CME: Understanding Pulmonary Vein Recordings: Implications for the Mapping and Ablation of Atrial Fibrillation

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CME: Understanding Pulmonary Vein Recordings: Implications for the Mapping and Ablation of Atrial Fibrillation
Utility of distal coronary sinus (CS) pacing during mapping of the left superior pulmonary vein (LSPV). On the first beat during sinus rhythm, it is difficult to distinguish between left atrial farfield signals and local pulmonary vein potentials, as they
Potentials recorded after ablation in the left superior pulmonary vein (LSPV). On the left panel, during distal coronary sinus (CS) pacing, it is unclear whether the remaining potentials (asterisk) on the circumferential mapping catheter are left atrial a
Targeting of left atrium to pulmonary vein breakthrough points guided by the circumferential mapping catheter. Mapping of left superior pulmonary vein (LSPV) is performed during distal coronary sinus (CS) pacing. The pacing artefact (S) is followed by an
Change in activation sequence observed during radiofrequency (RF) ablation at the ostium of the left superior pulmonary vein (LSPV). During RF ablation targeting LSPV 4-5 (asterisk), a delay and change in the PV activation sequence is observed on the last
Right superior pulmonary vein (RSPV) isolation during ongoing atrial fibrillation. (A) PV electrogram pattern recorded during atrial fibrillation on the circumferential mapping catheter with no consistent pulmonary vein activation sequence. (B) After init
(C) At the end of ablation, during ongoing atrial fibrillation, no pulmonary vein potentials are recorded on the circumferential mapping catheter. (D) Confirmation of the endpoint of PV isolation after restoration of sinus rhythm with no remaining PV pote
Pulmonary vein potentials (asterisks) are abolished during radiofrequency ablation in the left superior pulmonary vein (LSPV) while pacing the distal coronary sinus (CS). Only atrial farfield signals (A) are recorded on the circumferential mapping cathete
Recordings (200 mm/second) from the circumferential mapping catheter in the left inferior pulmonary vein (LIPV) during distal coronary sinus (CS) pacing illustrating one endpoint of electrical PV isolation. On the left panel, prior to ablation, the pacing
Recordings (100mm/second) during sinus rhythm before (left panel) and after (right panel) right superior pulmonary vein (RSPV) isolation. Abolition of the PVP (asterisk) is observed, and only right atrial farfield signals (RA) are recorded on the circumfe
Dissociation of pulmonary vein potentials (asterisks) after electrical isolation of left superior pulmonary vein (LSPV) during coronary sinus (CS) pacing. The discharges remained confined within the LSPV and have no relationship with atrial or ventricular
Author(s): 

Laurent Macle, MD and Peter G. Guerra, MD

The following activity is supported by an unrestricted educational grant from Biosense Webster a Johnson and Johnson company.

Atrial fibrillation (AF) affects up to 5% of the population over the age of 65,1 and it is associated with manifestations ranging from palpitations to heart failure. The prevalence of this arrhythmia is increasing over time, with some projections estimating that by the year 2050, a total of 5.6 million Americans will suffer from AF.2 Thromboembolic events are the most feared complication of this disease; approximately 30% of strokes occurring in patients over the age of 65 can be attributed to AF. Furthermore, data from the Framingham study has shown that AF is an independent predictor of mortality, with a relative risk 1.5-1.9 times greater than that of patients without arrhythmia.3

The difficulty in treating patients with paroxysmal AF is that contrary to patients with a persistent form of the arrhythmia, they tend to be particularly symptomatic of abrupt rhythm changes. In these patients in whom rhythm control appears to be more desirable, pharmacologic treatment has traditionally been the first-line approach. The efficacy of antiarrhythmic drug therapy for the maintenance of sinus rhythm in AF patients ranges from 37-65% (when using amiodarone4), although often at the expense of significant side effects and cost. Even when some measure of control is achieved, approximately half of the patients will experience recurrences within a year. Additionally, all antiarrhythmics carry the potential risk of inducing proarrhythmia, which ranges from 1 to 6 percent.5 For these reasons, alternative methods of treatment have been sought.

