Atrial Fibrillation
 RESOURCES FOR PATIENTS

BOSTON A-FIB SYMPOSIUM, January 13-14, 2006

The annual international Boston A-Fib Symposium is one of the most important conferences on A-Fib in the world. It brings together researchers and doctors who share the latest information. Unlike other heart related conferences, it concentrates only on A-Fib. But if you haven't read and understood most of A-Fib.com, it may be difficult reading.

OVERVIEW
    The dominant tone of the 2006 Boston A-Fib Symposium seemed to be one of caution.
    The first warning was about the re-occurrence of "silent" A-Fib in patients considered "cured' of their A-Fib. Dr. Hans Kottkamp of the University of Leipzig, Germany described the use of a seven-day ECG to monitor patients after they were “cured” of their A-Fib by catheter ablation. Over a twelve month period 50% to 60% of cured patients experienced reoccurrences of their A-Fib. 70% of the reoccurrences were silent (asymptomatic) A-Fib. (See Kottkamp.
    A similar alarm was sounded by Dr. Hugh Calkins of Johns Hopkins Hospital who reported results using a seven-day Holter monitor. Over a six month period 31% of "cured" A-Fib patients experienced re-occurrences of their A-Fib, but 82% of these re-occurrences were silent (asymptomatic) A-Fib. (See Calkins.
    Silent A-Fib can be just as harmful as symptomatic A-Fib, according to Dr. John Camm of St. George’s Medical School in London, England. (See Dr. Camm's presentation on Silent A-Fib in the Boston A-Fib Symposium 2004.)
    Caveat: for those of us who have been "cured" of our A-Fib by a catheter ablation procedure, we may still have re-occurrences of silent A-Fib which could be dangerous. It would be a good idea to discuss monitoring for silent A-Fib with your doctor.
   
    A common concern of many of the speakers was the recent deaths and traumatic events due to "atrio-esophageal fistula" where an unintended hole forms between the atrium and the esophagus. This may be due to using high wattage catheters in the back of the atrium near the esophagus. As one speaker put it, "There are only two kinds of Electrophysiologists---those who have not experienced a fistula (hole) in the esophagus and those who have!"
    To minimize the danger of esophageal fistula (holes), Dr. Andre d'Avila of Massachusetts General described an Esophageal Temperature Monitoring device that is inserted in the esophagus next to the heart to monitor whenever the esophagus increases in temperature due to ablation in the heart. But this device is not yet a guarantee of not harming the esophagus. (See d'Avila.)
    Another precautionary technique is to use a barium paste which the patient swallows to show where the esophagus lies in order to avoid making ablations near the esophagus. This was suggested by Dr. Fred Morady of the University of Michigan. (A possible danger of using barium paste in the esophagus is that barium might be breathed into the lungs and damage them.)
   
    Dr. Morady completely reversed his position of two years ago when he was a proponent of the Pappone high wattage catheter "Anatomically Based Circumferential PV Ablation" method. He has abandoned this ablation method in favor of a procedure which identifies spiking A-Fib signals and ablates only them. (See Morady.) It is this author's opinion that the Pappone high wattage catheter ablation procedure may pose serious dangers for patients and may be responsible for the recent deaths and traumatic events from atrio-esophageal fistula (holes).⁷⁹ Another possible complication from the high-wattage catheter is damage to the Phrenic nerve in the Pericardium around the heart which may result in breathing difficulties.

    A major, groundbreaking discovery was presented by Dr. Jose Jalife of SUNY Upstate Medical University in Syracuse, NY. He found that there are sites of high-frequency activity within a heart in A-Fib. When these sites are ablated, A-Fib can be terminated. (See Jalife.)

    How to detect "Complex Fractionated Atrial Electrograms," a new type of heart electrical signal, was discussed by the discoverer Dr. Koonlawee Nademanee of the Pacific Rim EP Research Institute in Inglewood, CA. "CFAE"s, when ablated, can eliminate A-Fib. (See Nademanee.)

    The Bordeaux group's newest procedures for curing Chronic A-Fib were discussed by Dr. Pierre Jaïs. He reported a success rate of 87% (which is remarkable considering how hard it is to cure Chronic A-Fib). (In a later follow-up study a success rate of 95% was reported using a second ablation procedure.^{92(Because of the importance of this article, the complete abstract is cited in the reference section.)} In this author's opinion, this is a major medical breakthrough in the A-Fib field.) He also identified several areas of the heart besides the Pulmonary Veins which produce A-Fib signals, including areas producing Dr. Nademanee's "Complex Fractionated Atrial Electrograms." (See Jaïs)
    (It seemed to this author that several leading doctors in A-Fib were moving to a more individualized approach to curing patients, rather than using a one-size-fits-all procedure. See the presentations of Dr.Jaïs, Dr. Morady, and Dr. Marchlinski.)

    Dr. Waldo's data and conclusions cast doubt on aspirin's effectiveness in preventing stroke from A-Fib. (See Waldo.)

    The Symposium also featured two demonstrations of catheter ablation viewed live via satellite. In France Dr. Michel Haïssaguerre of the Bordeaux group performed an ablation of a woman with Chronic A-Fib. Dr. Vivek Reddy from Massachusetts General Hospital in Boston performed an ablation demonstrating the use of an experimental Cryoablation balloon catheter.

    Also included is an update/summary of the 2006 Boston A-Fib Symposium by Drs. David Keane, Vivek Reddy and Jeremy Ruskin. Though written for the 2007 Symposium, it is included here---Update on Mechanisms and Therapy for A-Fib from the 11^th Annual Boston A-Fib Symposium 2006. (This update is written by doctors for doctors and may be somewhat difficult to read. However, it is an excellent summary not only of the main points of the 2006 Symposium but of all the issues of concern to A-Fib patients today.)

    Each presentation is listed by both the last name and by the topic of the presenter. If a doctor made more than one presentation, they are listed as (1) and (2). You can access a presentation either by the doctor's name or by the topic. (Due to inadequacies of the author, all presentations are not currently summarized.)

 

Dr. Pierre Jaïs, Hôpital Cardiologique du Haut-Lévêque, Bordeaux-Pessac, France discussed Strategies for Catheter Ablation of Long-Lasting Persistent Atrial Fibrillation

    Isolation of the Pulmonary Veins is effective in curing many patients with Paroxysmal (occasional) A-Fib. But this strategy isn't as effective in patients with long-lasting (Persistent and Chronic) A-Fib.
    For patients with long-lasting A-Fib a four-step procedure is used:
    1. Isolation (ablation) of the Pulmonary Veins.
    2. Isolation (ablation) of the inferior left atrium and Coronary Sinus.
    3.  Ablation of other atrial tissue with rapid or different electrical signals such as Continuous Fractionalized Electrograms (see Nademanee).
    4. Linear ablation of the left atrial roof and mitral isthmus.
    Cycle Length (how fast the A-Fib beats) was found to be very important. As the ablations continued the A-Fib cycles became longer, until the A-Fib stopped. People with the fastest A-Fib cycles were less likely to be cured.
    Continuous Fractionalized Electrograms were found throughout the heart and therefore couldn't be used to predict where to ablate. "Rapid or fractionalized electrograms were ubiquitous in both atria, and their interpretation could not be refined in terms of specificity and predictive value for ablation."
    In a later presentation of the results of the live Chronic A-Fib ablation, Dr. Jaïs identified the following sites in the heart that led to conversion from A-Fib to normal sinus rhythm:
    Pulmonary Veins 21%
    Coronary Sinus & Inferior Left Atrium 19%
    Left Atrial Appendage 17%
    Roof Line 12%
    Septum 11%
    Mitral Isthmus Line 10%
    Posterior Left Atrium 4%
    Superior Vena Cava 4%
    Mid Anterior Left Atrium 2%
    In two patients A-Fib ended when the right atrial septum was ablated. In patients who weren't cured, the right atrium had the most rapid A-Fib cycles, suggesting the both the left and right atria may be involved in maintaining A-Fib. (See http://www.medscape.com/viewarticle/515974)
    87% of patients in this study were cured of their long-lasting A-Fib. (In a later follow-up study a success rate of 95% was reported using a second ablation procedure.⁹² In this author's opinion, this is a major medical breakthrough in the A-Fib field. Before this study, curing Persistent/Chronic A-Fib was considered much more difficult and had a much lower success rate than for Paroxysmal (occasional) A-Fib)
    Identifying other areas of the heart (other than the Pulmonary Veins) and different electrical signals responsible for A-Fib may eventually help doctors find a way to achieve 100% success in curing A-Fib.

    Dr. Hans Kottkamp, University Leipzig - Heart Center, Dept. of Electrophysiology, Leipzig, Germany discussed The Frequency and Significance of Asymptomatic A-Fib After Catheter Ablation.

