Persistent A-Fib: Insights into Finding Additional Drivers May Shorten Ablation Procedures with Fewer Lesions
By Steve s. Ryan, PhD, July 2015
Dr. Pierre Jais of the French Bordeaux/LIRYC group gave a presentation on “The Spectrum of Atrial Tachycardias Following Ablation of Drivers in Persistent AF.”
He described a study of the ablation of 50 persistent A-Fib patients using ECGI to map and ablate A-Fib signal drivers.
A-Fib was terminated in 79% of patients, with 10% returned to sinus rhythm and the remaining 69% in tachycardias (but with no A-Fib).
For those still in arrhythmia, ECGI was used to map, analyze and diagnose the locations of the arrhythmias signals, and additional ablation lesions were performed. Identified were 25 macro-reentry circuits and 14 focal/localized-reentry circuits.
The reentry circuits found by ECGI were:
• common atrial flutter in 14 patients
• perimitral flutter in 9 patients
• roof dependent flutter in 2 patients
Dr. Jais showed many slides and videos of how ECGI mapped and analyzed where these arrhythmias were coming from and how they were ablated.
Dr. Jais’ Conclusions
Dr. Jais stated that the study data revealed, “the focal/localized-reentry were adjacent to drivers at 0.9cm from the core of driver with low voltage (0.5 mV)”.
To clarify, this means that the drivers of the remaining arrhythmias were located very close (adjacent) to the drivers previously mapped by ECGI.
Therefore, when ECGI locates an area of rotors and drivers, it is highly likely this is where the source of additional arrhythmias will most likely be found. This insight reduces or eliminates the need (and time) to search other areas of the heart thereby shortening procedure length and decreasing the number of lesions needed.
ECGI mapping and ablating is changing our understanding of and our techniques for ablating persistent A-Fib. If a patient has continued arrhythmias after the initial ablation, ECGI often can re-map and identify where the remaining arrhythmias are coming from, usually very near previously identified driver locations. This is a valuable insight for doctors doing ablations.
For patients, it may mean a shorter procedure time with fewer burns needed to eliminate the sources of A-Fib signals.
Last updated: Thursday, August 6, 2015
Atrial Fibrillation patients often search for unbiased information and guidance about medicines and drug therapy treatments. These are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer.)
11. “I am on Coumadin (warfarin) to thin my blood and prevent A-Fib blood clots. Do I now need to avoid foods with Vitamin K which would interfere with the blood thinning effects of Coumadin?” UPDATED
12. “The A-Fib.com web site claims that an A-Fib stroke is often worse than other causes of stroke. Why is that? If a clot causes a stroke, what difference does it make if it comes from A-Fib or other causes? Isn’t the damage the same?“
16. “I have to be on aspirin for stroke prevention. Which is better—the low-dose baby aspirin (81 mg) or a high dose (325 mg)? Should I take the immediate-release (uncoated) or the enteric-coated aspirin?”
17. “I don’t want to be on blood thinners for the rest of my life. I’ve had a successful catheter ablation and am no longer in A-Fib. But my doctor says I need to be on a blood thinner. I’ve been told that, even after a successful catheter ablation, I could still have “silent” A-Fib—A-Fib episodes that I’m not aware of. Is there anything I can do to get off of blood thinners?“
21. “I”ve read about a new anticoagulant, edoxaban, as an alternative to warfarin (Coumadin) for reducing risk of stroke. For A-Fib patients, how does it compare to warfarin? Should I consider edoxaban instead of the other NOACs?”
Last updated: Saturday, February 11, 2017
Atrial Fibrillation patients often have loads of “Why?” and “How?” questions. Here are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer.)
1. Causes: “Why does so much Atrial Fibrillation come from the Pulmonary Vein openings?”
Related Question: “What causes Paroxysmal A-Fib to turn into Persistent (Chronic) A-Fib?”
Related Question: “A-Fib and Flutter—I have both. Does one cause the other?”
2. Hereditary: “Is my Atrial Fibrillation genetic? Will my children get A-Fib too?”
3. PSVT: “Is Atrial Fibrillation (A-Fib) different from what doctors call Paroxysmal Supraventricular Tachycardia?”
4. Adrenergic/Vagal: “What is the difference between “Adrenergic” and “Vagal” Atrial Fibrillation? How can I tell if I have one or the other? Does it really matter? Does Pulmonary Vein Ablation (Isolation) work for Adrenergic and/or Vagal A-Fib?”
5. Stiff Heart: “I’ve heard about ‘stiff heart’ or diastolic dysfunction. When you have A-Fib, do you automatically have diastolic heart failure? What exactly is diastolic dysfunction?”
6. Stem Cells: “I’ve read about stem cells research to regenerate damaged heart tissue. Could this help cure A-Fib patients?”
