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Dr. Douglas L. Packer, MD, FHRS, Mayo Clinic, Rochester, MN

"Jill and I put you and your work in our prayers every night. What you do to help people through this [A-Fib] process is really incredible."

Jill and Steve Douglas, East Troy, WI 

“I really appreciate all the information on your website as it allows me to be a better informed patient and to know what questions to ask my EP. 

Faye Spencer, Boise, ID, April 2017

“I think your site has helped a lot of patients.”

Dr. Hugh G. Calkins, MD  Johns Hopkins,
Baltimore, MD


Doctors & patients are saying about 'Beat Your A-Fib'...


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Roy Salmon, Patient, A-Fib Free,
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"This book is incredibly complete and easy-to-understand for anybody. I certainly recommend it for patients who want to know more about atrial fibrillation than what they will learn from doctors...."

Pierre Jaïs, M.D. Professor of Cardiology, Haut-Lévêque Hospital, Bordeaux, France

"Dear Steve, I saw a patient this morning with your book [in hand] and highlights throughout. She loves it and finds it very useful to help her in dealing with atrial fibrillation."

Dr. Wilber Su,
Cavanaugh Heart Center, 
Phoenix, AZ

"...masterful. You managed to combine an encyclopedic compilation of information with the simplicity of presentation that enhances the delivery of the information to the reader. This is not an easy thing to do, but you have been very, very successful at it."

Ira David Levin, heart patient, 
Rome, Italy

"Within the pages of Beat Your A-Fib, Dr. Steve Ryan, PhD, provides a comprehensive guide for persons seeking to find a cure for their Atrial Fibrillation."

Walter Kerwin, MD, Cedars-Sinai Medical Center, Los Angeles, CA


AF Symposium & other medical conferences articles

Increasing Your Quality of Life: Catheter Ablation versus A-Fib Drugs

When seeking your Atrial Fibrillation cure, you’re often faced with the choices of catheter ablation versus antiarrhythmic drugs therapy.

We know from previous research studies that it’s safer to have an ablation versus living a life on antiarrhythmic drug therapy (AAD). (See Ablation Safer Than Life on Antiarrhythmic Drugs.)

But how do the two treatments compare when it comes to improvement in general health and ‘quality of life’?

Measuring ‘Quality of Life’

To determine success after treatment, researchers traditionally measure if A-Fib recurs using periodic ECGs. But this is “hardly a measure of successful treatment”, says Dr. Carina Blomstrom-Lundqvist, principal CAPTAF investigator from Uppsala University in Sweden.

CAPTAF stands for ‘Catheter Ablation compared with Pharmacological Therapy for Atrial Fibrillation‘.

The CAPTAF clinical trial is one of the first studies in which improvement in ‘quality of life’ was the goal. The trial compared the Atrial Fibrillation treatment effects of ablation versus antiarrhythmic drugs.

One-year results were presented in August at the 2017 European Society of Cardiology (ESC) Congress.

The CAPTAF Clinical Study

The CAPTAF trial enrolled 155 symptomatic patients with paroxysmal or persistent A-Fib at four Swedish centers and at one center in Finland.

Drug Therapies for Atrial Fibrillation, A-Fib, Afib

A-Fib Drug Therapies

All enrolled patients had to have failed one drug therapy (rate or rhythm control). The average age of the enrolled patients was 56 years. Nearly three-quarters had paroxysmal A-Fib. On average they had been diagnosed with A-Fib for about 5 years, and 70%-80% of the patients had severe or disabling symptoms.

Catheter ablation (RF)

Patients received a subcutaneously implantable cardiac monitor 2-m onths prior to the start of the study (to establish a baseline ‘burden’ of A-Fib, i.e. the proportion of time in A-Fib). Then participants were randomized to ablation with pulmonary vein isolation or antiarrhythmic drug therapy. (The study protocol required patients randomized to the ablation regimen to be completely off antiarrhythmic drugs by 6 months after their ablation procedure.)

The primary goal of the study was a change in general health-related quality of life.

CAPTAF Results: Overall Health & ‘Quality of Life’ Improved More after Ablation

Overall Health: After 12 months of follow-up, the ablation group showed a greater improvement in average overall health by 11.0 points versus 3.1 points improvement in the drug group (as measured by a standard survey instrument). The 8-point difference in gain between the two groups was statistically significant.

Quality of Life: The quality-of-life domains (general health, physical function, mental health, role-emotional, role-physical, and vitality) improved significantly more in the ablation group than in the drug group. No significant differences were shown in the remaining two domains (bodily pain and social functioning).

AF Burden: The AF burden of the ablation group was decreased by an average of 20% points versus 12% points among the group on antiarrhythmic drugs. The change from baseline did not reach statistical significance between treatment groups.

The complication rates were comparable between treatment groups.

Summarizing the Results

About the difference in quality of life, Dr. Carina Bloomstrom-Lindqvist, principal CAPTAF investigator, explained that continued treatment with an antiarrhythmic drug in the drug group of patients compared with no drug treatment in the ablated patients “is absolutely the explanation” for the observed difference in quality of life.

Regarding her findings, she said, “Using quality of life as the primary endpoint of a trial for the first time, we demonstrated that pulmonary vein isolation [PVI] is significantly more effective than antiarrhythmic drugs…even at an early stage of their disease.”

Want a Better Quality of Life? Get a Catheter Ablation

“Using quality of life as the primary endpoint…PVI is significantly more effective than antiarrhythmic drugs…”

The CAPTAF clinical study, though small, goes much further than previous studies and is a significant milestone for Atrial Fibrillation patients. This was one of the first studies to focus on quality of life after treatment.

The CAPTAF results prove scientifically that ablation works better for A-Fib patients than antiarrhythmic drugs (AADs).

If you have A-Fib and want to improve your quality of life―get a catheter ablation. It makes you feel better than a life on antiarrhythmic drugs.

Remember: Seek your Cure!
Anyone no longer in A-Fib can tell you how wonderful it is
to have a heart that beats normally again.

Resources for this Article

 

CASTLE AF Study: Live Longer―Have a Catheter Ablation!

Catheter ablation actually reduces death rates and hospital admissions. That’s the finding in the CASTLE AF trial, a key heart disease study, by Dr. Nassir Marrouche and his colleagues.

In a presentation at the 2017 European Cardiology Congress in Barcelona, Spain, Dr. Marrouche described CASTLE-AF study participants as having A-Fib, advanced heart failure (i.e., low ejection fraction) and an Implantable Cardioverter Defibrillator (ICD).

The multicenter CASTLE-AF trial focused on patients with A-Fib and systolic heart failure.

The CASTLE-AF trial enrolled 398 patients in 33 sites across Europe, Australia and the US between 2008 and 2016. Patients were randomized to receive either radiofrequency catheter ablation or conventional drug treatment.