    Dr. Kottkamp warned that patients "cured" of their A-Fib may have "silent" A-Fib reoccurrences. In his study 144 patients with A-Fib were treated by a combination of circumferential and linear lines (ablation lesions). 84% had occasional (Paroxysmal) A-Fib. A 7-day ECG was used before the ablation procedure, after the procedure, and at 3, 6 and 12 months after the procedure. Patients also kept a symptom log.
    Over a twelve month period 50% to 60% of "cured" patients experienced reoccurrences of their A-Fib. 70% of the reoccurrences were silent (asymptomatic) A-Fib.
    Though reoccurrence rates may vary, what is alarming about Dr. Kottkamp's study is the high rate of silent A-Fib in "cured" patients.

Dr. Hugh Calkins, Johns Hopkins Medical Institutions, Baltimore, MD talked about Defining Success Following A-Fib Ablation.

    Dr. Calkins' study concerned the reoccurrence of "silent" A-Fib in patients previously considered "cured" by a catheter ablation procedure, and reinforced Dr. Kottkamp's findings. In a six-month long study "cured" patients wore a 5-day Mobil Cardiac Outpatient Telemetry (MCOT) monitor which recorded their symptoms five days a month. They also kept a log of their symptoms. They telephoned in their monitored heart signals four times a day, and also whenever they had symptoms.
    "Cured" patients were found to be in A-Fib 31% of the time. 82% of these A-Fib attacks were silent (asymptomatic). (In this study 57% of patients who thought they were  experiencing A-Fib symptoms were actually in normal sinus rhythm. Symptoms of shortness of breath and chest discomfort were good predictors of being in A-Fib, whereas skipped beats was a poor predictor.)
    Dr. Calkins suggested a different way of defining success after AF Ablation which he called "reducing the A-Fib Burden," rather than complete elimination of A-Fib symptoms. For example, after a "successful" A-Fib Ablation a patient may go from constant (Chronic) A-Fib to occasional (Paroxysmal) A-Fib which is a "reduction of their A-Fib burden."
    Dr. Calkins discussed a common concern of the Symposium participants, that no current ablation catheters in use today are FDA approved for treating A-Fib. They are "off-label" which means they have been approved for other heart uses but not for treating A-Fib. (This is not unusual in the US medical field. Roughly half of today's current medical devices are used "off-label.")
    Current FDA guidelines for clinical studies of catheters say, "It is most appropriate to evaluate ablation therapy as a palliative therapy and select end points (results) that have the potential to clearly demonstrate a reduction in symptoms caused by A-Fib... For primary effectiveness end point the FDA recommends the relatively unambiguous end point of freedom from symptomatic A-Fib at one year. A blanking (healing) period may be reasonable of at least four weeks."
    Dr. Calkins suggested that being A-Fib symptom free for a year may be an unreasonably high bar to reach. If someone, for example, has a 15-minute A-Fib episode in month eleven, he/she fails the test and isn't considered cured. He recommended a "definition of success other than freedom from all A-Fib episodes."

Dr. Peter Kowey of Lankenau Hospital in Wynnewood, PA talked about Future Directions in Antiarrhythmic Drug Therapy.
 
    He discussed 10 areas of current research and clinical trials. (Most of the drugs mentioned below are still in clinical trials and have not been approved by the FDA.)
1. Carvedilol is a Beta Blocker that is also a Sodium Channel Blocker (Class I) and a Potassium Channel Blocker (Class III). It appears to prevent A-Fib in patients who’ve had a heart attack. (It has been approved by the FDA, but not for A-Fib.)
2. Azimilide Dihydrochlorid blocks both rapid and slow potassium channels in the heart (Class III). Though not very potent for A-Fib, it does seem to prevent shock from implantable defibrillators.
3. Dronedarone is a “congener” (a drug similar to) amiodarone which is currently the most effective antiarrhythmic drug, but also one with the most side effects. Dronedarone seems to have no thyroid or lung toxicity. It appears to work best in young people, and shouldn’t be used in cases of heart or renal failure. (This is perhaps the drug of most interest to A-Fib patients. To have a drug with the effectiveness of amiodarone, but without its side effects would be a major help to many A-Fib patients.)
4. Atrial Selective drugs such as RSD-1235 (only as an IV drug) and AVE 0118. These drugs are intended to affect the potassium current only in the atria and not the ventricles. (All current antiarrhythmic drugs tend to have an adverse effect on the ventricles.) RSD-1235 had an effectiveness of 55%-65% in clinical trials (this is a higher success rate then most antiarrhythmic drugs). (Atrial Selective drugs represent a potential major new development in treating A-Fib.)
5. Atrial Repolarizing Delaying Agents (ARDA) affect potassium and fast sodium currents. They seem to work well after cardioversion to prevent A-Fib from recurring.
6. Gap Junction Modulators. These work on the theory that loss of cell contact in the gap junction may contribute to developing A-Fib. (A gap junction is a junction between cell-types that allows different molecules and ions to pass freely between cells. In the heart, the signal to contract is passed through the gap junctions, allowing the heart muscle cells to contract in tandem.)
7. ACE-I/ARB (Angiotensin Converting Enzyme Inhibitor and Angiotensin Receptor Blocker) may be primary therapy for A-Fib in patients with Congestive Heart Failure and Hypertension. These tend to produce dilation and stretch-induced A-Fib which the ACE inhibitors decrease.
8. Anti-Inflammatory Statins may prevent A-Fib recurrence after cardioversion. Studies have shown that inflammation may be important in the development of A-Fib.
9. Fish oil consumption (from baked or broiled fish, not from fried fish) has shown a decrease in the risk of A-Fib. (This is an important finding for A-Fib patients. Fish oil, a natural remedy, may decrease the risk of getting A-Fib.)
10. Oral Anticoagulants to replace Coumadin. Ximelagatran, which many hoped would replace Coumadin, was rejected by the FDA because of liver toxicity. But there are many other drugs being investigated to replace Coumadin such as Dabigetran which is the furthest along in clinical trials. According to Dr. Kowey, maintaining proper anticoagulant levels “is the most important thing we do for patients.”
    In addition Dr. Kowey answered a question from the audience on home monitoring systems for Coumadin (warfarin). Currently they aren’t well accepted by patients and by insurers who are reluctant to pay for them, and they require a lot of maintenance. The need for monitoring is the single biggest impediment to using Coumadin, especially for young people. But, Dr. Kowey emphasized, if someone is motivated, home monitoring systems can be effective.

Dr. Andre d’Avila of Massachusetts General Hospital in Boston, MA discussed the Role of Esophageal Temperature Monitoring During A-Fib Ablation.

    Esophageal Temperature Monitoring is one of the methods currently being investigated to prevent Atrial Esophageal Fistula (puncturing of the Atrium and Esophagus) during an A-Fib procedure.
    Monitoring the position of the esophagus is important since its position varies from patient to patient and sometimes throughout the ablation process. But Dr. d’Avila stressed that only monitoring the position of the esophagus may be misleading. It may create a false sense of security and/or prevent important RF pulses from being delivered for fear of potential damage.
    It was thought that the presence of micro bubbles at the ablation site would indicate a high esophageal temperature reading. But Dr. d’Avila’s study showed very little correlation between micro bubbles and high esophageal temperature. “Despite the presence or absence of type 1 micro bubbles, you can have very high esophageal temperatures at very low power.”
    35 Watts can not be used as a cutoff for safety when one approaches the exterior wall (of the esophagus). Even at 15-30 Watts it is possible to record esophageal temperatures as high as 41 degrees.
    Dr. d’Avila stated his conclusions about the possibility of creating fistulas during the A-Fib procedure:
1. It doesn’t matter how experienced a doctor is doing ablations
2. It doesn’t matter what particular ablation technique is used (It seems to this author there is more of a chance of fistula using the Pappone high wattage drop and drag technique than with other methods.⁷⁹)
3. You can’t rely on the thickness of the left atrial tissue to decide whether or not you will be delivering a safe pulse.
4. Using low power may be helpful in avoiding fistula when ablating at the left atrial posterior wall, but may be misleading. You can have very high esophageal temperatures even at 20 Watts.
5. Short ablation times doesn’t seem to be very helpful. You can reach very high temperatures at only 20-30 seconds.
    Dr. d'Avila advocated using PVI guided by esophageal monitoring. But he pointed out the following limitations to this strategy:
    1. It depends on contact between the probe and the esophageal wall. The exterior wall of the esophagus may experience a higher temperature than registered by the esophageal monitor depending on the proximity of the probe to the esophageal wall. “The problem is when you don’t have high esophageal temperatures and you are very close to the esophagus. In that situation esophageal monitoring depends on contact and may create a false sense of security when normal temperatures are recorded during ablation.”
    2. General Anesthesia is needed to insert the esophageal probe.
    3. There is no animal model to prove this strategy.
    Dr. d’Avila concluded that:
    1. 80% of current procedures may produce high esophageal temperatures
    2. Monitoring of esophageal temperatures allows for the isolation of all Pulmonary Veins despite the proximity of the esophagus, since pulses may be delivered which do not result in high esophageal temperatures.
    3. “High esophageal temperatures indicate some sort of esophageal damage.”

 

Dr. Fred Morady of The University of Michigan discussed "An Individualized Approach to Catheter Ablation for Atrial Fibrillation."