7. EF: “What is the heart’s ejection fraction? As an A-Fib patient, is it important to know my EF?”
8. Anesthesia: “I read that the local anesthesia my dentist uses may trigger my A-Fib. Why is that?”
9. Fibrosis: “How can I determine or measure how much fibrosis I have? Can something non-invasive like a CT scan measure fibrosis?”
10. Treatment Options: “My surgeon wants to close off my LAA during my Mini-Maze surgery. Should I agree? What’s the role of the Left Atrial Appendage?”
Related Question: “My cardiologist recommends a pacemaker. I have paroxysmal A-Fib with “pauses” at the end of an event. Will they stop if my A-Fib is cured? I am willing, but want to learn more about these pauses first.”
Related Question: “My EP won’t even try a catheter ablation. My left atrium is over 55mm and several cardioversions have failed. I am 69 years old, in permanent A-Fib for 15 years, but non-symptomatic. I exercise regularly and have met some self-imposed extreme goals. What more can I do?
If you find any errors on this page, email us. Y Last updated: Tuesday, February 14, 2017
6. What causes Paroxysmal (occasional) A-Fib to turn into Persistent (chronic) A-Fib?
Researchers are still working to find the answer(s) to this question. We do know that some patients remain paroxysmal (usually with anti-arrhythmic therapy), while a large proportion progress to persistent A-Fib. (In a study of 5,000+ A-Fib patients, 54% of those on rate control meds went into permanent A-Fib within one year.)
The main trigger seems to be increased pressures in the left atrium that cause the muscle fibers within the pulmonary vein openings to start beating on their own.
Uncontrolled blood pressure, untreated sleep apnea and diabetes, or a worsening cardiomyopathy seem to be key factors that make people progress from Paroxysmal to Persistent A-Fib. Research tells us that even after a successful ablation for Persistent A-Fib, “the long term success rates depend mostly on treatment of hypertension and obstructive sleep apnea.”
What does this mean to you? The longer you have Atrial Fibrillation, the harder it can be to cure it. Consider working aggressively to stop your A-Fib as with antiarrhythmic meds or with a minimally-invasive Pulmonary Vein Ablation or a Mini-maze surgery. You don’t want to be part of the 54% whose A-Fib becomes permanent.
Atrial Remodeling and the Transition From Paroxysmal to Persistent AF by Dr Jose Jalife-2014 Boston AF Symposium
2014 Boston AF Symposium
Experiments in Atrial Remodeling in Sheep and the Transition From Paroxysmal to Persistent A-Fib
By Steve S. Ryan, PhD
Dr. Jose Jalife of the Center for Arrhythmia Research of the University of Michigan described his experiments inducing A-Fib in sheep by pacing their hearts. He is trying to discover the mechanisms underlying the transition from paroxysmal to persistent A-Fib.
Background: Some patients remain paroxysmal (usually with anti-arrhythmic therapy), while a large proportion progress to persistent A-Fib. (In a study of 5,000+ A-Fib patients, 54% of those on rate control meds went into permanent A-Fib in one year.)1
Previous presentation summary: This talk was a continuation of Dr. Jalife’s 2013 Boston A-Fib Symposium presentation on his experimental studies with sheep. (See A-Fib Produces Fibrosis—Experimental and Real-World Data.) He implanted pacemakers in the hearts of sheep; then induced A-Fib by pacing for 6-30 seconds, then stopped, then paced again, etc. He continued this sequence until the sheep were in persistent A-Fib. He left them in A-Fib for about a year. Dr. Jalife also had a control group of sheep who were monitored but not paced into A-Fib.
Pacing Sheep into A-Fib
Once pacing started in the sheep, it took around 5.5 days to produce the first A-Fib episode. It took around 7-9 weeks of pacing for the sheep to move from Paroxysmal to Persistent A-Fib. At that point the sheep stayed in Persistent A-Fib without any further need of pacing. Dr. Jalife’s sheep developed two major types of atrial remodeling:
- Structural Remodeling (Fibrosis)
- Electrical Remodeling (ion channel expression changes)
(In humans, remodeling usually also results in atrial dilation. Dr. Jalife’s sheep once in A-Fib also developed significant Atrial Dilation compared to a control group of sheep.)
Unlike humans, the sheep didn’t develop heart failure, left ventricle dilation and dysfunction, or tachycardia-induced cardiomyopathy despite being in A-Fib for more than a year. This is possibly because sheep have a very good AV Node (unlike most humans) which filters the A-Fib pulses from affecting the ventricles and keeps the ventricular rate low.
Genetic Differences in Sheep
But there were differences in the sheep. Some sheep transitioned into persistent A-Fib fast (<40 days) while others needed more pacing to transition into persistent A-Fib (>40 days). Sheep from the same herd would have the same diet, environment, etc. But genetically they must have been different in their ability to hold out from transitioning into persistent A-Fib.)