The study set out to definitively test the ability of A-Fib ablation to improve hard outcomes in patients with symptomatic paroxysmal or persistent A-Fib and a left ventricular ejection fraction (LVEF) of ≤35 percent (dangerously low percent). Median follow-up period was 37.8 months.

Results: Ablation Improves Quantity Not Just the Quality of Life

After catheter ablation, the death rate of trial patients was lowered by an amazing 47%! This is a lot better result than research studies using ICDs with drug therapy to lower the death rate in similar patients.

Before this study, catheter ablation was known to improve quality of life, but unexpected it also improved life outcomes (the quantity of life, how long one lives).

In addition, there may be a “major impact” on reducing costs associated with hospitalizations.

Ablation Improves Ejection Fraction

Once we study the soon-to-be published CASTLE-AF results, we can document what we’ve often observed anecdotally, that catheter ablation improves lower-than-normal ejection fraction and consequently cures a major component of heart failure.

Dr. Marrouche recommends EPs treating heart failure patients with A-Fib to “ablate them early on, very soon in the disease stage.”

My Anecdotal Evidence: Just last month I advised a 73-year-old man in persistent A-Fib to have an ablation by Dr. Andrea Natale. After only one month in sinus, his ejection fraction improved from a low 35% to a normal 55% (normal range is 50 to 75 percent)!

The CASTLE-AF study could pave the way for wider adoption of catheter ablation for treatment of A-Fib.

Even though he’s only a month into his blanking period, he feels terrific.

Wider Adoption of Catheter Ablation?

The CASTLE-AF study results could be a game changer for Atrial Fibrillation patients! Results could pave the way for wider adoption of catheter ablation and may prompt changes in current guidelines for treatment.

CASTLE-AF stands for Catheter Ablation versus Standard conventional Treatment in patients with LEft ventricular dysfunction and Atrial Fibrillation

Resources for this Article

Genetics of A-Fib—40% Increased Risk of Developing A-Fib If Relative Has It

AF Symposium 2012

Summary by Steve S. Ryan, PhD, January 2012

Patrick Ellinor, MD

Patrick Ellinor,

Genetics of A-Fib—40% Increased Risk of Developing A-Fib If Relative Has It

Genetic research in A-Fib, though in its preliminary stages, has the potential to be a game changer for patients with A-Fib. Dr. Patrick Ellinor of Mass General, Boston gave a presentation on the “Genetics of A-Fib: How Will We Translate GWAS Findings to Clinical Practice?”

A-Fib Is Inheritable

“If you have any immediate family with A-Fib, you have a 40% increased risk of developing A-Fib yourself. And the younger that someone in your family gets A-Fib, the more likely you are to have A-Fib.”

Screen for A-Fib?

If someone has A-Fib, should all their immediate family members be screened for A-Fib? Since in the US alone over three million people have A-Fib, it isn’t possible or practical to screen all family members for A-Fib. And even if we could screen everyone, we don’t yet have the means to prevent A-Fib from developing or even to identify patients with pre-A-Fib.

Editor’s Comments: If anyone in your immediate family has A-Fib, you are very likely to develop A-Fib yourself. You have to be more aware and vigilant than the average person. If, for example, you feel palpitations or a racing heart rate, take it very seriously. Don’t hesitate or delay in going to an Electrophysiologist (EP) to have yourself checked out. Make sure you tell your EP or Cardiologist that your relative has A-Fib.

Specific Genetic Chromosomes Associated With A-Fib

Dr. Ellinor identified the specific genetic chromosomes currently found to be associated with A-Fib:

  • 1q21
  • 16q22
  • and particularly 4q25

People with a particular combination of 3 genetic variants on chromosome 4q25 are six times more likely to develop A-Fib.

Further Research Needed

But current research has only revealed “associations.” Further research is needed to determine:

  1. Are these chromosomes associated with and/or do they cause an increased risk of A-Fib stroke, heart failure and death?
  2. Are these genetic variants associated with or do they indicate that a certain treatment should be used or that a certain outcome is more likely?
  3. How important are these genetic variants in the development of A-Fib?
  4. How do these genetic variants affect what types of arrhythmia develop? Do Paroxysmal A-Fib, Permanent A-Fib, or A-Flutter have different genetic profiles?
  5. And most importantly, how do these genetic variants work? What Is the mechanism behind the association?

“Right now all we have is an association.” “We don’t have a fundamental understanding as to how the variants themselves lead to the (A-Fib) disease.”

Warn all Your Immediate Family Members

If you have A-Fib, you must warn all your immediate family members that they have a good chance of getting it also. Even though we don’t know yet how to definitively prevent A-Fib, there are some precautions your family members can take:
  1. Avoid binge drinking and heavy partying.
  2. Avoid antihistamines and anything that can stimulate or trigger A-Fib. (see A-Fib Triggers) (This doesn’t necessarily include coffee. Some research indicates coffee may prevent A-Fib.)
  3. Be more attentive to overall health. Obesity, for example, is often a contributing factor to A-Fib. Sleep apnea is known to lead to A-Fib.
  4. Check for deficiencies in essential minerals (electrolytes) like magnesium or potassium? Are calcium levels too high (which may be a trigger for A-Fib)?
  5. Avoid or learn to cope with stress (not always possible).
    There is a tendency in all of us to not tell others if we are ill, perhaps because we perceive it as somewhat humiliating and a weakness in ourselves. But no one should be ashamed of having A-Fib. Most likely it isn’t anything we brought on ourselves. It’s genetic! It’s nobody’s fault!

We are not being fair to our family members by not telling them about our A-Fib. Don’t just mention it in passing. Sit down with them and tell them what A-Fib is like, and that they are at risk.

If you love your family, you owe it to them. This applies particularly to your brothers and sisters with whom you may have a loving but somewhat competitive relationship. Anyone in your immediate family must be warned.

If you find any errors on this page, email us. Y Last updated: Monday, May 1, 2017

Back to: 2012 AF Symposium

2017 AF Symposium: FIRM Rotor Mapping System During Live Ablation

Dr David Wilber Loyola University

D. Wilber

In a live case from the 2017 AF Symposium, Dr. David Wilber from Loyola University Medical Center showed how he uses the Topera FIRM rotor mapping system to identify rotors in conjunction with a PVI. (‘FIRM’ stands for Focal Impulse and Rotor Modulation.)

Dr. Wilber described how he first does voltage mapping while the patient is in normal sinus rhythm. He started in the right atrium, then moved to the left; he used the FIRM system to map where rotors were coming from. (In patients with persistent A-Fib, he typically finds as many as 4-8 rotors.) He mapped and ablated until there were no more rotors.

Only after using the FIRM system did he do a Pulmonary Vein ablation…Continue reading my report.