    Dr. Morady was formerly a proponent of the Pappone high wattage "Anatomically Based Circumferential PV Ablation" method. But after two episodes of esophageal fistula (holes in the esophagus), he now uses a variety of approaches depending on the individual patient. Dr. Morady’s reasons for this individualized approach are:
    1. A one-size-fits-all approach does not fit all patients. There is "a vast variability and differences between patients with A-Fib."
    2. An individualized approach requires less ablation of heart tissue which is better for patients. (Dr. Morady’s patients average about 32 minutes of ablation burn time, compared to 46 minutes with Circumferential PV Ablation.)
    3. An individualized approach can identify important drivers and triggers of A-Fib in patients, and thereby provide insights into the actual mechanisms of A-Fib.
    4. With this individualized approach, eliminating a patient’s A-Fib can be reliably demonstrated, (when a high dose of isoproterenol does not induce A-Fib).
    Before starting the ablation procedure, he uses a barium paste in the esophagus to avoid ablating near the esophagus. (Author's note: A possible danger of using barium paste in the esophagus is that barium might be breathed into the lungs and damage them. The author has no hard date to support this warning, only anecdotal reports.) Then he uses a lasso catheter to map the Pulmonary Veins.
    In the ablation procedure he first tries to eliminate Pulmonary Vein A-Fib triggers by Ostial PV Isolation. (He found in some patients that none of the Pulmonary Veins have A-Fib triggers.) If the patient’s A-Fib has not been eliminated by the PV ablation, he may use the following:
    Wide Area PV Ablation
    Linear Ablation
    Superior Vena Cava Isolation
    Ablation of Fractionated Electrograms in the Left Atrium (particularly the septum and roof of the heart), the Right Atrium, and the Coronary Sinus
    Ablation of Ganglionated Plexi
    Answering a question from the audience Dr. Morady said he uses an irrigated catheter with 20 second bursts of RF energy at 25-35 Watts.
    His success rate for Paroxysmal (occasional) A-Fib patients is 84% with an 18% redo rate.
    (To this author Dr. Morady’s individualized approach seems more promising for patients and safer. Dr. Morady gave many examples of the vast variability of patients with A-Fib, how a one-size-fits-all approach would not have eliminated many non-PV drivers. His individualized approach, like that of Dr. Jaïs and the Bordeaux group, may lead to finding more elusive A-Fib triggers and a higher success rate for A-Fib ablation.)

 

Dr. David C. Kress of the Midwest Heart Surgery Institute talked about "Advances in Surgical Therapy for A-Fib."

    Dr. Kress briefly discussed the classic Cox Maze 3 (open heart surgery in which the heart is cut and sewn back together to eliminate A-Fib) and the Radial Incision approach (Radial Maze). The Radial Maze produces better left atrial activation and better left atrial transport function (the left atrium pumps blood better^a). Though the Cox Maze 3 has a good success rate (97%), it is performed relatively infrequently because it is so traumatic for the patient.
    Dr. Cox also developed what he called a Mini Maze operation that involved fewer incisions in the heart and chest (a similar operation is the "Quarter 3"). But this operation still involved cardiopulmonary bypass, and the cutting and sewing of the heart. He also added a PV encircling lesion, left atrial isthmus lesion with coronary sinus lesion, and a right atrial isthmus lesion.
    A European version adds connecting lesions from the isolated PVs across the dome of the heart roof and over to the Mitral Valve.
    (Currently the term "Mini Maze" more often refers to the minimally invasive operations described below.)
    Dr. Kress mainly focused on minimally invasive surgery which does not involve open heart surgery. He explained that there are essentially two concepts for minimally invasive operations:
    Concept 1. Bilateral PV Isolation Using Bipolar RF (the Wolf Mini Maze), also called "Thorascopic Bipolar Isolation with EP Testing" by Dr. Randall K. Wolf. In the Wolf Mini Maze the surgeon cuts openings between the ribs, then uses a probe to punch through the pericardium (a sack around the heart) to access the heart (scissors or scalpels are not used). To encircle the PVs and heart, the lungs have to be alternately deflated and re-inflated. Using a bipolar RF clamp the surgeon makes transmural lesions (lesions that go through the wall of the heart) around the pulmonary veins and heart. The left atrial appendage is also cut and removed, and the opening of the left atrial appendage is stapled closed. The pericardium is then sewn back together. A patient can leave the hospital after only one or two days and can return to normal activities within a short time. (A video of this operation is found at http://www.or-live.com/healthalliance/1217/.)
    (The left atrial appendage is removed because clots are more likely to form in that area. There is some controversy about whether removal of the left atrial appendage is justified if the patient is no longer in A-Fib.)
    (The Journal of Thoracic and Cardiovascular Surgery has admonished a Un. of Cincinnati surgeon (Dr. Wolf) for failing to disclose financial ties to AtriCure, the West Chester, (Ohio) maker of heart-surgery equipment he and other researchers evaluated in a published study."⁸¹)
    Concept 2. Box Lesions around all four Pulmonary Veins using a Microwave Antenna (Saltman---the "Microwave MiniMaze"). Instead of bipolar RF clamps, the Microwave MiniMaze uses guide catheters to position microwave antennas around the Pulmonary Veins. Microwave energy is delivered at 65 Watts for 90 seconds. Also, a lesion is created from the left atrium appendage into the transverse sinus, connecting it to the Pulmonary Vein "box" lesion. The left atrial appendage is not removed but is usually stapled closed.
    Preliminary results are very positive. In a study by Dr. Wolf involving 27 patients, 91% were free of A-Fib after three months. According to Dr. Kress, "We can probably substitute the bipolar RF clamp operation (the Wolf Mini Maze) for the cut-and-sew portion of the Cox Maze 3." Dr. Kress also mentioned that there have been some instances of esophageal fistula in the early days of some of the Mini Maze operations.
    Dr. Cox wrote this comment on the minimally invasive operations. "None of the present energy sources...are capable of creating the left atrial isthmus lesion from the epicardial (outside the heart) surface, because of the necessity of penetrating through the circumflex coronary artery to reach the left atrial wall near the posterior mitral annulus."⁶⁶
    Dr. Kress also mentioned the work of Dr. Mack in Dallas who uses Argon Cryoablation in his Mini Maze operations. He reported a 90% success rate.
    Answering a question from the audience, Dr. Kress said that in the future surgeons and electrophysiologists might work together to identify conduction block and the presence of ganglia that produce A-Fib signals. Dr. Wolf (University of Cincinnati) and Dr. Jackman (Oklahoma University) are conducting a multi-center study involving this sort of collaboration.
    When asked why some patients required pacemakers after a Mini Maze, he hypothesized that the Mini Maze lesions may affect the blood supply to the sinus node which may result in Sick Sinus Syndrome.
    (From this patient’s perspective, operations such as the Wolf Mini Maze are no longer "experimental." These minimally invasive operations represent a new option for the treatment of A-Fib. The Mini Maze is probably a very important option for someone who can not tolerate anticoagulants. But a word of caution---these are surgical operations with the potential risks and complications of surgery.)
    ^aThe Radial Maze was developed by Dr. Cox as a refinement of his Maze operation. He found that in patients after the Maze operation, "left atrial transport function was significantly less than in normal control subjects." He hypothesized this was because:
    1. the incisions isolating the pulmonary veins also eliminate approximately 29% of the left atrium from contributing to the transport function.
    2.  because of the complexity of the incisions, they may inhibit the activation and contraction of nearby atrial segments.
    3. the incisions may prolong atrial activation time, thereby desynchronizing the atria and ventricles.
    4. some of the Maze incisions may interrupt the atrial coronary arteries, impairing heart circulation.
    Whereas in the Radial Maze operation the incisions parallel the direction of the atrium's activation and the direction of the blood supply. No part of the atrium is electronically or mechanically isolated. This produces better left atrial activation and better left atrial transport function.
    Annals of Thoracic Surgery 1999;67:27-35.

 

Dr. Koonlawee Nademanee of the Pacific Rim EP Research Institute in Inglewood, CA discussed Automating the Detection of Complex Fractionated Atrial Electrograms (CFAEs).

