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Atrial Fibrillation (AF) Disclaimer 2 All St. Jude Medical products should be used only according to FDA approved indications. Discussion surrounding therapeutic techniques in no way constitutes a recommendation of or training toward the utilization of St. Jude Medical products Objectives 3 To understand the Clinical Considerations of the physician when dealing with AF To understand the Mechanisms and Causes of AF To learn to visualize Significant Anatomy relevant to AF To discuss Tools and Techniques relevant to treating AF Clinical Considerations Epidemiology Atrial fibrillation is the most common clinically significant cardiac arrhythmia in the world. Approximately one third of hospitalizations for cardiac rhythm disturbance 2.3 million people in the United States and 4.5 million in the European Union have paroxysmal or persistent AF Hospital admissions for AF have increased by 66% due to the aging population Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 4 Clinical Considerations Epidemiology AF is associated with an increased long-term risk of stroke, heart failure, and allcause mortality, especially in women The mortality rate of patients with AF is about double that of patients in NSR and is linked to the severity of underlying heart disease The most devastating consequence of AF is stroke as a result of thromboembolism 1 out of every 6 strokes occurs in patients with AF ACCF/AHA Pocket Guideline. Management of Patients with Atrial Fibrillation. Adapted from the 2006 ACC/AHA/ESC Guidline and the 2011 ACCF/AHA/HRS Focused Updates) 5 Clinical Considerations Risk Stratification CHADS2 Score Prior Cerebrovascular accident (CVA) Prior transient ischemic attack (TIA) Age History of hypertension (HTN) Diabetes Heart failure (HF) ACCF/AHA Pocket Guideline. Management of Patients with Atrial Fibrillation. Adapted from the 2006 ACC/AHA/ESC Guidline and the 2011 ACCF/AHA/HRS Focused Updates) 6 7 O nl y Clinical Considerations Clinical Presentation Symptomatic or asymptomatic, even in the same patient up to 21% of newly diagnosed patients with newly diagnosed AF are asymptomatic Symptoms associated with AF vary with: ventricular rate underlying functional status duration of AF presence and degree of structural heart disease individual patient perception Most patients with AF complain of palpitations, angina, dyspnea, fatigue, or dizziness Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 9 Clinical Presentation Initial Evaluation 10 Characterize the pattern of the arrhythmia How long have they had it? How long have they experienced symptoms? Cardioversions in the past? What drugs are they on? Determine underlying causes (heart failure, pulmonary problems, hypertension, or hyperthyroidism) Define associated cardiac and extracardiac conditions Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Classification of AF 11 First detected episode Permanent (Cardioversion failed) Recurrent (After 2 episodes) AF Persistent 7days – 1 year ACCF/AHA Pocket Guideline. Management of Patients with Atrial Fibrillation. Adapted from the 2006 ACC/AHA/ESC Guidline and the 2011 ACCF/AHA/HRS Focused Updates) Paroxysmal (selfterminates) 12 Clinical Presentation Patient Management 13 Four Main Issues that must be addressed 1. Prevention of systemic embolization (clot) 2. Rate control 3. Rhythm control 4. Choosing between rhythm and rate control Choice of therapy is influenced by: Patient preference Associated structural heart disease Severity of symptoms Whether the AF is recurrent paroxysmal, recurrent persistent, or permanent (chronic) In addition, patient education is critical, given the potential morbidity associated with AF and its treatment. Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Electrocardiographic Features 14 15 Electrocardiographic Characterized by rapid and irregular atrial fibrillatory waves (f waves) and lack of clearly defined P waves Features Best seen Lead V1 and in the inferior leads (II, III, and AVF). Rate of the fibrillatory waves -- between 350 and 600 beats/min The atrium twitches “like bags of worms” Ventricular response is typically irregularly irregular at a rate of 90-170 beats/min Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Pathophysiology Although useful, this classification does not account for all presentations of AF and is not clearly related to any specific pathophysiology or mechanism of arrhythmogenesis Pattern of AF may change in response to treatment Paroxysmal often progresses to Persistent Persistent can deteriorate into Permanent or Chronic Persistent may become Paroxysmal with drug therapy or catheter ablation Distinction between classifications is not only a function of the underlying arrhythmia, but also the clinical pragmatism of the patient and physician Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 16 Mechanisms Two concepts of the underlying mechanism of AF have received considerable attention: 1. Factors that trigger the onset of AF 2. Factors that perpetuate AF Patients with