2017 AF Symposium: Live Case of Ablation with FIRM Mapping System

Dr David Wilber Loyola University

D. Wilber, MD

In a live case, Dr. David Wilber from Loyola Un. Medical Center in Chicago, IL showed how he uses the Topera FIRM rotor mapping system to identify rotors in conjunction with a PVI. ‘FIRM’ stands for Focal Impulse and Rotor Modulation.

Patient background: The patient was a 54-year-old male in persistent A-Fib for 7 months, obese with a BMI of 31, hypertension, diabetes, and obstructive sleep apnea. He was symptomatic, with fatigue and decreased exercise tolerance. An MRI showed his Left Atrium was 15.5% fibrotic. (If using Dr. Nassir Marrouche’s Utah I–IV Classification System to rate the patient’s amount of fibrosis, this patient would be “Utah Stage 2”, i.e., a reasonable candidate for a catheter ablation.)

Voltage & FIRM Mapping: Rotors Ablated First

FIRM mapping display of left atrial rotor during atrial fibrillation.

FIRM mapping display of left atrial rotor during atrial fibrillation.

In live video streaming from Chicago, Dr. Wilber described how he first does voltage mapping while the patient is in normal sinus rhythm. He started in the right atrium, then moved to the left; he used the FIRM system to map where rotors were coming from. (In patients with persistent A-Fib, he typically finds as many as 4-8 rotors.) He mapped and ablated until there were no more rotors.

Only after using the FIRM system did he do a Pulmonary Vein ablation (PVI).

He explained that the concept of terminating A-Fib during a PVI ablation doesn’t work with the FIRM system. Instead, he looks to ablate rotational areas (which are usually 2.2 cm across). He does this by using a Contact Force sensing catheter usually at 35 watts for 30 sec.

During this ablation, he found one rotor at the base of the Left Atrial Appendage (LAA). (In the followup panel discussion, Dr. Andrea Natale commented that he and his colleagues now look first for A-Fib signals in the LAA.)

FIRM Rotors Hard to See

VIDEO examples: Dr. Wilber showed a video using FIRM in which [even to my untrained eye] it was easy to see a rotor. But he showed other videos where the overlapping, swirling waves made it difficult to see where exactly a rotor was coming from.

Editor’s Comments:
This patient was at great risk of recurrence after a catheter ablation, because of his various illnesses (comorbidities). By restoring him to normal sinus rhythm, he would be able to exercise and develop life-changing habits to reduce his obesity, diabetes, and hypertension.
ECGI CardioInsight system: Focal and re-entrant driver maps

ECGI CardioInsight system: Focal and re-entrant driver maps

Abbott Topera FIRM vs Medtronic ECGI CardioInsight:  In comparison to the ECGI CardioInsight system where the rotors and focal sources are very obvious (even to untrained observers), the FIRM system display of rotors are often confusing and hard to identify. Dr. Wilber acknowledged that it takes study and experience with the FIRM system to use it effectively.
To me, the Abbott Topera FIRM system seems hard to use. In head-to-head competition with the Medtronic ECGI CardioInsight system, I predict the FIRM system will probably not survive.
The Medtronic ECGI CardioInsight system has been in limited use in Europe and in 2017 has begun a limited rollout in the U.S.

For more on the Medtronic ECGI CardioInsight, see my article: ECGI Mapping Now Available in U.S.

For more about Dr. Nassir Marrouche’s Utah I–IV Classification System, see my article: Fibrosis Risk and the U. of Utah/CARMA website.

Reference for this Article

2017 AF Symposium: Preventing Esophageal Fistula

Report 14 from the 2017 AF Symposium summarizes a live ablation using a new tool to protect the esophagus.

The Problem: During an ablation, doctors take great precautions to not heat or injure the esophagus which lies behind the posterior wall of the left atrium. Injuring the esophagus can, in very rare cases, cause an atrial esophageal fistula which can be fatal.

Fear of causing esophageal injury can cause the EP to modify the ablation lesion set delivery, thereby reducing ablation success.

New Solution: an Esophagus displacement tool.

Use of the esophagus displacement tool, EsoSure Esophageal Retractor

The EsoSure Esophageal Retractor allows doctors to re-position a section of the esophagus away from the nearby heart tissue and avoid the heat generated during ablation.

Live streaming ablation: In this re-do ablation, entrainment (pacing) mapping was used to identify non-PV triggers.

Since they had to ablate in the posterior of the left atrium next to the esophagus, they simply moved the EsoSure Retractor up and down to displace the esophagus. The EPs remarked they could now ablate at a higher wattage without fear of harming the esophagus. …continuing reading my report…

2017 AF Symposium: Movin’ it—Protecting the Esophagus During Ablation

2017 AF Symposium

Movin’ it: Protecting the Esophagus During Ablation

Live case presenters: Drs. Rodney Horton, Amin Al-Ahmad and David Burkhardt from the Texas Cardiac Arrhythmia Institute at St. David’s Medical Center in Austin, TX. Moderator: Dr. Andrea Natale.

Patient background: A 79-year-old female needed a ‘re-do’ second ablation. She had persistent A-Fib and hypertension. Her first ablation was August 15, 2016 where they couldn’t terminate her Flutter. Because the temperature probe in her esophagus showed a rise in temperature when they tried to ablate certain areas, “we were not as aggressive as we would have liked.”

The Danger: Esophageal Fistula

During an ablation, doctors take great precautions to not heat or injure the esophagus which lies behind the posterior wall of the left atrium. Injuring the esophagus can, in very rare cases, cause an atrial esophageal fistula which can be fatal.

Fear of causing esophageal injury can cause the EP to modify the ablation lesion set delivery, thereby reducing ablation success by:

1. Reducing the wattage or amount of energy delivered to the left atrium wall which causes less complete scarring; and/or

2. Relocating the ablation lesion to a less desirable area

For this patient: During her first ablation: the doctors noticed a rise in temperature of the probe inserted in her esophagus, so her doctors stopped ablating in that area. Consequently, the A-Fib signal source(s) in that area were not isolated effectively. Result: her A-Flutter was not terminated.

Solution: Esophageal Displacement Tool

The esophagus is not a rigid, inflexible pipe but rather like a hose made out of flexible muscle fibers. It can naturally migrate side-to-side 2-3 cm on its own.

For this live streaming ablation, a new esophagus displacement tool was used: the EsoSure Esophageal Retractor. The tool allows doctors to re-position a section of the esophagus away from the nearby heart tissue and avoid the heat generated during ablation.

The inventor of the device, Steven W. Miller, RN and EP nurse, demonstrated his device to me at the AF Symposium Exhibit Hall.

EsoSure Esophageal Retractor: Shape adjusts to body temperature at A-Fib.com

EsoSure Esophageal Retractor: Shape adjusts to body temperature

At room temperature, the stylet is fairly straight which allows it to be easily inserted into a commonly used gastric tube which is routinely placed down the esophagus by the anesthesia staff. But as the stylet warms to body temperature, it takes on a greater curve. He inserted the stylet into warmed water. You could see how the stylet changed shape and developed a greater curve.