    Dr. Nademanee is the discoverer of CFAEs, a new tool to help doctors identify sources of A-Fib signals in the heart.
    Dr. Nademanee defined Complex Fractionated Atrial Electrograms as follows: (an electrogram is a picture of the electrical activity of the heart as sensed by a pacemaker or catheter in the heart).
    "a) atrial electrograms that have fractionated (divided) electrograms composed of two deflections (turns or bends) or more, and/or have a perturbation (disturbance) of the baseline with continuous deflection of a prolonged activation complex (a long A-Fib signal),
    b) atrial electrograms with a very short cycle length (< 120 ms).
In general, CFAEs are usually low voltage multiple potential signals between 0.05-0.25 mV (milleVolts)."
    These low voltage signals are close to the levels of background noise found in heart monitoring systems, and require operator experience and expertise to manually identify them. "...identifying and tagging CFAEs...is subjective and heavily dependent on operator experience."
    Manual mapping of the CFAEs is always done while the patient is in A-Fib. If the patient is in normal sinus rhythm, A-Fib is induced by giving the patient isoproterenol or through atrial pacing (using an electrical signal to stimulate the heart). Once the CFAEs are located during CARTO mapping (a mapping system that uses a special catheter to generate 3-D maps of the heart), the CFAEs are ablated. If the A-Fib or Atrial Flutter continues, the remaining sources of A-Fib signals are identified and ablated. If the A-Fib and/or Atrial Flutter are not successfully terminated, external cardioversion is performed.
    (Dr. Nademanee’s approach differs from other doctors in that he first identifies and ablated CFAEs, then he looks for other sources of A-Fib signals in the heart. Whereas Dr.Jaïs and Dr. Morady, for example, first try to identify and ablate sources of A-Fib in the Pulmonary Vein openings before identifying and ablating other sources of A-Fib such as CFAEs.)
    Dr. Nademanee described new software that identifies the CFAEs and displays them in a CARTO map. The CFAEs are color coded according to the degree of fractionated signals and their cycle lengths. This software provides better accuracy and considerably shortens the time of mapping. However, manual evaluation and editing of the resulting map is necessary, "because the (current) software has inherent weakness in detecting noise and also precisely recognizing the beginning and end of the complex."
    (From this patient’s perspective, CFAEs and the software used to identify them may prove to be an important tool to help find and ablate the more elusive sources of A-Fib in the heart.)

 

Dr. Warren Jackman of the University of Oklahoma discussed the Relationship Between Locations of Autonomic Ganglionated Plexi and Sites of Complex Fractionated Atrial Electrograms and/or High Frequency Electrograms During A-Fib.

    Dr. Jackman discussed the location and importance of Autonomic Ganglionated Plexi. (The Autonomic Nervous System controls the heart and smooth muscle tissue and involuntary actions.) (Ganglionated Plexi are areas of the atria containing clusters of nerve cells.) There are seven areas of Autonomic Ganglionated Plexi in the atria, four in the left atrium, three in the right. These Ganglionated Plexi areas are located near but not in the Pulmonary Veins, and may be involved in producing Complex Fractionated Atrial Electrograms and A-Fib.
    In experimental studies using dog models, it was found that areas of Fractionated Atrial Potentials are close to and are "located primarily in the regions surrounding Ganglionated Plexi." ("Fractionated Atrial Potentials" is the name Dr. Jackman uses for Dr. Nademanee’s "Complex Fractionated Atrial Electrograms.") According to Dr. Jackman, "There is a distinct relationship or requirement for some degree of stimulation from the Ganglionated Plexi in order to have Fractionated Electrograms."
    He also hypothesized that stimulating the Ganglionated Plexi increases calcium loading and calcium release which may trigger Fractionated Electrograms ("Calcium Transient Triggered Firing Hypothesis").
    (Dr. Jackman’s studies may make it easier to identify and locate Complex Fractionated Atrial Electrograms since they are located primarily in the Ganglionated Plexi areas. They may also show how Fractionated Electrograms and A-Fib are generated.)

Dr. Frank Marchlinski of the University of Pennsylvania discussed "Non-Pulmonary Vein Triggers for A-Fib: Provocation, Recognition, Location, and Relationship to Chronicity of A-Fib."

    Dr. Marchlinski described the protocol for ablating patients with A-Fib that he and his colleagues use:

1. He begins by using programmed stimulation to screen for Accessory Pathway/AVNRT (Atrioventricular Node Reentry Tachycardia). In AVNRT the AV Node develops two pathways instead of one, allowing a signal to go down one pathway, then back up the other pathway to the atrium (Reentrant Circuit) resulting in Supraventricular Tachycardia (speeding up the heart beat). He found that 4% of his patients who had A-Fib actually had AVNRT instead, and could be cured without having to go through a regular Pulmonary Vein Ablation (Isolation) procedure.
2. Both before and after PV isolation he initiates PV and non-PV triggers for A-Fib:
       -If a patient is in Persistent/Permanent A-Fib, he first cardioverts them, then identifies areas of early reoccurrence of A-Fib.
       -If a patient is in sinus rhythm, he gives them isoproterenol in increments of 3, 6, 12, 20 mcg/minute to stimulate them into A-Fib (with a Median dose of 12 mcg/minute).
       -If the spontaneous triggers still haven't been provoked, he induces A-Fib by burst pacing. He cardioverts the patient, then identifies areas of early reoccurrence of A-Fib.
       -He then repeats this initiation of A-Fib while administering low dose isoproterenol.

    This protocol adds about 1/2 hour to the ablation procedure time.
    Dr. Marchlinski and his colleagues found that 15% of their patients had non-Pulmonary Vein A-Fib triggers (113 out of 761 patients), and 3% had only non-PV triggers. These non-PV triggers were found in the following areas of the heart:
        Right Atrial Appendage
        Superior Vena Cava
        Crista Terminalis
        Tricuspid Valve Annulus
        Eustachian Ridge
        Fossa Vallis
        Septum
        Posterior Wall of Left Atrium
        Mitral Annulus
        Epicardial Coronary Sinus
    Preliminary data suggest that such factors as gender, race and type of A-Fib may influence where non-PV triggers are found.
    ---Women have more only non-PV triggers than men;
    ---Race seems to affect where non-PV triggers are found in the heart;
    ---Patients with Persistent/Permanent A-Fib seem to have more non-PV triggers.
    In addition, Dr. Marchlinski found that patients with only non-PV triggers had a higher success rate of being cured of A-Fib than other patients (91%).
    (Dr. Marchlinski and his colleagues' work seems to be very promising for patients.
    By limiting ablation only to identified trigger sites, he decreases the amount of burn lesions in the heart versus one-size-fits-all procedures. This lowers the risk of ablation proarrhythmia [where the ablation process may stimulate arrhythmias], and decreased atrial circulation and transport [blood doesn't circulate in the heart walls as well and the heart doesn't pump as well because of ablation lesions].
    By identifying patients with AVNRT and with only non-PV A-Fib triggers, he seems to increase their chances of being cured of A-Fib. Whereas with a one-size-fits-all approach, many non-PV triggers may not be ablated or isolated.
    By adding to our knowledge of non-PV A-Fib trigger sites, he increases our understanding of the physiology and anatomy of A-Fib. His work seems related to and moving in the same direction as that of Dr. Jaïs and Dr. Morady.)

Dr. David Wilber of Loyola University Medical Center discussed "Left Atrial Function & Remodeling Before and After Catheter Ablation or Surgery for A-Fib"

    Dr. Wilber’s presentation focused on the structural and mechanical changes that affect the heart in A-Fib, and whether any of these remodeling effects can be reversed by eliminating  patients' A-Fib. Some of the remodeling effects associated with A-Fib are:
    a) Increased left atrial size
    b) Decreased left atrial contractual and reservoir function (reservoir function refers to the capacity of the left atrium to expand and accept blood flow)
    c) Pulmonary Vein expansion
    d) Atrial fibrosis (the formation of fibrous tissue) and scarring
    e) Increase in Left Ventricle size, decrease in LV Systolic and Diastolic function.
    When a patient is restored to normal sinus rhythm (after an ablation procedure or after surgery), how much of this remodeling effect is reversed? Dr. Wilber discussed several surgical and catheter ablation studies that addressed this question.
RADIAL MAZE SURGERY STUDIES
    In one study, after patients were restored to normal sinus rhythm, left atrial size declined and contractual function improved, but they didn't return to normal. "In every surgical study, (left atrial) function, even though it returned, it remained at dramatically reduced levels." Most of the improvement occurred in the first month.
    A second provocative surgical study investigated whether the Radial Maze linear lesions operation impaired atrial function even though it cured the patients' A-Fib. After two years, cured patients in the treatment group still had an abnormal, stiff left atrium. Also, their left atrium volume was 30% more than normal, and their atrial function was still reduced. Whereas, in the control group who were cured by cardioversion, the left atrium returned almost back to normal. (This study may be particularly important for young people or athletes with A-Fib who are considering a catheter ablation procedure or surgery. A successful cardioversion may be better at restoring normal heart function after A-Fib than surgery or extensive catheter ablation procedures.)
CATHETER ABLATION STUDIES
    After successful ablation, Dr. Pappone found a 15-20% reduction in size of the left atrium, and some improvement in atrial function. A Dr. Chen study and a Dr. Hopkins study, using the less destructive Segmental Ostial ablation procedure, found a decrease in volume both in the left atrium and the pulmonary vein openings. A Netherlands study using a more extensive procedure with circumferential ablation and linear lesions, also found a reduction in size of the left atrium. A Un. of Michigan study using circumferential ablation and linear lesions found a decrease in left atrium size, but also the Ejection Fraction (how well the atrium pumps) fell even further than before the successful A-Fib ablation.
    A Bordeaux group study using Pulmonary Vein Isolation (Segmental) and Linear Lesions with an average follow-up of eleven months showed that left atrial volumes fell, but also that left atrial contractual and filling function almost returned to normal for Paroxysmal patients. For Chronic patients, left atrial contraction was low after ablation, but after eleven months it improved considerably. The study also showed improvements in ventricular, diastolic and systolic function. This improvement occurred even if patients had reoccurrences of A-Fib. According to Dr. Wilber, this data is somewhat at odds with other studies of catheter ablation.
CONCLUSION
    Dr. Wilber concluded that most of the data showed that after successful A-Fib ablation:
    1. There is a moderate decrease in size of the left atrium, but it doesn't return to normal.
    2. Left Atrial contractual and reservoir functions remain abnormal.
    (Perhaps the most important point Dr. Wilber raised concerned, "...the potential deleterious (bad) effects of (catheter) ablation procedures on contractual and reservoir functions (of the left atrium)... Can we design a procedure that will optimize recovery?" Particularly for young people and athletes, years down the road how will their left atrial dysfunction affect their quality of life, exercise tolerance, performance, etc?
    Another very important point he raised was that the more extensive ablation procedures may be related to or cause decreased atrial function.) 
   