Different trials attempting to suppress AF with atrial pacing or more sophisticated overdrive pacing algorithms have shown mixed results with this form of therapy providing, at best, a reduction in the AF burden. Palliative measures such as ablation of the atrioventricular node and pacing have been effective in reducing the symptoms related to AF. However, it is important to bear in mind that this is by no means a curative strategy, and the persistence of AF requires that the patients remain anticoagulated. Furthermore, rendering patients completely pacemaker-dependent is not always an attractive proposition.

Curative therapies are currently being developed both by surgeons and electrophysiologists based on either eliminating the initiating triggers for AF or modifying the substrate for its maintenance. Multiple reentrant wavelets are necessary for perpetuating AF. Surgical incisions (atriotomies) have been shown to prevent paroxysmal or chronic AF by depriving the wandering of wavelets of the spatial extent necessary for their persistence. The challenge for electrophysiologists has been to recreate the success of the surgical approach by using radiofrequency (RF) ablation catheters to create linear lesions in lieu of surgical incisions. However, linear ablation is limited by the fact that current catheters are designed to create point lesions, thus, the catheter must be dragged across the endocardium in order to create a complete line of block. This can be particularly difficult in the ridges and valleys of the posterior left atrium, and incomplete linear lesions may form the substrate for a reentrant arrhythmia.6

References: 

1. Fuster V, Ryden LE, Asinger RW, 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. Circulation 2001;104:2118–2150.2. 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. Benjamin EJ, Wolf PA, D'Agostino RB, et al. Impact of atrial fibrillation on the risk of death: The Framingham Heart Study. Circulation 1998;98:946–952.4. Roy D, Talajic M, Dorian P, et al. Amiodarone to prevent recurrence of atrial fibrillation. Canadian Trial of Atrial Fibrillation Investigators. N Engl J Med 2000;342:913–920.5. Guerra PG, Talajic M, Roy D, et al. Is there a future for antiarrhythmic drug therapy? Drugs 1998;56:767–781.6. Packer D, Johnson S. Origin of unablated discontinuities in linear lesions in the canine atrium (Absr). J Am Coll Cardiol 1998;31:254A.7. Jais P, Haissaguerre M, Shah D, et al. A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation 1997;95:572–576.8. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659–666.9. Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: Electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation 1999;100:1879–1886.10. Gerstenfeld EP, Guerra P, Sparks PB, et al. Clinical outcome after radiofrequency catheter ablation of focal atrial fibrillation triggers. J Cardiovasc Electrophysiol 2001;12:900–908.11. Haissaguerre M, Jais P, Shah D, et al. End point of successful ablation of atrial fibrillation initiated from the pulmonary veins. Pacing & Clin Electrophysiol 1999;22:711.12. Haissaguerre M, Jais P, Shah DC, et al. Electrophysiological end point for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci. Circulation 2000;101:1409–1417.13. Shah D, Haissaguerre M, Jais P, et al. Left atrial appendage activity masquerading as pulmonary vein potentials. Circulation 2002;105:2821–2825.14. Macle L, Jais P, Weerasooriya R, et al. Irrigated-tip catheter ablation of pulmonary veins for treatment of atrial fibrillation. J Cardiovasc Electrophysiol 2002;13:1067–1073.15. Haissaguerre M, Shah DC, Jais P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation 2000;102:2463–2465.16. Yamane T, Shah DC, Jais P, et al. Electrogram polarity reversal as an additional indicator of breakthroughs from the left atrium to the pulmonary veins. J Am Coll Cardiol 2002;39:1337–1344.17. Oral H, Knight BP, Ozaydin M, et al. Segmental ostial ablation to isolate the pulmonary veins during atrial fibrillation: Feasibility and mechanistic insights. Circulation 2002;106:1256–1262.18. Macle L, Jais P, Scavee C, et al. Electrophysiologically guided pulmonary vein isolation during sustained atrial fibrillation. J Cardiovasc Electrophysiol (in press).19. Lu TM, Tai CT, Hsieh MH, et al. Electrophysiologic characteristics in initiation of paroxysmal atrial fibrillation from a focal area. J Am Coll Cardiol 2001;37:1658–1664.

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