Depending on how the stylet is positioned, it can displace the esophagus up to 2-3 cm to the left or right depending on each person’s anatomy.

Using the EsoSure Retractor, the EP can easily and safely move the esophagus away from any area being ablated. It is FDA approved and has been used by different practitioners more than 700 times without damaging the esophagus.

Live Case Using the EsoSure Retractor

In this re-do ablation, the 79-year-old female patient was in A-Fib when the ablation started. They cardioverted her, but she went right back into A-Fib.

Entrainment (pacing) mapping was used to identify non-PV triggers. Since they had to ablate in the posterior of the left atrium next to the esophagus, they simply moved the EsoSure Retractor up and down to displace the esophagus. It seemed very easy to do.

The EPs mentioned that, with the use of this displacement device, they could now ablate at a higher wattage without fear of harming the esophagus. They also ablated the Left Atrial Appendage area to restore her to sinus rhythm.

What Patients Need to Know

Displacing the esophagus is a major medical advance: The EsoSure Esophageal Retractor is a major medical advance that will significantly improve not only the safety but the effectiveness of catheter ablations. Compared to any other gear in the ablation lab, the EsoSure Retractor is inexpensive ($365-$395 depending on quantity ordered). Any EP lab can and should use it, (or something similar).

Esophagus injury: All too often the esophagus lies behind the right pulmonary vein openings. Doctors have to limit both the placement and the power of their lesions out of fear of damaging the esophagus.

But being able to move the esophagus solves this problem. Ablations will be more effective, and the danger of producing an Atrial Esophageal Fistula (while rare) will be greatly reduced, if not eliminated. It will also reduce ablation procedure time.

Ask your EP: If you are scheduling an ablation, ask your doctors about their plan to prevent esophageal injury.

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Saturday, March 11, 2017

Reference for this Article

2017 AF Symposium LIVE VIDEO: Can Adding Fibrosis Improve Ablation Success?

Updated March 9: We added two new slides comparing the patient’s initial and subsequent DE-MRI images.

Report 13 from 2107 AF Symposium: In a live ablation from from Mass. General Hospital in Boston, Drs. Heist and Van Houzen demonstrated a pioneering strategy to treat Atrial Fibrillation patients with patchy fibrotic areas of tissue. This tissue perpetuates A-Fib.

First, a DE-MRI scan defines and measures the heart’s areas of fibrosis. Next, the doctors ablated (or filled in) these patchy areas with more fibrosis (i.e., ablation scarring) turning the patchy areas into dense fibrotic areas. Transforming patchy fibrotic tissue to dense fibrotic tissue stops A-Fib signals from perpetuating in that tissue.

It may seem counter-intuitive―create more fibrosis to make patients A-Fib free. Read more about this innovative strategy.

2017 AF Symposium Live Video: Adding Fibrosis to Improve Ablation Success?

2017 AF Symposium

Live Case: Can Adding Fibrosis Improve Ablation Success?

Updated March 13: We added two new slides.

Streaming video of an ablation by Drs. Kevin Heist and Nathan Van Houzen from Massachusetts General Hospital (MGH) in Boston, MA (moderator, Dr. Moussa Mansour).

Patient background: The case of a 62-year-old male with symptomatic persistent A-Fib, despite a previous ablation 8/9/2016. Propafenone, amiodarone, and an electrical cardioversion weren’t effective. The patient had been taken off amiodarone a week before this ablation. They cardioverted him into sinus rhythm to better measure areas of low voltage (areas of fibrosis). Low voltage areas were defined as less than 0.5 V.

Mapping Views: Lesions and Remaining Fibrosis From First Ablation

THE TOP SLIDE: The RF point-by-point ablation lesions from the patient’s first ablation done months before the live case.

RED dots represent a greater force or more time making the lesion; PINK dots represent a lower efficiency lesion due to proximity to the esophagus.

Some of these PINK dot area had reconnected and had to be re-ablated during the live case.

(“PA” is  the left atrium viewed from the back.)

THE BOTTOM SLIDE: The MRI done shortly before the live case. The BLUE areas are normal atrial tissue. The RED areas are fibrotic/scarred areas. Some of the red areas in this PA view were not ablated during the first procedure and represent spontaneous fibrosis.

Live: Ablating Areas of Fibrosis

In this live procedure from Boston, MA, Drs. Heist and Van Houzen did a normal PVI and found evidence that some areas from the patient’s previous ablation had reconnected.

The innovative aspect of this ablation is they also ablated areas of fibrosis. ‘Spontaneous fibrosis’ tends to be patchy in a way that perpetuates A-Fib.

Ablating or filling in these patchy areas with more fibrosis (i.e., ablation scarring) turns the patchy areas into dense fibrotic areas which can’t conduct or perpetuate A-Fib.

They first performed a Delayed Enhancement MRI (DE-MRI) scan of this patient’s heart in order to define and measure the areas of fibrosis.

The EPs then ablated (filled in) areas of this fibrosis, turning these patchy fibrotic regions into denser fibrotic areas. These dense fibrotic areas no longer conducted or perpetuated A-Fib.

Two months after the ablation the patient is doing well in sinus rhythm. Whereas after his first ablation, he experienced early recurrence.

What Patients Need to Know

Who Benefits from this Strategy? Adding or filling in patchy fibrotic areas with more fibrosis through ablation is a very innovative ablation strategy.

It is being applied to patients with persistent or persistent long-standing A-Fib who usually have more fibrosis, but is also being applied to paroxysmal patients who have had a durable (successful) PVI but are still in A-Fib (they often have some fibrotic areas).

The term ‘spontaneous fibrosis’ refers to fibrosis (scarring) which occurs naturally, that is, without a doctor’s procedural intervention.

Impractical for Diffused Fibrosis: This strategy doesn’t work if someone has a generalized distribution of fibrous tissue throughout their atrium. It would require ablation of the whole atrium creating too much fibrosis and causing other heart function problems.

Isn’t Creating More Fibrosis Dangerous for Patients? It certainly does seem counterintuitive―create more fibrosis to make patients A-Fib free. But we are looking at patients who already have patches of fibrosis. (If we could turn these fibrotic areas back into smooth heart muscle, then this strategy wouldn’t be necessary.)

This strategy can make people with difficult A-Fib cases A-Fib free, and make a huge difference for patients who have failed ablations.

While this strategy is exciting, we are only at the very beginning stages of this research.

Acknowledgements:

Nassir Marrouche MD

N. Marrouche MD

Dr. Nassir Marrouche: The concept of ablating areas of fibrosis was conceived by Dr. Nassir Marrouche of the University of Utah (CARMA). Dr. Marrouche has started DECAAF II, a clinical study on fibrosis to compare ablation of fibrosis areas to standard PVI ablation.