Dr. Douglas Packer of the Mayo Clinic in Rochester, MN discussed "Surgical and Catheter-Based Strategies for Stroke Prevention in A-Fib"

    One of the major dangers of having A-Fib is the risk of stroke. Dr. Packer cited some sobering statistics concerning A-Fib related strokes:
    ---Of the 500,000 strokes per year in the U.S., 25% are caused by or are related to A-Fib.
    ---70% of A-Fib related stroke patients die or develop severe neurological problems.
    ---Patients with A-Fib have 5 to 6 times greater probability of having  a stroke and 18 times greater probability of an embolic event (a clot that doesn't cause a stroke).
    ---35% of A-Fib patients who are not treated with anticoagulants will have a stroke in their lifetime.
    ---Strokes are age dependent. For A-Fib patients over 80 years old, 30-35% of strokes are attributed to A-Fib.
    Dr. Packer pointed out that most strokes come from the Left Atrial Appendage (91%) which is a very complicated structure with often more than one lobe. In A-Fib the flow of blood from the Left Atrial Appendage is particularly poor. Clots can easily form and cause stroke.
REMOVING THE LEFT ATRIAL APPENDAGE
    He cited a surgical study in which 25% of patients undergoing open heart surgery had their Left Atrial Appendage cut out. In the follow-up study patients who did not have a stroke were usually the ones who had had their Left Atrial Appendage removed. Though there is controversy about this because of bleeding and partial ligations (sewing up the cut heart).⁶⁷
    Dr. Packer discussed whether catheter based procedures can close off the Left Atrial Appendage (LAA) without the risks of surgery. Catheter based Occlusion Devices (PLATTO, Watchman) are currently in clinical trials. In this procedure a catheter guide sheath with the Occlusion Device is positioned inside the Left Atrial Appendage, then the sheath is withdrawn and the device expanded to tighten in place and close off the LAA. This procedure takes about one hour. Preliminary results seem promising.
    (Dr. Packer raised an important question of who would receive or need these Occlusion Devices. When and if these Occlusion Devices are approved, should a doctor doing a catheter ablation procedure routinely close off the Left Atrial appendage in case a patient's A-Fib isn't completely cured? Or should an Occlusion Device only be used for patients who need to be off of anticoagulants?
    Dr. Packer raised another very important point both for doctors and for patients. He read a letter from a major insurance company which rejected a patient for coverage based on the patient being on coumadin, "...because of the many unforeseen complications and side effects which may result from the continued use of coumadin." It's very alarming that insurance companies would take over the role of the doctor and dictate what meds a doctor and patient can use. It would be a major crisis for A-Fib patients if people taking coumadin were routinely denied health insurance. However, pragmatic reality could one day dictate the use of Occlusion Devices, so that someone with A-Fib wouldn't have to take coumadin and could be covered by medical insurance.)

Dr. Carlo Pappone of San Raffaele University Hospital in Milan, Italy discussed "The Use of Remote Magnetic Navigation in Catheter Ablation for A-Fib."

    Dr. Pappone showed a video of a stereotaxis robotic navigation system which uses a computer and magnetic fields to image the heart and control the ablation catheter. The system synchronizes fluoroscopic and CARTO mapping to create a 3-D real time image of the heart. This system produces perfect ablation lines and uses a maximum of only 4 grams of pressure on the heart wall. Soon the system will be able to do automatic ablations and remote robotic ablations just by moving a mouse. Dr. Pappone thinks this robotic navigation technique will be the most important application for A-Fib in the next two years.
    Dr. Pappone said that he averages only 45 minutes doing a Circumferential Pulmonary Vein Ablation (he can do seven ablations a day). (See  Pappone and the Pappone Method.) He now uses an irrigated catheter with a 4mm tip at a maximum of 65° at 70 Watts.
    Dr. Pappone also talked about a new refinement of his Circumferential Pulmonary Vein Ablation procedure. He found that ablating the vagal ganglia (areas of the heart where vagal reflex can be stimulated) significantly reduces recurrence of A-Fib after 12 months.
    In another study Dr. Pappone compared A-Fib patients who had a Circumferential Pulmonary Vein Ablation procedure with patients who received antiarrhythmic drug therapy. After a median follow-up of 900 days, survival for ablated patients was longer than among patients treated medically, and the same as healthy persons. Ablated patients' "Quality of Life" reached normal levels at six months and remained unchanged after one year. This differed from patients receiving medical therapy. "Pulmonary vein ablation improves mortality, morbidity, and quality of life as compared with medical (drug) therapy."
    Dr. Pappone discussed that catheter ablation is difficult to do on A-Fib patients who have an artificial Mitral Valve, because of the increased risk of damage to it. But he found that Circumferential Pulmonary Vein Ablation is feasible for patients with an prosthetic Mitral Valve, with outcomes similar to those of standard patients.
    (Author's Note: Dr. Pappone's Circumferential Pulmonary Vein Ablation procedure may become the ablation procedure used by most doctors and medical centers, because it is more cost effective, easier to learn, and is less dependent on operator skill than other procedures. However, there are currently some criticisms of this procedure that patients should be aware of:
    ---The use of high wattage catheters may lead to damage of the esophagus [see d'Avila] and Atrial Esophageal Fistula---a hole in the atrium and esophagus which often results in death.
    ---The extensive scarring of the atrium in Dr. Pappone's procedure may possibly lead to impaired functioning of the left atrium [see Wilber].)
 
Dr. Vivek Reddy of Massachusetts General Hospital in Boston, Massachusetts discussed "The Use of Remote Robotic Navigation in Catheter Ablation for A-Fib."

      Dr. Reddy described a system that uses a robotic arm catheter ("Steerable Guide Catheter") with a deflectable sheath that can bend in multiple levels and directions.  This "sheath-within-a-sheath" system uses both an internal guide sheath and an outer sheath (which bend and move independently) to remotely navigate and ablate within the heart.
    This robotic catheter system is combined with electroanatomical mapping and 3-D Computed Tomography (similar to a CAT Scan). The physician, using a 3-D joystick, sees both a cartoon rendering of what the system estimates the catheter is doing, and real time fluoroscopic (X-ray) images. The system software combines the images. Any standard ablation catheter can be used with this system. Dr. Reddy described how in going through the transseptal wall, for example, one operator uses the joystick while another is at the operating table to advance the needle and dilator through the transseptal wall.
    In discussing safety issues Dr. Reddy said this robotic catheter system maintained firm contact with heart tissue to produce better lesions, but that there might be a potential for perforation. Future systems should have "contact sensing strategies" to identify the degree of contact or pressure of the catheter on the heart tissue. "This is probably the future for all catheter ablation procedures."
    Dr. Reddy mentioned that Dr. Natale at the Cleveland Clinic and Drs. Haïssaguerre and Jaïs in Bordeaux, France have also used this system, but only around 30 patients have been treated so far.
    Dr. Reddy described how using this system cured a patient in Chronic A-Fib which is harder to cure than other types. After ablating the Pulmonary Veins, he made roof and Mitral isthmus lines. Then he made several lesions near the base of the Left Atrial Appendage, along the anterior Septum, and in areas of Fractionated Potentials. At this point, the A-Fib rhythm organized into Atrial Flutter, a more organized arrhythmia. He then went into the right atrium and made a Cavotricuspid isthmus lesion line which put the patient into sinus rhythm.
    Dr. Reddy said he believes that remote navigation for catheter ablation, whether magnetic (see Pappone) or robotic, will change the field of catheter ablation for A-Fib.

Dr. Moussa Mansour of Massachusetts General Hospital in Boston, MA discussed "Three Dimensional Left Atrial Anatomy: Implications for Catheter Ablation."