All ventricular parameters remained normal in the paced sheep, except for atrial dilation and the markers of fibrosis which increased progressively as the sheep went from paroxysmal to persistent A-Fib. Fibrosis appeared in the right atrium, left atrium and the posterior left atrium. This fibrosis was the result of collagen deposition in the atria which is a permanent remodeling effect of A-Fib.
Dr. Jalife showed slides of a normal pig’s heart compared to a pig in persistent A-Fib. Well over ½ the atria seemed fibrotic.
Mechanisms of Electrical Remodeling
As expected, sustained A-Fib shortened the atrial action potential duration and refractory period. Also, rotor frequencies were increased. For example, in one sheep the dominant frequency of the first episode of paroxysmal A-Fib was 7.3 Hz, but increased progressively to 10.3 Hz during the transition to persistent AF. When AF in that sheep became persistent, the dominant frequent had stabilized at 11.3 Hz and remained constant for up to a year.
In perhaps the most important findings of Dr. Jalife’s experiments, the rate of increase in dominant frequency correlated strongly with the time at which AF stabilized. In other words, although the progression from paroxysmal to persistent A-Fib varied from one animal to another, the rate of dominant frequency increase could be used to forecast the time at which AF became persistent.
In other words, although the progression from paroxysmal to persistent A-Fib varied from one animal to another, the rate of dominant frequency increase could be used to forecast the time at which AF became persistent.
Dr. Jalife and his team also identified the mechanisms of electrical remodeling in sheep, which ion channels in the heart are responsible for transitioning sheep from paroxysmal to persistent A-Fib. Sodium and calcium heart electrical currents were lowered, while potassium and IK1 currents were increased. These electrical changes were associated with gene expression changes “in the alpha subunits of the L-type calcium (CACNA1C) and sodium (SCNSA) channel protein.”
- “Sustained AF reduces L-type calcium (Caᵥ1.2) and sodium (Naᵥ1.5) protein expression”
- “Sustained AF reduces the rapid sodium inward (INa) and L-type calcium (ICaL) currents”
- “Sustained AF reduces the transient outward current (Ito)”
- “Sustained AF increases the inward rectifying potassium current (IK1) and protein expression of the Kir2.3 channel”
The sheep model explains the structural and electrical remodeling that occurs in humans.
As in humans, there is a variable progression in time from paroxysmal to persistent A-Fib.
The rate of dominant frequency increase during such a progression predicts the time at which AF stabilizes and becomes persistent, reflecting changes in Action Potential Duration and densities of ICaL, IK1, INa and Ito.
Predicting the transition from paroxysmal to persistent A-Fib is feasible, at least in some patients, by measuring the increase in dominant frequency over time.
No one seeing Dr. Jalife’s presentation could doubt that A-Fib produces fibrosis. (Though even among sheep in the same environment, diet, etc. and with a similar gene pool, there were differences in how fast the individual sheep progressed to persistent A-Fib.) As patients with A-Fib, we have to base our medical decisions on the conclusion that A-Fib produces fibrosis; that if we stay in A-Fib over a significant period of time, we will progressively develop fibrosis which is currently irreversible and can lead to a host of other heart problems.
A common strategy today…is to leave you in A-Fib but control your heart rate by the use of beta-blockers, etc. But leaving you in A-Fib produces fibrosis which is irreversible and very damaging to the heart.
A common strategy today for treating A-Fib is to leave you in A-Fib but control your heart rate by the use of beta-blockers, calcium-channel blockers, etc. But leaving you in A-Fib produces fibrosis which is irreversible and very damaging to the heart. If your doctor wants to leave you in A-Fib, Dr. Jalife’s experiments would recommend that you get a second opinion, and ASAP.
One of the major advantages of a successful catheter ablation (and surgery) is it probably reverses the electrical remodeling effect of A-Fib. This makes intuitive sense. A heart beating in normal sinus rhythm (NSR) doesn’t usually produce those weird ion channel currents. But more research needs to be done before we can conclude this. However, a successful catheter ablation does not reverse fibrosis (structural remodeling), though it may reduce atrial dilation.
By identifying the actual mechanisms of electrical remodeling, Dr. Jalife’s ground-breaking experiments may lead to new therapies and drugs to combat not only the transition from paroxysmal to persistent A-Fib, but how to prevent patients from developing A-Fib in the first place. And using dominant frequency to predict when a patient is transitioning to persistent A-Fib, can be an invaluable tool for doctors (and reassuring for patients).