Known for the completed DECAAF study, Dr. Mansour is now collaborating with Dr. Marrouche on the DECAAF II study, and Massachusetts General Hospital (the originating site of this live streaming video) is one of the participating sites. For more, see my 2017 AF Symposium article A-Fib Increases Fibrosis.

Dr. Kevin Heist: I would like to thank Dr. Kevin Heist, Mass. General Hospital, for patiently explaining to me the concept, rationale and strategy of ablating areas of fibrosis. (I really needed his help!)

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Monday, March 13, 2017

Reference for this Article

2017 AF Symposium: LIVE Video Ablation With Non-Contact Catheter Mapping

The Acutus Medical Non-Contact basket catheter with multiple electrodes

The Acutus Medical Non-Contact basket catheter with multiple electrodes

Report 12 from 2107 AF Symposium: In a live case from Prague, the Czech Republic, the EPs used the non-contact basket catheter to generate a 3D anatomy of the patient’s left atrium.

They produced propagation maps which looked like rotor action seen in other mapping systems, but sharper and with high resolution.

During the ablation, they used Acutus Medical’s basket catheter to re-map the left atrium. This showed that there were gaps in the ablation of one of the right vein openings which they corrected. …Read my full report…

Live Case: Non-Contact Ultrasound Basket Catheter Dipole Density Mapping

2017 AF Symposium

Live Case: Ablation Using Non-Contact Ultrasound Basket Catheter Dipole Density Mapping

Illlustration: Acutus Medical Non-Contact Dipole basket catheter with multiple electrodes.

Acutus Medical Non-Contact Dipole basket catheter with multiple electrodes.

Video streaming of an ablation from Na Homolce Hospital in Prague, the Czech Republic with Drs. Peter Neuzil, Jan Petru, and Jan Skoda.

The doctors used a new high resolution mapping system from Acutus Medical to identify in real time where his A-Fib signals were coming from.

Patient background: A 68-year-old man in paroxysmal A-Fib had a CHA2DS2-VASc score of 4 with hypertension and a pulmonary embolism. He had had a PVI in January 2011 and a repeat PVI to fix gaps in April 2011. His A-Fib recurred in 2014. Electrical cardioversions didn’t work.

Non-Contact Mapping with Ultrasound-Electrode Catheter

VIDEO: For a more detailed explanation of the Non-Contact Dipole Density AcQ Imaging and Mapping, see the video from Acutus Medical.(1:54)

The Acutus Medical Non-Contact Dipole Density AcQ Imaging and Mapping catheter uses a basket catheter with multiple electrodes and ultrasound anatomy reconstruction.

‘Non-contact’ means the basket catheter can float freely in the left atrium and doesn’t have to be applied to the surface of the heart to generate A-Fib maps.

The basket catheter has six splines each with eight nodules that contain 48 ultrasound transducers and 48 electrodes. The ultrasound pings the atrium wall and rapidly produces a 3D left atrium anatomy.

Electrical Measurement: Dipole Density vs Voltage

For over one hundred years, voltage has been the major electrical measurement in cardiac medicine. The limitation with using voltage in electrophysiology is that the reading includes both the localized charge (Dipole Density) as well as the sum of the surrounding sources providing a broad, blended view of cardiac activity.

According to Acutus Medical, by eliminating these surrounding sources, and using dipole density (instead of voltage) the field of view becomes sharper and narrower.

This more precise electrical activation is displayed as a Dipole Density map on a 3D ultrasound reconstruction of the heart.

Acutus Medical Illustration: localized charge (Dipole Density) with the sum of the surrounding sources

Acutus Medical Illustration: localized charge (Dipole Density) with the sum of the surrounding sources

Live Streaming Video: Ablation from Prague

In the live case, the EPs used the non-contact basket catheter to generate a 3D anatomy of the patient’s left atrium.

They produced propagation maps which looked like rotor action seen in other mapping systems, but sharper and with high resolution.

During the ablation, they used the basket catheter to re-map the left atrium. This showed that there were gaps in the ablation of one of the right vein openings which they corrected. When they made a mitral isthmus line, the patient’s A-Fib terminated which restored him to normal sinus rhythm.

What Patients Need To Know

May Replace Contact Mapping: Non-contact mapping is a significant innovation in catheter ablation and may eventually replace existing contact mapping catheters and make ablations easier. It also seems to require less technical skill than in a traditional contact mapping system.

“Non-contact mapping is a significant innovation and may eventually replace existing contact mapping catheters.”—Steve Ryan

No Radiation & Instantaneous: Using ultrasound to produce a 3D rendering of the heart is innovative and could change the way the anatomy of the heart is generated for an ablation. And unlike a CT scan, it doesn’t use radiation. Also, unlike a CT scan, the ultrasound images of the heart are generated instantaneously in real-time.

Higher Resolution: Dipole Density mapping may prove to be a higher resolution system than current mapping systems.

Not Yet Available in U.S.: But don’t expect the Acutus Medical System to become available in the U.S. any time soon. It isn’t yet FDA approved or available for sale in the U.S.

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If you find any errors on this page, email us. Last updated: Thursday, March 2, 2017

Reference for this Article

2017 AF Symposium: Three New Reports—Genetic A-Fib and LIVE Streaming Video Ablations

Live Streaming Video from AF Symposium at A-Fib.com

To my 2017 AF Symposium Overview, I added how we observed in-progress A-Fib procedures via streaming video from five locations spanning the globe, and heard from the EPs performing the ablations. Continue to the Video Overview…

Report 11: LIVE! Ablation Using CardioFocus Laser Balloon

CardioFocus HeartLight Laser Balloon catheter

CardioFocus HeartLight Laser Balloon catheter

Video streaming from Na Homolce Hospital in Prague, The Czech Republic. Drs. Peter Neuzil, Jan Petru and Jan Skoda did an ablation using the CardioFocus HeartLight Endoscopic Visually Guided Laser Balloon (FDA approved April 4, 2016).

The doctors showed how they could directly see the Pulmonary Vein opening they were ablating (unlike RF and CryoBalloon systems). The center of the catheter has an endoscopic (looking inside) camera.

(To me, this is a major advantage and ground-breaking improvement for patients.)

Read more of my report, and see a short video clip with an actual view of the pulmonary veins during an ablation. …Continue reading my report….

Report 10: LIVE! Two Procedures—but Different Left Atrial Appendage Occlusion Devices

Featuring the Amplatz Amulet from St. Jude Medical and the LAmbre from LifeTech Scientific.

Amplatz Amulet occlusion device by St. Jude Medical - A-Fib.com

Amplatz Amulet occlusion device by St. Jude Medical

Live from Milan, we watched the doctors insert an Amplatz Amulet into the LAA of a 78-year-old women who had a high risk of bleeding.