     Dr. Mansour presented data that 42% of A-Fib patients have an atypical, unusual left atrium structure. This complex anatomy of the left atrium must be understood in order to perform a safe and effective ablation procedure. Some of the non-normal anatomical structures often found in the left atrium are:

1. Instead of the normal four Pulmonary Veins, 16-26% of patients have a fifth vein between the right superior and right inferior Pulmonary Veins.  Instead of isolating (ablating) around each of the right PVs, all three Pulmonary Veins must be isolated as a single group.
2. Approximately 3% of patients have a third Pulmonary Vein above the right superior PV. A normal circular ablation (isolation) around the right superior PV might damage and/or close this third PV. The encircling ablation lesions must be made wider to include this third vein.
3. In 16-32% of patients the left superior and left inferior Pulmonary Veins have a common opening which can be quite large. Normal circular mapping catheters are too small to adequately map this opening, and ablation catheters can mistakenly ablate within this opening and damage it. Imaging techniques such as Intracardiac Ultrasound (Echo) can be used to identify and isolate this large vein opening.
4. Many patients have ridges in their atrium, particularly between the Left Atrial appendage and the Left Superior Pulmonary Vein. It's hard to position an ablation catheter over these ridges. An ablation line must instead be made at the base of the Left Atrial Appendage.
5. The Mitral Valve Isthmus is often very long and may extend beyond the Coronary Sinus. Ablation of the Mitral Isthmus can be challenging. Creation of an incomplete line can leave gaps which can result in atypical flutter after PV Isolation. Completion of this line requires ablation within the Coronary Sinus in 50% of patients.
6. Pulmonary Vein openings are often not circular but can be oval and irregular, requiring careful placement of the isolating ablation lines.  

    Dr. Mansour also pointed out that both the Cardiac Cycle (the beating of the heart) and the Respiratory (breathing) Cycle change the location of the Pulmonary Veins. Any imaging technology must record images of the inside of the heart at the same place in the Cardiac and Respiratory Cycles.
    Dr. Mansour concluded that pre-procedure imaging and mapping is essential for patients having an A-Fib ablation procedure, in order to determine whether the patient has a typical or atypical atrium.
    (Author's Note: A one-size-fits-all ablation strategy may not work for the many patients who have an atypical atrium structure.) 

Dr. Marcus Wharton of the Medical University of South Carolina in Charleston, SC discussed "Atypical Atrial Flutter During and After A-Fib Ablation: Incidence, Physiology, and Management."

    After an A-Fib ablation procedure, some patients develop Atrial Flutter. Conditions that contribute to developing Flutter are:
    ---Chronic or Persistent A-Fib
    ---A past history of Flutter
    ---Atrial disease, scarring, and/or previous heart surgery
    ---An enlarged left atrium
    In addition, patients undergoing a Wide Area Circumferential Ablation procedure (see Pappone Method) have a 3-35% chance of developing flutter in the long term.
TYPICAL ATRIAL FLUTTER
    Dr. Wharton described Typical Atrial Flutter as Flutter originating in the Right Atrium. During an A-Fib ablation procedure, he routinely ablates the Cavotricuspid Isthmus (the area between the Tricuspid Valve Annulus and the Inferior Vena Cava in the right atrium) to prevent Right Atrial Flutter. If this Cavotricuspid Isthmus is not ablated, 10-15% of patients will develop Typical Atrial Flutter.
ATYPICAL ATRIAL FLUTTER
    He described Atypical Atrial Flutter as coming from the Left Atrium. The mechanisms or patterns of Left Atrial Flutter are:
    1. Macroreentry around the Pulmonary Veins ("Macroreentry" refers to  abnormal Flutter electrical circuits circling around the atrium)
    2. Macroreentry through gaps in linear lesions
    3. Macroreentry in the Pulmonary Veins
    4. Focal Flutter signal sources within the Pulmonary Veins
    5. Focal Flutter signal sources other than within the Pulmonary Veins.
    Within the first two months after catheter ablation to cure A-Fib, 9% of patients will develop Atypical Atrial Flutter. But most of these patients can be cardioverted and will return to normal sinus rhythm. However, 2-3% may remain in Atrial Flutter.
    Approaches to cure Flutter in these patients are:
    1. Re-isolate the Pulmonary Veins and non-PV focal sources to eliminate the triggers for Flutter.
    2. Make Mitral Isthmus and Left Atrial Roof lesion lines to cut off Macroreentry circuits around the Pulmonary Veins and Mitral Annulus. Dr. Wharton pointed out that it's difficult to achieve complete block when making these line lesions. And any gap may actually be "proarrhythmic" (may increase Macroreentry Flutter circuits). "If we can't achieve complete isolation, we potentially may be creating more harm than good with these lesions." He also pointed out that in two-thirds of his patients, in order to achieve complete block, the Mitral Isthmus line lesion had to be extended to ablate within the Coronary Sinus (which can be risky).
CONCLUSION
    Dr. Wharton concluded that Mitral Isthmus and left Atrial Roof lesion lines may improve success rates in curing/preventing Atrial Flutter in all varieties of A-Fib. He also suggested that ablating Complex Fractionated Atrial Electrograms and Autonomic Denervation (ablating sites or ganglia of the Autonomic nervous system) may also help cure Atrial Flutter.
    (For someone considering a Right Atrium Ablation procedure to cure Flutter, some Flutter may originate from the left atrium. Consequently, a Right Atrium Ablation procedure might not cure Atrial Flutter.)

Dr. Michael R. Gold of the Medical University of South Carolina in Charleston discussed "Pacing to Prevent A-Fib and CHF (Congestive Heart Failure)---the Role of Lead Position and Pacing Algorithms."

    Older A-Fib patients often have bradycardia (slow heart rate) from sick sinus syndrome. Pacing (the insertion of a  pacemaker) helps these patients, but is of no benefit to A-Fib patients who don't have Bradycardia.
    Dr. Gold stated that pacing "...is not curative therapy" for A-Fib. Though atrial pacing may reduce A-Fib, the improvement is modest. "Pacing should be used primarily in (A-Fib) patients who need pacing for other reasons." Dr. Gold pointed out that earlier retrospective (after the fact) studies had shown a marked reduction of A-Fib with atrial based pacing compared with ventricular pacing alone (VVI mode). But more recent prospective randomized studies have shown a more modest benefit.
    Discussing the various pacing methods for A-Fib, Dr. Gold stated that Atrial Pacing (AAI mode) is more effective than Right Ventricular Pacing (DDD mode) which may actually increase A-Fib.
    Other pacing methods and factors that improve A-Fib are:
    ---Cardiac Resynchronization pacing (CRT), a biventricular pacing mode.
    ---Dynamic Atrial Overdrive pacing where the atria are paced 100% of the time.
    ---Placing the pacemaker leads in the high Septum area works better than placing the leads in non-Septum areas.
    Ablation of the AV Node and insertion of a permanent pacemaker was a common A-Fib treatment. However, it is now used less frequently in the era of ablation procedures which cure A-Fib. There is a small risk of sudden death following AV Node ablation, which can be minimized with higher pacing rates in the first several months following ablation.
    Answering a question from the audience about Implantable Defibrillators, Dr. Gold saw no role for them unless a patient needed ventricular defibrillation. 
    (At one time it was hoped that atrial pacing therapy might one day become a cure for A-Fib. Recent research cited by Dr. Gold shows that pacing modestly improves A-Fib but doesn't cure or prevent it. Pacing should be used primarily for A-Fib patients who need pacing for other reasons.)

Dr. Jose Jalife of SUNY Upstate Medical University in Syracuse, NY discussed "The Relationship Between High-Frequency Fractionated Electrograms and Reentrant A-Fib Drivers in the Posterior Left Atrium."

    (Dr. Jalife described what may be a major new discovery in the treatment of A-Fib.) He found that there are sites of high-frequency activity within a heart in A-Fib. When these sites are ablated, A-Fib can be terminated.
    He used spectral analysis and dominant frequency mapping to produce 3-D color coded images of the heart with the lower frequencies in red and the higher in purple.
    He found that patients with Paroxysmal (occasional) A-Fib had high (Dominant) Frequencies mostly in the Pulmonary Vein openings, whereas Persistent or Chronic patients had sites of Dominant Frequencies more scattered throughout the left atrium. Also, Persistent/Chronic patients had higher Dominant Frequencies. This may be do to the remodeling effect of A-Fib which over time changes the substrate (structure) of the heart.
    He hypothesized that ablating areas of high (dominant) frequency may become an alternative to making linear lesions in the atrium which are hard to make, are associated with an increased procedural risk, and may be proarrhythmic (may increase A-Fib).
    He also related his work to that of Dr. Nademanee's Complex Fractionated Atrial Electrograms (CFAEs). "Unlike what Nademanee suggests, CFAEs do not correspond to the highest dominant frequency sources. Our results strongly suggest that the region harboring the A-Fib source shows the highest dominant frequency and the highest degree of organization, but is surrounded by complex fractionated activity. Therefore, CFAEs may point to the location of adjacent high frequency sources."
    (In this author's opinion Dr. Jalife's discovery of High (Dominant) Frequencies and their role in A-Fib is a major breakthrough in catheter ablation for A-Fib.)
    Dr. Jalife also presented an analysis of the previous year's Boston A-Fib Symposium (2005). Four different approaches to catheter ablation for A-Fib are emerging:⁸⁸

1. Isolation of triggers and reentrant circuits in the Pulmonary Veins (Dr. Haïssaguerre).
2. Disruption of the substrate for perpetuating rotors in the Antra of the Pulmonary Veins and the posterior left atrium (Dr. Pappone).
3. Targeted ablation of Ganglionated Autonomic Plexi in the Epicardial Fat Pads (Dr. Jackman).
4. Disruption of putative dominant rotors in the atria as recognized by High Frequency Complex Fractionated Electrograms during mapping of atrial fibrillation (Dr. Nademanee).