frequent, self-terminating episodes of AF are likely to have a predominance of factors that trigger AF Patients with AF that does not terminate spontaneously are more likely to have a predominance of factors that perpetuate AF This generalization has clinical usefulness, but there is considerable overlap of these mechanisms in the typical AF patient Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 17 Mechanisms of Initiation Stable focus (PAC) or reentrant circuit with activation arising from this focus too rapid to be conducted uniformly throughout the atria Rapid propagation of the wave fronts breaks up into irregular wavelets Mechanism of initiation of AF is not certain in most cases and likely is multifactorial 18 Murgatroyd, F.D., Krahn, A.D., Klein, G.J., Yee, R.K, & Skanes, A..C(2001). Atrial Arrhythmias. In Murgatroyd, F.D., Krahn, A.D., Klein, G.J., Yee, R.K, & Skanes, Handbook of Cardiac Electrophysiology (55-71). London: ReMEDICA Publishing Limited Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Mechanisms of Initiation AF Triggers Premature Atrial Complexes (PACs) from the Pulmonary Veins (PVs), Coronary Sinus (CS), Superior Vena Cava (SVC), Ligament of Marshall, Left Atrial chamber, RA chamber (crista terminalis) Sympathetic or Parasympathetic stimulation Other Supraventricular Tachycardia (SVT) 19 AVRT, AFL, AVNRT Identification and treatment of triggers may be curative Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Mechanisms of Initiation Triggering foci of rapidly firing cells within the sleeves of atrial myocytes extending into the PVs have been clearly shown to be the underlying mechanism of most paroxysmal AF Thoracic veins are highly arrhythmogenic PV-LA Junction has discontinuous myocardial fibers separated by fibrotic tissues and, therefore, is highly anisotropic More information can be found on page 210 20 Mechanisms of Perpetuation 21 Multiple wavelets of depolarization propagate within the atria. These can divide, coalesce extinguish each other as they travel in an apparently random fashion, seeking tissue that is excitable. Results in electrical and structural remodeling Atrial Dilation Decreased Atrial Refractoriness Larger Hearts Fibrillate Easily (Elephant and Whale) Smaller Hearts Do Not Fibrillate Easily (Mice) Murgatroyd, F.D., Krahn, A.D., Klein, G.J., Yee, R.K, & Skanes, A..C(2001). Atrial Arrhythmias. In Murgatroyd, F.D., Krahn, A.D., Klein, G.J., Yee, R.K, & Skanes, Handbook of Cardiac Electrophysiology (55-71). London: ReMEDICA Publishing Limited Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Anatomy Nathan, H., et al. “The Junction Between the Left Atrium and the Pulmonary Veins: An Anatomic Study of Human Hearts.” Circ, Vol. 34, (1966): 412-422. Print. 22 Anatomy Nathan, H., et al. “The Junction Between the Left Atrium and the Pulmonary Veins: An Anatomic Study of Human Hearts.” Circ, Vol. 34, (1966): 412-422. Print. 23 Anatomy Armour, J.A. ET AL. “Gross and Microscopic Anatomy of the Human Intrinsic Cardiac Nervous System.”The Anatomical Record. Vol. 247.(1997):289–298. Print. 24 Anatomy Armour, J.A. ET AL. “Gross and Microscopic Anatomy of the Human Intrinsic Cardiac Nervous System.”The Anatomical Record. Vol. 247.(1997):289–298. Print. 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 Electrophysiology Study Pre-Procedure Considerations Stop antiarrhythmic medications more than 5 days before Anticoagulated with warfarin (INR, 2 to 3) for more than 4 to 6 weeks before the ablation procedure Warfarin usually stopped 2 to 5 days before the procedure TEE to screen for LA thrombus (mandatory in patients who are in AF at the time of the procedure) Optional magnetic resonance (MR) imaging or contrastenhanced, multi-slice CT scan of the LA with 3-D reconstruction Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 41 Electrophysiology Study Pre-Procedural Planning Considerations Conscious sedation or general anesthesia? Transseptal access tools and sheaths Diagnostic catheters HIS CS PV TEE Intracardiac Echo (ICE) Item 100057675 Rev A Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 42 Spectrum of Techniques Elimination of Triggers Pulmonary Vein Triggers Segmental Ostial Pulmonary Vein Isolation Circumferential Antral Pulmonary Vein Isolation Substrate Modification Wide Area Circumferential (WACA) Linear Atrial Method Complex Fractionated Atrial Electrogram (CFAE) Central Nervous System Denervation Non-Pulmonary Vein Triggers Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 43 44 Focal Pulmonary Vein 1998 Haissaguerre demonstrated that PAF initiated by spontaneous triggers (94% within the PVs) Triggers AF initiated with a burst of rapid firing from foci within 2 to 4 cm of the ostium of the PV Advantages Shorter procedure time, less fluoroscopy, potential cure Can be done without a 3D Mapping System Limitations: High Rate of PV stenosis Probability of more than one culprit vein Frequent recurrences Difficult to elicit PV arrhythmia in the EP laboratory to allow adequate mapping. Does not address reentry in the