These doctors did something I had never seen before. They made a physical model of the woman’s LAA, then showed how the Amplatz Amulet fit into the model. This helped AF Symposium attendees see how the Amplatz Amulet actually worked. …Continue reading my report…

Report 9: World-Wide Studies on Genetic A-Fib

DNA: Double helix graphic at A-Fib.com

Dr. Patrick Ellinor of Mass. General Hospital, Boston MA, reported the biggest news is that A-Fib genetic research is increasing exponentially. The AFGen Consortium website lists 37 different studies and world-wide institutions studying A-Fib genetics with over 70,000 cases. Within the next 10 years, Dr. Ellinor and his colleagues hope to identify over 100 different genetic loci for A-Fib.

Dr. Ellinor reported that using a genetic “fingerprint” of A-Fib helps to identify those patients at the greatest risk of a stroke. (There’s a 40% increased risk of developing A-Fib if a relative has it.)…Continue reading my report…

About the Annual AF Symposium

The annual AF Symposium brings together the world’s leading medical scientists, researchers and EPs to share recent advances in the treatment of atrial fibrillation. You can read all my summary reports on my 2017 AF Symposium page.

2017 AF Symposium More Reports: Obesity & A-Fib and Increasing Fibrosis

Another two summary reports from the January 2017 AF Symposium. Here’s the entire list of my reports from the 2017 AF Symposium.

Report 7: A-Fib Increases Fibrosis by 5%-10% Per Year

Dr. Nassir Marrouche of the University of Utah (CARMA), Salt Lake City, UT continued his ground-breaking work using MRI to investigate Atrial Fibrillation. Some of the major contributions Dr. Marrouche’s MRI research has made include that patients with high fibrosis levels are at greater risk of stroke and that they may be precluded from a successful catheter ablation.

He showed how current MRI testing also measures fibrosis in 3D to better gauge its thickness. Read about his latest research on A-Fib patients and fibrosis.

Report 8: New Insights into the Effects of Obesity on Atrial Fibrillation

Dr. Jose Jalife of the University of Michigan, Ann Arbor, MI, discussed the “Obesity Paradox”, a hypothesis that obesity may be protective and associated with greater survival with certain chronic diseases. Dr. Jalfie showed how and why this is not the case with A-Fib.

Under normal conditions, the surface of the heart is covered by fat stored in the tissue. A-Fib is often associated with increased volume of epicardial fat… Continue reading Dr. Jalife’s research findings.

See the entire list of my reports from the 2017 AF Symposium.
Look for another report soon.

2017 AF Symposium Video Streaming: Ablation using CardioFocus Laser Balloon

2017 AF Symposium

Live Case: Ablation using CardioFocus Laser Balloon

Video clip: :16 sec view of pulmonary view opening during ablation with HeartLight System; from ‘Ablate What You See & See What You Ablate’.

Video streaming from Na Homolce Hospital in Prague, The Czech Republic. Drs. Peter Neuzil, Jan Petru and Jan Skoda, in their second live case, did an ablation using the CardioFocus HeartLight Endoscopic Visually Guided Laser Balloon (FDA approved April 4, 2016).

Direct Visualization

The doctors showed how they could directly see the Pulmonary Vein opening they were ablating (unlike RF and CryoBalloon systems).

The center of the catheter has an endoscopic (looking inside) camera. (To me, this is a major advantage and ground-breaking improvement for patients.) (Watch :13 video clip)

Laser Energy For Ablation

CardioFocus HeartLight Laser Balloon at A-Fib.com

CardioFocus HeartLight Laser Balloon

In the center of the catheter is an optical fiber which produces an arc of laser (near infrared) energy. When they applied this laser energy, it looked like a green flashing light that circled the PV.

The doctors said that watching this circulating green arc allowed them to visually see if they were making complete circular lesions of the PV.

They later used a regular Lasso catheter to check for ablation integrity.

Variable Diameter Compliant Balloon

The doctors also showed how the CardioFocus HeartLight system uses a variable diameter compliant balloon which can be sized to fit into a wide range of PV openings.

See our library of videos about Atrial Fibrillation

One preliminary research article suggested that the Laser Balloon system clinical outcomes were an improvement over CryoBalloon ablation. 

VIDEO ANIMATION: For a one-minute animation of how the CardioFocus HeartLight system works, see Visually Guided Ablation.

Editor’s Comments:
The CardioFocus HeartLight Laser Balloon catheter seems like a major advance in the treatment of A-Fib, To be able to look directly at the PV opening instead of using fluoroscopy, etc. should make an EP’s ablation task much easier and potentially more effective. And having a variable diameter compliant balloon is an added plus.
But when I talked with the CardioFocus rep at the AF Symposium exhibit hall, he said they were in the process of rolling out the Laser Balloon system to various centers. It may be a short while till the system is up and operational nationwide in the U.S. (It’s already in use in Europe.) We will try to list which centers use the Laser Balloon system.
If real world experience proves its effectiveness, the CardioFocus HeartLight Laser Balloon system may eventually make CryoBalloon ablation a secondary player.

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Sunday, February 12, 2017

Resources for this article

2017 AF Symposium: New Reports on Reversing Fibrosis and Hypercoagulability & NOACs

I’ve been a busy writer since attending the 2017 AF Symposium in January. Here are two more summary reports.

Report 5Some Forms of Fibrosis May Be Reversible: Research with Overweight Sheep 

In a very hopeful study for Atrial Fibrillation patients, Dr. Stanley Nattel of the University of Montreal, Montreal, Canada concluded that some forms or types of fibrosis are indeed reversible.

Steve with Shannon Dickson, editor of The A-Fib Report

Steve with Shannon Dickson, editor of The A-Fib Report

He described his experiments with overweight sheep. A 30% weight lost reduced fibrosis as well as inflammation and incidence of A-Fib. Continue reading….

Report 6: Hypercoagulability May Cause A-Fib, NOACs May Prevent It 

Novel oral anticoagulants (NOACs) may both prevent and stop A-Fib, according to a thought-provoking hypothesis by Dr. Ulrich Schotten of the University of Maastricht, Maastricht, The Netherlands.

His different, somewhat contrary hypothesis flips the current thinking― that hypercoagulability increases and promotes A-Fib (versus A-Fib increasing hypercoagulability).

Working with specially designed mice with increased thrombin activity (hypercoagulated mice), Dr. Schotten found that these mice had increased atrial fibrosis and A-Fib, and a hypercoagulated state promotes atrial fibrosis…Continue reading….

See the entire list of my reports from the 2017 AF Symposium.
Look for three more reports soon.