(Dr. Jalife may have discovered a fifth approach---the use of High (Dominant) Frequencies to identify and ablate A-Fib signals in the heart.)

Dr. Patrick Ellinor of Massachusetts General Hospital in Boston, MA discussed "Advances in the Genetics of Atrial Fibrillation."

    Dr. Ellinor discussed whether there were "phenotypes" or genetic predictors for A-Fib. In his study at MGH he found that 30% of Lone A-Fib patients had a family history of A-Fib. Some studies have identified chromosome 10 and the genes KCNQ1 and KCNJ2 as related to A-Fib. But current research hasn't been able to identify the dominant genes or gene mutations that may predict A-Fib.
    Dr. Ellinor welcomes individuals with a family history of A-Fib (generally 3 or more members of a family) to participate in the study to identify genes for A-Fib. You can contact him directly to learn more about the study.
    Patrick T. Ellinor, MD, PhD
    Cardiac Arrhythmia Service
    Massachusetts General Hospital
    55 Fruit St., GRB 109
    Boston, MA 02114
    617-726-5067
    Fax: 617-726-2155
    E-mail: pellinor at partners dot org (Dr. Ellinor's E-mail address is spelled out to prevent automatic search engines from flooding him with advertisements.)

Dr. Albert Waldo of University Hospitals of Cleveland Cardiology/Case Western Reserve Un. discussed "2006 ACC/AHA/ESC Guidelines for the Treatment of A-Fib - Update and Critique: Impact of A-Fib Guidelines on Clinical Practice."

    One of the major problems facing both patients with A-Fib and doctors who treat them is how to prevent stroke. Current medical guidelines^a for A-Fib patients with risk factors for stroke recommend using an oral "vitamin K antagonist" such as warfarin (an antagonist works against the coagulation vitamin K). Risk factors for stroke are: prior ischemic (clotting) stroke, transient ischemic attack or systemic embolism (blood clot), being over 75 years old, impaired left ventricular systolic function, hypertension, and diabetes melltius.
    A-Fib patients 65-75 years old, even without any risk factors for stroke, are at intermediate risk of stroke and should be on warfarin. "The relative risk of ischemic stroke increases by 1.4 per decade beginning at age 65 years." (A 1.4 increased risk means someone is 1.4 times more likely to have a stroke than a normal person.) According to Dr. Waldo, "aspirin only may not be an appropriate recommendation for patients between 65-74."
    If an A-Fib patient is younger than 65 years old with no heart disease, guidelines recommend aspirin (325 mg/d) or no therapy. If there is heart disease with no risk factors for stroke, aspirin (325 mg/d) is recommended.
Doubts About Aspirin Therapy
    Dr. Waldo raised concerns about aspirin therapy. Citing several studies Dr. Waldo indicated that, "warfarin is far superior to aspirin in diminishing the risk of stroke."⁷³,⁷⁴ Also, should a stroke occur on aspirin, it is usually more severe and has a significantly higher mortality when compared with warfarin therapy (with the INR maintained in the therapeutic range of 2.0-3.0). ("INR" stands for International Normalized Ratio and is a means of measuring the level of warfarin in the blood stream.) Dr. Waldo recommended that, "the use of aspirin really needs to be reconsidered or at least more seriously tested."  "...if one needs protection against stroke, one needs a vitamin K antagonist (warfarin)."
    Bleeding Risk From Warfarin   
    Dr. Waldo addressed concerns about bleeding risk (cerebral hemorrhage stroke) in patients taking vitamin K antagonists (warfarin). The relative risk of ischemic (clotting) stroke increases with age, as does the risk of a hemorrhagic stroke when taking warfarin. But "the risk of ischemic stroke (in an A-Fib patient not taking warfarin) is considerably greater than the risk of intracranial bleeding."⁷⁵ Dr. Waldo also pointed out that an increased risk of hemorrhagic stroke does not occur until a patient's INR reaches 3.9-4.0 (a normal therapeutic warfarin INR range is 2.0-3.0).
    Should Warfarin Be Stopped After A Successful A-Fib Ablation?
    Common practice today is to terminate oral anticoagulation therapy 3-6 months following an apparently successful cure. But recent studies indicating reoccurrences of often silent A-Fib after ablation raise some doubts about this practice (see Kottkamp and Calkins). In his practice Dr. Waldo  keeps "cured" A-Fib patients with risk factors for stroke on warfarin.
Warfarin Under-Prescribed
    In a study of hospitals treating A-Fib patients, 20% of high risk patients didn't receive any anticoagulation therapy, and 24.7% only received aspirin when according to the guidelines they should have received warfarin. "The patients who need (warfarin) the most seem to be getting it the least."
    (Author's Note: Dr. Waldo's data and recommendations against aspirin and in favor or warfarin are very important for A-Fib patients. As Dr. Waldo put it, "Stroke is a fate worse than death." Since aspirin is far less effective than warfarin in preventing stroke, A-Fib patients with risk factors for stroke on aspirin therapy should seriously consider changing to warfarin.)
    (Added August 14, 2007: The Center for Shared Decision Making gives somewhat controversial odds of getting an A-Fib stroke depending on one's overall heart health (http://www.dhmc.org/webpage.cfm?site_id=2&org_id=108&morg_id=0&sec_id=0&gsec_id=39685&item_id=39691):
Under age 65 with no history of hypertension, stroke, arterial embolism, left ventricular dysfunction, or TIA:
        Chance of stroke in two years 2 out of 100
        Taking daily coated aspirin 1.5 out of 100
        Taking daily warfarin 1 out of 100
    Age 65-75 with no history of hypertension, stroke, arterial embolism, left ventricular dysfunction, or TIA:
        Chance of stroke in two years 4 out of 100
        Taking daily coated aspirin 3 out of 100
        Taking daily warfarin 2 out of 100
    Over age 75, or under age 75 with history of hypertension or left ventricular dysfunction:
        Chance of stroke in two years 12 out of 100
        Taking daily coated aspirin 9 out of 100
        Taking daily warfarin 4 out of 100
    Any age with a history of TIA, stroke or arterial embolism, or over age 75 with a history of hypertension or left ventricular dysfunction:
        Chance of stroke 20 out of 100
        Taking daily coated aspirin 16 out of 100
        Taking daily warfarin 7 out of 100
    ^aThere are two main sets of guidelines for the use of anticoagulants for A-Fib patients: the American College of Chest Physicians (ACCP) guidelines published in October 2004, and the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) guidelines published in September 2001 (currently under revision). Both sets of guidelines are generally compatible with each other, but there are differences. For example, the ACC/AHA/ESC guidelines use age 60 as a cut off for some considerations, whereas the ACCP uses age 65.

Debate and Discussion: "Catheter Ablation Should Be First Line Therapy in Selected Patients with A-Fib." Pro: Dr. Andrea Natale, The Cleveland Clinic Cleveland, OH. Con: Dr. Eric Prystowsky, The Care Group, Indianapolis, IN.

    The debate addressed a question that is very important to A-Fib patients: should drug therapy be tried first, or should a catheter ablation procedure be the first choice? Most current guidelines for treating A-Fib state that drug therapy should be tried first.

MEDICATION THERAPY
    Both Dr. Natale and Dr. Prystowsky were in general agreement that current drug therapies have limited effectiveness and can have dangerous side effects.
    Dr. Natale discussed the role of Rate Control (using medicines to control the heart rate, but leave the heart in A-Fib) and Rhythm Control (using antiarrhythmic medicines to try to stop A-Fib) in treating A-Fib. The AFFIRM clinical studies found no mortality difference between Rate Control and Rhythm Control. However, Dr. Natale pointed out that the AFFIRM study did not compare patients in Rate Controlled A-Fib with patients in normal sinus rhythm (the goal of catheter ablation). In fact, the AFFIRM investigators concluded, "the presence of sinus rhythm was one of the most powerful independent predictors of survival, along with the use of warfarin... Patients in sinus rhythm were almost half as likely to die compared with those with A-Fib."
    Dr. Natale pointed out that the AFFIRM study was not really an endorsement of Rate Control drugs. Rather it illustrated how ineffective and dangerous current antiarrhythmic drugs can be. "...data from several trials have demonstrated that the success of antiarrhythmic medications (AAMs) in maintaining sinus rhythm is borderline, at best, with increasing failure rates over time... AAMs clearly do not cure A-Fib; at best, they are a palliative treatment used to reduce the burden of A-Fib as opposed to eliminating it altogether. ...in our experience rhythm control is not only ineffective and poorly tolerated, but only delays an inevitable ablation."
    In addition, AAMs frequently cause debilitating side effects. Amiodarone, possibly the most effective AAM, is associated with the most dangerous side effects: intolerable skin discoloration, pulmonary fibrosis, damaged thyroid, and neurological or ophthalmic problems. Also, AAMs may increase mortality. "Both cardiac mortality and arrhythmic death were significantly increased, particularly in patients with heart failure."
    Dr. Prystowsky concurred with Dr. Natale about "the limited long-term efficacy and high incidence of side effects for antiarrhythmic medications."
     CATHETER ABLATION (PVI) THERAPY
    Both doctors' PRO and CON arguments on using catheter ablation as a first-line therapy far treating A-Fib are listed in the following table.