substrate (persistent or chronic pts) Requires double or triple transseptal access Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Focal Pulmonary Vein Triggers 45 Pulmonary Vein Stenosis Kato et al. “Pulmonary vein anatomy in patients undergoing catheter ablation of atrial fibrillation: lessons learned by use of magnetic resonance imaging.” Circulation. Vol.107. (2003): 2004-10. Print. Robbins, ER, et al, “Pulmonary vein stenosis after catheter ablation of atrial fibrillation.” Circulation Vol. 98 (1998) :1769. Print Focal Pulmonary Vein Triggers Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 46 Segmental Ostial Pulmonary Vein Isolation Map segments of the ostium at which muscle fibers extending from the LA into the PV are present (PV muscle potentials) Advantages: No risk of PV stenosis Easy to identify PV potentials Short case times, less fluoroscopy Eliminates the need for detailed mapping of spontaneous ectopy Limitations 1-4 PVs (Time vs. Recurrence) Anatomical variance between PVs can add to difficulty and time Does not account for reentry in the substrate Requires double or triple transseptal access Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 47 Segmental Ostial Pulmonary Vein Isolation Kato et al. “Pulmonary vein anatomy in patients undergoing catheter ablation of atrial fibrillation: lessons learned by use of magnetic resonance imaging.” Circulation. Vol.107. (2003): 2004-10. Print. More information can be found on page 232-33 48 Segmental Ostial Pulmonary Vein Isolation Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 49 Segmental Ostial Pulmonary Vein Isolation Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 50 Segmental Ostial Pulmonary Vein Isolation Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 51 Circumferential Antral Pulmonary Vein Isolation Focusing on the outermost atrial side of the antral-LA junction rather than at the ostium. Advantages: Isolates PVs and accounts for foci in the antrum Does does not rely on localizing the sites of electrical breakthroughs into the PV easier to perform during AF Easier to account for variation in PV anatomy (e.g. common antrum) Begins to account for reentry in the substrate Less chance for PV stenosis Modifies posterior wall and areas of CNS innervation Limitations Longer cases and more potential for complications (other than stenosis) Can create AT/AFL post procedure Relies upon a good 3D reconstruction/registration of anatomy Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 52 Circumferential Antral Pulmonary Vein Isolation Kato et al. “Pulmonary vein anatomy in patients undergoing catheter ablation of atrial fibrillation: lessons learned by use of magnetic resonance imaging.” Circulation. Vol.107. (2003): 2004-10. Print. 53 Circumferential Antral ICE Guided Positioning at the PV Pulmonary Vein Isolation antrum The anatomical region within the ablation circles typically encompasses the entire posterior wall, LA roof, and anteroseptal extension of the right PVs ICE can help visualize evolving microbubble formation during tissue heating. Microbubble formation, however, is not a straightforward surrogate for tissue heating Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 54 Circumferential Antral Pulmonary Vein Isolation Endpoint electrical isolation of all four PVs (just like segmental ostial PVI) Reconfirmation of isolation after 60 min has been suggested to detect early recurrence of PV conduction Studies using ICE-guided circumferential PV isolation have reported a success rate after the first procedure of about 80%, with higher success rates seen in younger patients with paroxysmal AF One study compared segmental ostial PV isolation and circumferential extraostial PV isolation. At 11 ± 3 months’ follow-up, 60% of patients in the segmental group were free of AF, compared with 75% of patients in the circumferential group Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 55 Wide Area Circumferential (WACA) Advantages Efficacy is not dependent upon complete and lasting PV disconnection from the LA Can be done with a single transseptal access Eliminates AF by addressing other mechanisms Substrate reentry, CNS denervation, Ligament of Marshall, Bachmann’s Bundle Tailored lesion sets to accommodate unusual anatomy Does not require identification of PV potentials Risk of PV stenosis is decreased Limitations More lesions = longer cases and more potential for complications (other than stenosis) Can create AT/AFL post procedure Relies upon a good 3D reconstruction/registration of anatomy Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 56 Wide Area Circumferential (WACA) Can use activation mapping in correlation with voltage mapping to assess lesion sets PVI Isolation is not required Termination of AF occurs in about one third of pts If AF does not terminate, cardioversion is performed at the end of the procedure If AF recurs immediately, the completeness of the lines is reassessed and additional lines should be considered WACA ablation may create macroreentrant circuits in the LA, mediating