I asked my EP why running with a 150 heart rate is ok, but not AFIB tachycardia. She said it is the "sustained" tachycardia that is the problem. Not 2 15 minute episodes.

Remodeling is in 2 forms... electrical and physical. You explained the electrical very well. The physical has to do with larger atrial size and fibrosis. Both encourage afib. Even in athletes. Sometimes it progresses and sometimes it doesn't. Taking care of yourself by what you eat, triggers, sleep, all the normal healthy stuff and controlling your rate are all good. I don't think "weaker" is the right word. They can do MRIs to determine atrial size and fibrosis.

Thank you for your response Petey. At what point do you think a doctor orders an MRI to assess Atrial size or fibrosis? Perhaps, after inconclusive findings on Echo or maybe at the preference or discretion of the doctor? One more question if you don't mind....I remember some months back you mentioned in a post that rate control acts as a "governor" on your heart during exercise. (I may have misspelled that word). I understood this to mean that the medication would only allow your heart rate to increase only to a point. Does rate medication also lower your resting heart rate? If so, then I am thinking a person's max heart rate and target heart rate zones would have to be adjusted as well? If a person can tolerate exercise, tolerates their medication and AF is well managed, will rate medication allow a person to get a good cardio work out for weight management or reduction?

Here is my experience and what I know from being a gym rat. It general, they say that your "target" heart rate should be 220 minus your age equals your maximum heart rate. 85% of your maximum heart rate is your target heart rate that is, the optimum zone for maximum benefit. So, if a person is 60, their maximum heart rate is 160 (220-60), and their target rate is 136 (85% of 160). I wouldnt worry about going slightly under or over.
Some interesting stuff about rate control they used to think that strict rate control, that is, a resting heart rate of 60-80, was very important to be maintained. During a 6 minute walk, 110 was the goal. Well, they found that even if your resting heart rate was between 60-100 and your 6 minute walk produced above 110 (say 130), there was no difference in long term outcomes. Heart failure is the thing they were trying to avoid. That is because a long term heart rate that is high can weaken the heart. Another fact, afib type heart failure is reversible after rate control is under control.
So what is normal resting heart rate by definition? Between 60-100. If you have a resting heart rate of 59, that is bradycardia. If your rate is 101, that is tachycardia. Thats a pretty wide normal range. As far as endurance athletes are concerned, they usually fall into the bradycardia range and it is benign (although increased atrial size and bradycardia make athletes more prone to afib they think). Athletes like to brag about their resting heart rate of 30-60. Remember when you were taught that 72 bpm was the norm? So all of these numbers are guidelines and your overall heart health and how you feel is what really matters. Low blood pressure is the same if it is 98 over 62 for example, they say that is fine if you arent dizzy.
Concerning remodeling electrical remodeling is progressive they say. It makes it harder to eliminate afib they think, because it makes afib the new normal, with many electrical pathways for afib to travel to the ventricles. I have never heard of anyone saying that atrial size actually weakens the heart, it just makes you more susceptible to afib. Again, athletes hearts are remodeled to adjust to the high output required and they have larger atria. Larger atria mean more places to have afib electrical impulses. No-one comes out and says it, but it seems to mean more why the remodeling occurred. For example, if it was from high blood pressure or leaky valves, that is not good. But maybe it is the cause that matters. Afib can cause larger atria also, they believe.
Concerning rate control and workouts for me, my resting heart rate on rising is about 60 same when I am asleep. It is from 60-80 at rest during the day. It seems my heart rate goes up to 130 when I really push it. So I am in a good zone. I have heard some serious athletes complain about not getting workout level heart rates. I believe it is in the adjusting of the medication. I am on Bystolic, a beta blocker. It has been consistent.
One interesting thing in my case. .. as you know I am in persistent afib after about 20 minutes on the treadmill, if I push hard, my heart rate goes down to about 80 or less and I can breathe even better I am wondering if I am self converting. My portable EKG machines dont allow you to measure when I am moving when testing. Maybe I need another stress test with EKG at the doctors office.
Finally, they should just measure your atria when you are diagnosed, along with all the other stuff on an MRI also, I presume that you had a stress test with all this stuff? They should be measuring all your heart sizes, blockages, mitral regurgitation, etc. I think you have to ask for the fibrosis test. Google Utah score before you go to the doctor.