One of the scariest parts of Dr. Jalife’s presentation was how fast he could pace those sheep into persistent A-Fib. Obviously sheep aren’t people. But we know that for most people, there is a relatively short window of time when they progress from paroxysmal to persistent A-Fib (about a year). When you have A-Fib, you can’t count on genetics, diet, life style, environment, etc. to protect you from progressing to persistent A-Fib. Right now we just don’t know why some people stay paroxysmal for years, while most become persistent after a relatively short time. Worst case scenario, you have about a year. Act accordingly.
- Peykar, S. Atrial Fibrillation. Cardiac Arrhythmia Institute/Sarasota Memorial Hospital website. Last accessed Jan 5 2013. URL:http://caifl.com/arrhythmia-information/atrial-fibrillation/↵
Steve’s Lists of A-Fib Doctors by Specialty
Steve has prepared these lists of doctors treating atrial fibrillation patients by specialty to help you find doctors with a particular expertise.
- US EPs with FHRS-designation performing A-Fib ablations: Listed by State/City
- US EPs Using Cryoballoon Ablation
- US EPs Installing the Watchman Device
- US Surgeons performing Maze and Mini-Maze operations
- US Centers performing the Hybrid Surgery/Ablation procedure
- EPs Specializing in Persistent/Long-Standing Persistent A-Fib (US and International)
- EPs using Contact Force sensing catheters
Notice: unlike other directories, A-Fib.com offers no preferential listings or placement. No doctor or facility pays, provides services, etc. to be listed. We accept no fee, benefit or value of any kind for listing a specific doctor or medical center. A-Fib.com is not affiliated with any practice, medical center or physician.
If you know the name of the doctor or practice, use the “Search our site” box (upper right on this page) to get to the right Directory page. Then, open your browser’s ‘Find on Page’ feature (‘CTRL+F’) to locate the name on the page.
Disclaimer: this directory is provided for informational purposes only. We make no endorsement of a specific physician or medical facility. Choosing a physician is an important decision and should be based upon your own investigation of each physician’s training, education and experience. These listings offer you the opportunity to locate and contact a healthcare professional directly.
A-Fib.com is your independent source of unbiased information about Atrial Fibrillation, resources and treatments.
Last updated: Monday, April 24, 2017
EPs Specializing in Persistent/Long-standing Persistent A-Fib (US and International) a List from A-Fib.com
Doctors Specializing in Persistent/Long-standing Persistent A-Fib (US and International)
Persistent A-Fib and Long-standing Persistent A-Fib are often difficult to cure. If you are highly symptomatic, you may need a highly skilled, experienced specialist. This list is a starting point for you.
|DOCTOR OR MEDICAL CENTER||US CITY/STATE OR COUNTRY||COMMENT|
|The French Bordeaux Group||Bordeaux, France||Step wise ablation technique with 95% success rate in curing Chronic A-Fib after two ablations.|
|Dr. Robert A. Schweikert||Akron, OH||—|
|Dr. Fred Morady||Ann Arbor, MI||Developed Ablation Frontier’s Multi Electrode catheters for Chronic A-Fib still in clinical trials (11/20/09)|
|Dr. Patrick M. Hranitzky||Durham, NC||Uses stepwise approach.|
|Dr. Kevin J. Makati||Tampa, FL||—|
|Dr. Andrea Natale
Dr. J. David Burkhardt
|Dr. Andrea Natale
Dr. Steven C. Hao
Dr. Rick Hongo
|San Francisco, CA||—|
|Dr. James Ong||Tarzana, CA||—|
|Dr. Carlo Pappone||Cotignola, Italy||Uses step wise technique, though different than Bordeaux group.|
|Dr. Sidney Peykar||Sarasota, Florida||Uses Bordeaux step wise technique and trained in Bordeaux.|
|Dr. Robert Eckart||Sarasota, Florida|
|Dr. Vivek Reddy||New York, NY||Uses step wise technique, though different than Bordeaux group.|
|Dr. Darryl S. Wells||Seattle, WA||Does CryoBalloon ablation.|
|Dr. William H. Sauer
Dr. Ryan G. Aleong
|Aurora, CO||Modified step-wise approach.|
|Dr. J. Marcus Wharton||Charleston, SC||—|
|Dr. Wilber Su||Phoenix, AZ||—|
NOTICE: we offer no preferential listings. We accept no fee, benefit or value of any kind for listing a specific doctor or medical center. A-Fib.com is not affiliated with any practice, medical center or physician.
HOW TO FIND THE CONTACT INFO: Use the “Search our site” box (upper right on this page) to get to the right Directory page. Then, open your browser’s ‘Find on Page’ feature (‘CTRL+F’) to locate the name on the page.
Disclaimer: this directory is provided for your convenience only. We make no endorsement of a specific physician or medical facility. Choosing a physician is an important decision and should be based upon your own investigation of each physician’s training, education and experience. This directory offers you the opportunity to locate and contact a healthcare professional directly.
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Last updated: Saturday, May 14, 2016