention in patients with nonrheumatic atrial fibrillation. Stroke. 2007;38(2):624-630.
13 Cox JL, Ad N, Palazzo T. Impact of the maze procedure on the stroke rate in patients with atrial fibrillation. J Thorac Cardiovasc Surg. 1999;118(5):833-840.
14 Madden JL. Resection of the left auricular appendix; a prophylaxis for recurrent arterial emboli. J Am Med Assoc. 1949;140(9):769-772.
15 Cox JL. Cox JL. The surgical treatment of atrial fibrillation: IV. Surgical technique. J Thorac Cardiovasc Surg. 1991;101:584-592.
16 National Institute for Health and Care Excellence. Atrial fibrillation: the management of atrial fibrillation CG180 2014;
17 American College of Cardiology/American Heart Association Task Force on Practice Guidelines, Society of Cardiovascular Anesthesiologists, Society of Thoracic Surgeons, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients with Valvular Heart Disease): developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2006;48(3):e1-e148.
18 Bartus K, Bednarek J, Myc J, et al. Feasibility of closed-chest ligation of the left atrial appendage in humans. Heart Rhythm. 2011;8(2):188-193.
19 Bartus K, Han FT, Bednarek J, et al. Percutaneous left atrial appendage suture ligation using the LARIAT device in patients with atrial fibrillation: initial clinical experience. J Am Coll Cardiol. 2013;62(2):108-118.
20 Finta B. Percutaneous transpericardial left atrial appendage closure with the LARIAT device. EP Lab Digest. 2013;13(7):22-24.
21 Gunda S, Kanmanthareddy A, Vallakati A, et al. Characterization of pleural effusion after left atrial appendage exclusion using the Lariat procedure. J Cardiovasc Electrophysiol. 2015;26(5):515-519.
22 Lee RJ, Bartus K, Bednarek J, et al. Criteria for success of left atrial appendage ligation by a novel catheter-based suture ligation procedure. J Am Coll Cardiol. 2011;57(14s1):e66.
23 Lee RJ, Bartus K, Yakubov SJ. Catheter-based left atrial appendage (LAA) ligation for the prevention of embolic events arising from the LAA: initial experience in a canine model. Circulation: Cardiovascular Interventions. 2010;3(3):224-229.
24 Massumi A, Chelu MG, Nazeri A, et al. Initial experience with a novel percutaneous left atrial appendage exclusion device in patients with atrial fibrillation, increased stroke risk, and contraindications to anticoagulation. Am J Cardiol. 2013;111(6):869-873.
25 Miller MA, Gangireddy SR, Doshi SK, et al. Multicenter study on acute and long-term safety and efficacy of percutaneous left atrial appendage closure using an epicardial suture snaring device. Heart Rhythm. 2014;11(11):1853-1859.
26 Price MJ, Gibson DN, Yakubov SJ, et al. Early safety and efficacy of percutaneous left atrial appendage suture ligation: results from the U.S. transcatheter LAA ligation consortium. J Am Coll Cardiol. 2014;64(6):565-572.
27 Stone D, Byrne T, Pershad A. Early results with the LARIAT device for left atrial appendage exclusion in patients with atrial fibrillation at high risk for stroke and anticoagulation. Catheter Cardiovasc Interv. 2013:86(1):121-127.
28 Afzal MR, Kanmanthareddy A, Earnest M, et al. Impact of left atrial appendage exclusion using an epicardial ligation system (LARIAT) on atrial fibrillation burden in patients with cardiac implantable electronic devices. Heart Rhythm. 2015;12(1):52-59.
29 Badhwar N, Lakkireddy D, Kawamura M, et al. Sequential percutaneous LAA ligation and pulmonary vein isolation in patients with persistent AF: initial results of a feasibility study. J Cardiovasc Electrophysiol. 2015:26(6):608-614.
30 Han FT, Bartus K, Lakkireddy D, et al. The effects of LAA ligation on LAA electrical activity. Heart Rhythm. 2014;11(5):864-870.
31 Pillarisetti J, Reddy YM, Gunda S, et al. Endocardial (Watchman) vs epicardial (Lariat) left atrial appendage exclusion devices: understanding the differences in the location and type of leaks and their clinical implications. Heart Rhythm. 2015;12(7):1501-1507.