Well thats a brief summary.

petey

http://healthsciences.utah.edu/carma/images/3rdArticle.pdf

Utah scoring, ablation staging, and Fibrosis

Atrial fibrillation (AF) is associated with atrial electrical,
contractile, and structural remodeling. Several different
structural markers have been proposed and associated with
ablation outcomes. However, modalities allowing providers
to accurately and prospectively assess atrial structural arrhythmic
substrate and to individually predict treatment outcomes
are still lacking.
Although AF ablation seems to be a valid therapeutic
option, the effectiveness of the procedure has been demonstrated
only in a moderate percentage of the AF patient
population. Thus, the dilemma lies in defining the appropriate
ablation candidate that would profit most from an invasive
procedure. Furthermore, success of the radiofrequency
(RF) ablation procedure correlates with the appropriateness
No disclosures.
Address for correspondence: Nassir F. Marrouche, M.D., Executive
Director, Comprehensive Arrhythmia Research and Management Center,
Division of Cardiology, University of Utah Health Sciences Center, Suite
4A100 SOM, 30 N 1900 E, Salt Lake City, UT 84132. Fax: 801-585-1601;
E-mail: nassir.marrouche@hsc.utah.edu
Manuscript received 19 August 2010; Revised manuscript received 8
September 2010; Accepted for publication 13 September 2010.
doi: 10.1111/j.1540-8167.2010.01941.x
of transmural left atrial lesion. However, accurate intraprocedural
assessment of lesion formation remains yet to be
determined.
Gadolinium is a magnetic resonance imaging (MRI) contrast
agent, which allows differentiation between healthy and
abnormal myocardial tissue due to differential washout kinetics.
These properties have led to the development of late
gadolinium enhancement (LGE)-MRI. By using custommade
high-resolution LGE-MRI sequences, we have been
able to define areas of enhancement within the atrial wall,
which correspond to intramyocardial fibrosis and/or ablation
scar.1
In this article, we describe an MRI-based tailored approach
to manage patients with AF. Our protocol begins
with clinical staging of AF capable of predicting ablation
success and patients stroke risk. Finally, we demonstrate
the use of MRI in planning redo AF ablation procedures,
and an overview of our work in the field of real-time
MRI.

Atrial Fibrosis, Not Afib Type, Linked to Atrial Fibrillation Strokes
February 23, 2011 at 3:29 pm 6 Comments
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Researchers at the Comprehensive Arrhythmia Research and Management Center (CARMA) in Utah have been studying the relationship between atrial fibrillation, atrial fibrosis, and catheter ablation outcomes for many years. Now, theyve applied their knowledge of quantifying atrial fibrosis to stroke risk assessment and found that the amount of atrial fibrosis, not type of afib, is independently associated with stroke.

The long version:

February 24, 2011 New research showing a link between atrial fibrosis (hardened tissue in the atrium) and stroke was just published in the Journal of the American College of Cardiology. Doctors at the Comprehensive Arrhythmia Research and Management Center (CARMA) in Utah have been studying the relationship between atrial fibrillation, atrial fibrosis, and catheter ablation outcomes for many years. Now, theyve applied their knowledge of quantifying atrial fibrosis to stroke risk assessment.

Atrial Fibrosis and Remodeling

If left untreated, atrial fibrillation can lead to atrial fibrosis, which is called remodeling or substrate modification. Once the atrial substrate has been modified, it becomes increasingly difficult to treat atrial fibrillation. In the past, it was thought that only persistent forms of atrial fibrillation caused substrate modification. However, doctors at CARMA have shown that even patients with paroxysmal afib can have extensive remodeling. Dr. Nassir Marrouche, Executive Director of CARMA, presented research on this and how atrial fibrosis can affect catheter ablation outcomes at Heart Rhythm Society 2010.