2017 AF Symposium: LIVE VIDEO! Two Procedures—Different Left Atrial Appendage (LAA) Occlusion Devices

AF Symposium 2017

LIVE VIDEO! Two Procedures—Different Left Atrial Appendage (LAA) Occlusion Devices

This live streaming video session from Milan, Italy, featured two Left Atrial Appendage occlusion devices: the Amplatz Amulet from St. Jude Medical and the LAmbre from LifeTech Scientific.

LAA Closure Using the Amplatz Amulet (St. Jude Medical)

Amplatz Amulet occlusion device by St. Jude Medical - A-Fib.com

Amplatz Amulet occlusion device by St. Jude Medical

Live from Milan, Drs. Claudio Tondo, Antonio Dello Russo, Gaetano Fassini, and Massimo Moltrasio inserted an Amplatz Amulet (St. Jude Medical) into the Left Atrial Appendage of a 78-year-old women who had a high risk of bleeding. (The LAA is the origin of 90%-95% of Atrial Fibrillation-related clots).

Model of Patient’s LAA: These doctors did something I had never seen before. They made a physical model of the woman’s LAA, then showed how the Amplatz Amulet fit into the model. This isn’t done in all cases of LAA occlusion, but was very helpful for the AF Symposium attendees to see how the Amplatz Amulet actually worked.

Illustration of placing the Amplatz Amulet (St. Jude Medical) in the left atrial appendage

Illustration of placing the Amplatz Amulet (St. Jude Medical) in the left atrial appendage

The doctors also demonstrated how they could easily retract and recapture the device (which isn’t easy to do with the Watchman occlusion device [Boston Scientific]).

Like the Watchman device, the Amulet also has hooks to hold the device in place.

VIDEO ANIMATION: showing how the Amplatz Amulet device is installed (1:14 min.) from St. Jude Medical.
Watchman device - A-Fib.com

Watchman occlusion device by Boston Scientific

It seemed very easy to insert the Amplatz device. It closed off the LAA opening with the bottom part completely covering the LAA opening into the left atrium.

For most patients, this might be an advantage of the Amplatz device over the Watchman occlusion device which doesn’t have this overlap and can sometimes leak around the edges.

But, on the other hand, once the Amplatz device is in place, the overlap of the LAA would prevent ablation and electrical isolation of the LAA should that be necessary. But in most cases, this isn’t often required.

Second LAA Closure Using the LAmbre (LifeTech Scientific)

LAmbre (LifeTech Scientific) occlusion device at A-Fib.com

LAmbre (LifeTech Scientific) occlusion device

Later in the session when the moderators cut back to the live video stream from Milan, the EPs inserted a LAmbre (LifeTech Scientific) device in the LAA of a second patient. She was a 50-year-old woman who had a very small LAA. She had suffered two ischemic strokes within a month of each other, but she had bleeding problems when she took warfarin and dabigatran (Pradaxa).

[She was definitely between a rock and a hard place. Ischemia refers to a restriction or blocking of blood supply as by A-Fib clots. She needed to be on blood thinners to prevent A-Fib clots from forming particularly in her LAA, but couldn’t tolerate blood thinners which caused her bleeding problems. An LAA occlusion device was pretty much her only option.]

The LAmbre LAA occlusion device (LifeTech Scientific) seems similar to the Amplatz (St. Jude Medical) as both are fully recapturable and repositionable within the LAA. But each has its own anchor design to hold the device in place. But the LAmbre can fit into smaller size Left Atrial Appendages.

Both the Amplatz Amulet and the LAmbre occlusion devices are approved for use in Europe, but neither is approved yet in the U.S. (Not surprising since the U.S. approval  of the Watchman device also lagged the European approval.)

I predict the Amplatz Amulet from St. Jude Medical will soon be approved by the FDA for use in the U.S.

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Monday, June 12, 2017

2017 AF Symposium: World-Wide Studies on Genetic A-Fib

Patrick Ellinor, MD

P. Ellinor, MD

AF Symposium 2017

World-Wide Studies on Genetic A-Fib

Dr. Patrick Ellinor of Massachusetts General Hospital, Boston MA, updated everyone on the world-wide effort to identify the genetic basis of A-Fib.

What are the genetic variants associated with A-Fib? In previous research Dr. Ellinor showed, among other findings, that A-Fib is inheritable and that there is a 40% increased risk of developing A-Fib if a relative has it. (See my earlier report: Genetics of A-Fib 2012 AF Symposium.)

World-Wide Effort to Study A-Fib Genetics and Genome Sequencing

The biggest news is that A-Fib genetic research is increasing exponentially. The AFGen Consortium website lists 37 different studies and world-wide institutions studying A-Fib genetics with over 70,000 cases. Within the next 10 years, Dr. Ellinor and his colleagues hope to identify over 100 different genetic loci for A-Fib.

There’s a 40% increased risk of developing A-Fib if a relative has it.

A-Fib Genetic “Fingerprint” May Help Identify Those at Risk of Stroke

Dr. Ellinor reported that using a genetic “fingerprint” of A-Fib helps to identify those patients at the greatest risk of a stroke. While still a research tool, this approach could be used to identify those patients at risk for either developing A-Fib or a stroke.

A-Fib genetic research and genome sequencing could someday identify the pathways and potential therapeutic targets of A-Fib.

In the future, genetic research may refine stroke risk models such as CHA2DS2-VASc and HAS-BLED to better target who may actually need anticoagulants and who can safely take them.

Participate in A-Fib Genetic Studies

Familia Atrial Fibrillation at A-Fib.comIf you and at least 3 other members of your family have A-Fib, you can become involved in this potentially very important research. Contact the studies at Mass. General Hospital or Vanderbilt University.

Patrick T. Ellinor, MD, PhD, Director, Cardiac Arrhythmia Service
Marisa Shea, RN,  Research Nurse
Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114
617-724-7780, Email: mshea1(at)partners.org

Vanderbilt University also welcomes families with A-Fib for their genetic studies. Contact the Vanderbilt Atrial Fibrillation Registry (they also have an AF Ablation Registry)

Diane Crawford, RN
Vanderbilt University Medical Center, 1266 MRB IV, Nashville, TN 37232-0575
(615) 322-0067, Email: Diane.n.crawford(at)vanderbilt.edu

Recent Post: For more about genetic Atrial Fibrillation, see my post, Inherited A-Fib? Is it More Risker for Family Members?

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Monday, February 6, 2017

2017 AF Symposium: New Insights into the Effects of Obesity on Atrial Fibrillation

Jose Jalife, MD

Jose Jalife, MD

AF Symposium 2017

New Insights into the Effects of Obesity on Atrial Fibrillation

Dr. Jose Jalife of the University of Michigan, Ann Arbor, MI, discussed the “Obesity Paradox”. The Paradox is a hypothesis that obesity may be protective and associated with greater survival with certain chronic diseases. Dr. Jalfie showed how and why this is not the case with Atrial Fibrillation.