conversion of AF into AFL Inducibility of AF after ablation was found to be a significant independent predictor of recurrent AF Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 57 Linear Left Atrial Success of surgical linear lesions has led to the development of the catheter-based approach Address the substrate Preevent reentry Eliminate non-PV foci Roof line, mitral isthmus line, cavotricuspid isthmus line Used to do posterior and anterior lines deemed proarrhythmic or dangerous Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 58 Complex Fractionated Atrial Electrograms (CFAE) Map sites with complex fractionated atrial electrograms (CFAEs) during AF May represent continuous reentry of the fibrillation waves into the same area or overlap of different wavelets entering the same area at different times May indicate the presence of a driver or a rotor What defines a CFAE? “CFAEs are defined as (1) atrial electrograms that are fractionated and composed of two deflections or more, and/or have a perturbation of the baseline with continuous deflection of a prolonged activation complex over a 10-second recording period, or (2) atrial electrograms with a very short CL (120 milliseconds or less) averaged over a 10-second recording period” An important limitation of this approach is that the visual appearance of CFAEs is variable and they are often of very low amplitude Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 59 Complex Fractionated Atrial Electrograms (CFAE) Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 60 Autonomic Nervous System Denervation Hyperactivity of the intrinsic autonomic nervous system constitutes a dysautonomia that can lead to a greater propensity for AF Denervation of the autonomic nerves at a few specific sites on that heart that are directly related to arrhythmia formation Ganglionated plexuses are located predominantly in six regions of the atria. In the LA, they are located around the antral regions of the PVs and in the crux. In the RA, they are localized at the junction of the RA and SVC How do you know where they are? Anatomy or vagal response using high-frequency electrical nerve stimulation Endpoint, Outcome, and Repeatability? Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier 61 Superior Vena Cava Isolation62 Proximal SVC contains cardiac muscles connected to the RA, and atrial excitation can propagate into the SVC The SVC myocardial extension harbors most (up to 55%) non-PV triggers of AF (especially in females), and elimination of SVC triggers is associated with improved long-term maintenance of sinus rhythm post–AF ablation. Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Cryothermy Biomechanics Biophysics 63 Pressurized cryorefrigerant Nitrous Oxide (N20) 3 Phases of lesion formation 1. Freeze/thaw phase 2. Hemorrhagic-inflammatory phase 3. Replacement-fibrosis phase Andrade, J, et al. “The Biophysics and Biomechanics of Cryoballoon Ablation.” Pacing and Clinical Electrophysiology.Vol. 35:9, (2012): 1162–1168. DOI: 10.1111/j.1540-8159.2012.03436.x Challenges 64 Phrenic Nerve Palsy (PNP) Pulmonary Vein Stenosis Andrade, J, et al. “The Biophysics and Biomechanics of Cryoballoon Ablation.” Pacing and Clinical Electrophysiology.Vol. 35:9, (2012): 1162–1168. DOI: 10.1111/j.1540-8159.2012.03436.x References 65 Cox JL. “Cardiac surgery for arrhythmias.” PACE. Vol. 27. (2004):266-282. Print. Fuster V, et al. “ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology.” Circ., Vol. 104, (2001): 2118-2150. Print. Issa, Z.F., Miller, J.M., & Zipes, D.P. (2009). Atrial Fibrillation. In Z.F. Issa, J.M. Miller & D.P. Zipes, Clinical Arrhythmology and Electrophysiology (208-284). Philadelphia: Saunders Elsevier Kato et al. “Pulmonary vein anatomy in patients undergoing catheter ablation of atrial fibrillation: lessons learned by use of magnetic resonance imaging.” Circulation. Vol.107. (2003): 2004-10. Print. Konings KT et al. “High-density mapping of electrically induced atrial fibrillation in humans.” Circ. Vol. 89. (1994):1665. Print. Murgatroyd, F.D., Krahn, A.D., Klein, G.J., Yee, R.K, & Skanes, A..C(2001). Atrial Arrhythmias. In Murgatroyd, F.D., Krahn, A.D., Klein, G.J., Yee, R.K, & Skanes, Handbook of Cardiac Electrophysiology (55-71). London: ReMEDICA Publishing Limited Nathan, H., et al. “The Junction Between the Left Atrium and the Pulmonary Veins: An Anatomic Study of Human Hearts.” Circ, Vol. 34, (1966): 412-422. Print. Robbins, ER, et al, “Pulmonary vein stenosis after catheter ablation of atrial fibrillation.” Circulation Vol. 98 (1998) :1769. Print Wijffels et al. “Atrial fibrillation begets atrial fibrillation.” Circ. Vol. 92, (1995):1954.Print. Andrade, J, et al. “The Biophysics and Biomechanics of Cryoballoon Ablation.” Pacing and Clinical Electrophysiology.Vol. 35:9, (2012): 1162–1168. DOI: 10.1111/j.1540-8159.2012.03436.x . Thomas, D., Katus, H., and Voss, F. “Asymptomatic pulmonary vein stenosis after cryoballoon catheter ablation of paroxysmal atrial fibrillation.” Journal of Electrocardiology 44 (2011) 473–476.