    Dr. Natale argued that, in contrast to Rate Control and Antiarrhythmic drug therapies, catheter ablation (PVI) offers the possibility of a lasting cure. Citing recent studies from several different medical centers, an overall success rate of over 80% is currently being achieved, which is 2- to 3-times better than anything achievable with AAMs. In all these centers there was a very low incidence of complications.
    In a controlled, long-term study, patients who underwent A-Fib ablation had significantly improved survival compared to patients who received antiarrhythmic medications, suggesting that A-Fib ablation might be considered as a first-line strategy.⁸³ Also, in the RAAFT study (Radiofrequency Ablation for Atrial Fibrillation Trial) comparing A-Fib ablation as first-line therapy to AAMs, A-Fib recurred in 65% of AAM patients compared to only 13% of ablation patients.
    Dr. Prystowsky indicated that the long-term efficacy of A-Fib ablation isn't definitely known. Perhaps, "...pulmonary vein isolation procedures may not result in long-term clinical success after initial clinical success."
    He also stated that with regards to A-Fib patients at high risk for stroke, "there is no long-term follow-up showing a reduction in stroke risk in patients apparently cured of A-Fib with catheter ablation." Such patients may need constant long-term monitoring with, for example, an implanted loop recorder.
    There is also a significant variance of success among medical centers using similar techniques of ablation. "Because the procedures are technically challenging and highly operator dependent," the safety and efficacy of catheter ablation varies by doctor and medical center. Only 8% of medical centers worldwide do more than 300 A-Fib ablations a year.
    He also thought the Complications Rate after A-Fib ablations may be under-reported due to publication bias. He was particularly concerned about Atrio-Esophageal Fistula. "Risk factors for this potentially fatal complication have not been established." He mentioned that catheter ablation may sometimes damage the vagal nerve system with unknown long-term consequences. He expressed concern about the recent studies indicating "silent" A-Fib recurrences after ablation which would lower the reported success rate (see Kottkamp and Calkins).
    SHOULD PATIENTS RECEIVE A-FIB ABLATION AS A FIRST CHOICE?
    Both doctors basically agreed that A-Fib ablation should be offered as a first-line therapy to some patients, but not to all. They differed slightly when describing the patients who should be offered A-Fib ablation as first-line therapy.
    According to Dr. Natale, at the present time A-Fib ablation as first-line therapy should not be offered to all patients with A-Fib. Large-scale, comparative clinical trials need to be performed before recommending ablation as a first choice for a very broad population of A-Fib patients.
    Ablation should be offered as a first-line therapy to highly symptomatic patients with recurrent A-Fib (not related to other, curable causes), who have already failed drug therapy, with minimal or moderate structural heart disease.  Also, ablation may particularly benefit younger patients with lone A-Fib for whom very-long-term antiarrhythmic and anticoagulation pose higher risks and lifestyle costs.
    However, Dr. Natale predicted that in the near future A-Fib ablation can be offered as first-line therapy to a broader A-Fib population. He cited data showing that good success rates are already being achieved in A-Fib patients with impaired left ventricular function, previous cardiac surgery or valvular heart disease, and advanced age. The only group that seems destined to fail ablation is that with extensive, preexistent scarring (atrial myopathy).
    Dr. Prystowsky stated that catheter ablation might be considered as an initial therapy in the following cases:
    ---patients with very symptomatic A-Fib who refuse antiarrhythmic medications,
    ---patients in whom the only antiarrhythmic choice is long-term amiodarone,
    ---possibly patients at high risk of stroke who refuse or cannot take long-term warfarin therapy,
    ---young patients with paroxysmal A-Fib and sinus node dysfunction who may not tolerate antiarrhythmic medications without a permanent pacemaker.
THE IMPORTANCE OF EXPERIENCED DOCTORS AND CENTERS
    Both doctors recognized that operator experience, skill and use of advanced technology affect the success rates of  A-Fib Ablation. Dr. Natale stated that only centers with considerable experience in performing A-Fib ablation should consider offering ablation as first-line therapy, because currently success is highly operator dependent.
    Answering a question from the audience, Dr. Prystowsky reported that Wellpoint Inc. has a policy of not paying for a PVI unless a patient has failed two antiarrhythmic drugs. (This appears to be another disturbing example of insurance companies making decisions that should be left to the doctor and patient.)
    (Editor's Note: From this patient's perspective, catheter ablation should be considered as first-line therapy for many A-Fib patients. According to Dr. Natale, "The lack of efficacy and known harm of alternative pharmacological therapy for A-Fib cannot be underestimated." Whereas catheter ablation has a high success rate, is most likely a permanent cure, and is a low risk procedure. However, for best results a patient may need to go to centers with considerable experience in performing catheter ablations for A-Fib [over 300/year].)

Panel and Audience Discussion: How We Approach Catheter Ablation for A-Fib Today: Tailoring Procedures to Individual Clinical Scenarios and Optimizing Safety and Effectiveness. Moderator: Dr. Jeremy Ruskin. Panelists: Dr. Warren Jackman, Dr. Pierre Jaïs, Dr. Steven Kalbfleisch, Dr. Karl Heinz Kuck, Dr. Francis Marchlinski, Dr. Andrea Natale, Dr. Douglas Packer, Dr. Carlo Pappone, Dr. Vivek Reddy, Dr. David Wilber

    The panel moderator, Dr. Jeremy Ruskin of Massachusetts General, pointed out that catheter ablation, while still considered "new," has been used to cure A-Fib patients for eleven years. He asked the panelists to describe their current strategies for Paroxysmal (occasional), Persistent (lasting over 24 hours but can be cardioverted) and Chronic (permanent) A-Fib patients.
Dr. David Wilber, Loyola Un. Medical Center, Chicago
Paroxysmal:
      Pulmonary Vein (PV) Isolation is the cornerstone of our approach. We use electrograms to confirm isolation.
    Then we use an individualized approach. If there is scarring and/or fibrous tissue in the atrium and we can still induce A-Fib, we ablate areas of low voltage (less than 0.5mV) and areas of Complex Fractionated Atrial Electrograms (CFAEs). If A-Fib can still be induced, we use linear lesions. But this rarely happens with Paroxysmal patients. At the end we use high dose isoproterenol (20 micrograms/min.) to try to induce A-Fib to make sure there are no focal drivers anywhere else. Because we regularly use anesthesia, we wake up patients at the end of the procedure. We are concerned about sedation suppressing some of the A-Fib drivers.
Persistent and/or Chronic:
    We again begin by ablating (isolating) the Pulmonary Vein (PV) openings. Then we ablate CFAEs. Then we look at the right atrium, particularly the Coronary Sinus and Superior Vena Cava. Then we use linear lesions. Our ideal end point is non-inducibility of A-Fib. But with Chronic patients this may not be a realistic goal. For Chronic patients we are happy if we can maintain sinus rhythm, ablate CFAEs, and have good lesion sets.

Dr. Karl Heinz Kuck, St. George Hospital, Hamburg, Germany.
    We spend a lot of time creating the true anatomy of the heart by imaging techniques. What some people call the outside of the Pulmonary Vein Ostia (openings), we would call the inside.
Paroxysmal/Persistent:
    We use Circumferential Isolation outside the ostia and make sure the isolation is permanent.
Chronic:
    The Circumferential Isolation procedure works for approximately 50% of Chronic patients. We don't know yet which strategy is better than that. There are so many CFAEs in the heart. Is 115 burns enough? We need more experience.

Dr. Douglas Packer, The Mayo Clinic, Rochester, MN.
Paroxysmal:
    We start with PV Circumferential Ablation, then move to non-PV foci (A-Fib trigger sources), then make linear lesions, making sure there are no gaps in the lesion lines. 
Persistent/Chronic:
    We start with a wider area Circumferential Ablation of the PVs, then ablate areas of CFAEs. We have been discouraged by ablation of CFAEs alone, which don't terminate Chronic A-Fib. We then ablate in the Coronary Sinus, Posterior Mitral Annulus and Septum using linear lesions.

Dr. Warren Jackman, Un. of Oklahoma, Oklahoma City, OK.
Paroxysmal:
    We start by mapping the left atrium and PVs using ICE to mark key landmarks. We identify and ablate the four Ganglionated Plexi areas in the left atrium. If A-Fib continues, and it usually does, we will cardiovert the patient to terminate the A-Fib. Then we will look for areas of spontaneous firing and do a complete Antrum PV Isolation. If we can still induce microreentry tachycardias by 4 micrograms/min of Isoproterenol, we will make linear lesions.
Chronic:
    We ablate Ganglionated Plexi, then CFAEs, cardiovert, then do Antrum Isolation, then move to the