Under normal conditions, the surface of the heart (epicardium) is covered by fat stored in the tissue (called adipose tissue).

A-Fib is often associated with increased volume of epicardial fat. This increased volume lengthens the duration of A-Fib episodes and results in fibrotic remodeling of the adipose tissue.

In addition, fatty acids both shorten the ‘action potential’ and increase the ‘dominant frequency’ (factors in the initiation and maintenance of AF signals). This leads to fibrosis (fibrofatty infiltration) of the epicardial fat. Altogether, they perpetuate Atrial Fibrillation signals and episodes.

“Obesity Paradox” Doesn’t Apply

Excessive epicardial fat is bad for those with A-Fib. Thanks to Dr. Jalife’s research, we can rule out the “Obesity Paradox” with regards to obesity and A-Fib. Increased epicardial fat:

• Increases the duration of A-Fib
• causes fibrotic remodeling of the adipose tissue
• Increases fatty acids

Thanks to Dr. Jalife we are beginning to understand how and why obesity affects the heart and A-Fib.

Surgery of Obese Patient―My Observations

At a 2016 conference in Zürich, I watched a live A-Fib surgery of an obese patient. It was incredible how many layers of yellow fat bundles the surgeon had to cut through before reaching the heart.

If a video of this surgery were shown to A-Fib patients who are significantly overweight, it could be quite motivating. When you actually see the epicardial fat layers Dr. Jalife talks about, it makes a frightening, ‘come-to-Jesus’ impression.

What Patients Need to Know

Weight Loss and A-Fib: Research has shown that just losing weight and exercising, by themselves, can reduce and even eliminate A-Fib.

Recurrence Rates: In addition, many EPs today won’t perform a catheter ablation on someone who is obese, because their recurrence rates are very high compared to normal patients.

If you have A-Fib and are significantly overweight (not just a few pounds), you can expect to hear a lecture from your EP/doctor that you should lose some weight.

For more, see Weight Loss Key to Reverse Atrial Fibrillation, Improve Ablation Success.

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Friday, March 3, 2017

A-Fib Increases Fibrosis by 5%-10% Per Year

Nassir Marrouche MD

N. Marrouche MD

AF Symposium 2017

A-Fib Increases Fibrosis by 5%-10% Per Year

Dr. Nassir Marrouche of the University of Utah (CARMA), Salt Lake City, UT continued his ground-breaking work using MRI to investigate Atrial Fibrillation.

Some of the major contributions Dr. Marrouche’s MRI research has made include that patients with high fibrosis levels are at greater risk of stroke and that they may be precluded from a successful catheter ablation.

(For more about stroke risk, see Dr. Marrouche’s High Fibrosis at Greater Risk of Stroke and Precludes Catheter Ablation: Lessons Learned from the DECAAF Trial.)

Magnetic resonance imaging (MRI) is a technique that uses a magnetic field and radio waves to create detailed images of organs.

Fibrosis Develops Rapidly, Within One Year

Dr. Marrouche’s latest research shows that about 35% of patients with A-Fib will experience more than 5%-10% of fibrotic changes within 1 year. (This is a frightening statistic, since fibrosis is currently considered irreversible.)

He also described how the more fibrosis a patient has, the more likely the patient will have a recurrence after an A-Fib ablation.

He also showed how current MRI testing also measures fibrosis in 3D to better gauge its thickness.

New Study Ablating Fibrosis

Dr. Marrouche also described a new clinical trial (DECAAF II) that will compare standard Pulmonary Vein Isolation (PVI) ablation to ablation of fibrosis areas. See http://www.decaaf.org

The more fibrosis a patient has, the more likely the patient will have a recurrence after an A-Fib ablation.

What Patients Need To Know

A-Fib produces fibrosis quickly and harms your heart permanently. This fibrosis produces collagen and scarring in the heart which is a permanent remodeling effect of A-Fib.

And what a wake-call for A-Fib patients―that A-Fib fibrosis can and does develop so rapidly! Within one year of living in A-Fib, your heart can become 10% fibrotic which is irreversible. How truly frightening!

Dr. Marrouche’s Message: Don’t live in A-Fib! The message from Dr. Marrouche’s research is obvious. Don’t live in A-Fib!!! Do everything you can to be restored to normal sinus rhythm.

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Monday, March 6, 2017

2017 AF Symposium: Some Forms of Fibrosis May Be Reversible

Dr. Stanley Nattel, U of Montreal

S. Nattel, MD

AF Symposium 2017

Some Forms of Fibrosis May Be Reversible

Background: Fibrosis is tissue with fiber-like characteristics; over time it makes the heart stiff, less flexible and weak, overworks the heart, reduces pumping efficiency and leads to other heart problems.

Dr. Stanley Nattel of the University of Montreal, Montreal, Canada discussed whether fibrosis is reversible. In a very hopeful study for Atrial Fibrillation patients, he concluded that some forms or types of fibrosis are indeed reversible.

Heart Attack Fibrosis

Dr. Nattel described a typical heart attack victim who experiences actual heart tissue damage and areas of heart tissue death. In these damaged heart areas, fibrous tissue replaces dead cardiomyocytes (scarring). This form of fibrosis may be irreversible.

A 30% weight lost reduced fibrosis in overweight sheep, as well as inflammation and incidence of A-Fib.

Interstitial (A-Fib) Fibrosis

But A-Fib fibrosis is often “purely interstitial” or reactive to the A-Fib. (“Interstitial” refers to the space between cells or myocytes.) This type of fibrosis may indeed be reversible.

Dr. Nattel described his experiments with overweight sheep. A 30% weight lost reduced fibrosis (collagen formation) in these overweight sheep, as well as inflammation and incidence of A-Fib.

(For more research findings, see Dr. Jose Jalife’s experiments in sheep which reduced fibrosis by 50%: The Holy Grail: Preventing A-Fib by a GAl-3 Inhibitor.)

What Patients Need to Know

Some A-Fib Fibrosis May Be Reversible: This is encouraging for A-Fib patients. Even if you develop fibrosis from being in A-Fib, some of this fibrosis may be reversible.

Returning to normal sinus rhythm may reverse a good deal of fibrosis in your heart.

But much more research needs to be done to figure out how best to reverse A-Fib fibrosis. And some long-term A-Fib fibrosis may indeed be irreversible when it produces lasting scarring (dead fibrotic tissue).

Don’t Live in A-Fib and Develop Fibrosis: If you have A-Fib, you are most likely developing a fibrotic heart. The good news from Dr. Nattel (and Dr. Jalife) is that returning to normal sinus rhythm may reverse a good deal of fibrosis in your heart.

In spite of what you hear in today’s media and advertisements, don’t just live in A-Fib and develop fibrosis! Seek your cure!

Return to 2017 AF Symposium Reports
If you find any errors on this page, email us. Last updated: Friday, March 3, 2017

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