Atrial Fibrosis and Stroke

Researchers at CARMA evaluated the atrial fibrosis of 387 patients using delayed enhancement magnetic resonance imaging (DE-MRI). Patients were categorized into four groups depending on the level of fibrosis. Stage I patients had the lowest amount of atrial fibrosis, at less than 8.5% of the left atrium. Stage IV patients had the highest, at more than 21.1% of the left atrium.

Analysis showed that extensive substrate modification was independently associated with stroke. Stage IV patients were four times more likely to have a stroke than patients with a low level of atrial fibrosis. (The odds ratio for having a stroke was 3.91 for Stage IV patients compared to only 0.07 for Stage I patients.)

The researchers compared the level of remodeling with patients CHADS2 risk scores. Of note, 16.5% of patients with a CHADS2 score of 0 (low risk) and 18.5% of patients with a CHADS2 score of 1 (intermediate risk) had Stage IV atrial fibrosis.

The study had two other important findings. First, the type of atrial fibrillation, paroxysmal or persistent, did not have an impact on the likelihood of stroke rate. Second, gender did. Women were three times more likely to have a stroke than men. Because men tend to get treatment for atrial fibrillation sooner than women, the researchers hypothesized that women in the study had more extensive remodeling than men, which led to a higher stroke rate.

Although doctors at CARMA dont believe that atrial fibrosis evaluation should replace CHADS2, they think their staging system could help determine which patients should be placed on anticoagulation. For instance, a patient may be deemed to have low stroke risk based on a CHADS2 score of zero, but if that patient has extensive atrial fibrosis, that patient may be at high risk for stroke and need to be placed on anticoagulation medication.

Comment: Many afib patients are placed on rate control medication, which helps alleviate the symptoms of atrial fibrillation but doesnt put the heart back into normal sinus rhythm. Thus, atrial fibrillation can continue and lead to substrate modification, which allows more afib to occur (Afib begets afib). This new research from CARMA shows that this also increases the risk of stroke. If this applies to you, this new finding may be a subject for discussion with your doctor.

I have to laugh at the last paragraph... the writer (her comment is in the last paragraph and isn't part of the study)doesn't like rate control... but the study says persistent afib doesn't affect fibrosis any more than paroxysmal afib. So that doesn't make sense. If you are in persistent or longstanding persistent (permanent) afib, you are probably on rate control and/or rhythm control isn't working, otherwise you wouldn't be in afib... so there must be something else going on that causes one person to have fibrosis and not another. Look again at the study... stage 4 fibrosis differences between paroxysmal and persistent afib was only 2%!!! Measuring fibrosis IS a valid way of predicting ablation success probability however.

Petey: Your experience with heart rate and rate control is encouraging information. I appreciate the input.

I never had an MRI and my last echo was done right after my last ablation (10 months ago) to ensure the pericardial effusion resolved. My LA size was 3.2 cm at that time. The report permeters indicated that my LA size is within range (1.9 to 4.0 cm). I have mitral valve prolapse with trace regurgitation but my doctor has not seems concerned with this since my LA is not enlarged. I had a stress test done 1 1/2 years ago when diagnosed with inconclusive results so my Cardio at the time did performed a heart cath.

It sounds like an MRI, to determine fibrosis and potential ablation success, could be very beneficial for many people. I am going to bring this up to my Cardio as it relates to stroke risk. It sounds like they can really make an accurate decision on blood thinner therapy based on an MRI finding more so than CHADS. I am a 0 on CHADS and am on 325mg aspirin only.

Additionally, If I were to attempt further ablations in the future, I think I would pretty much insist on having an MRI, after reading some of the studies you posted about MRI, assessing fibrosis to determine potential ablation success. It is also interesting in the posted info that paroxsysmal AF may be associated with some fibrosis/remodeling. Thanks for all this great information!

3.2 is great. Did you know that a centimeter is 1/4 inch? That means normal range is between 1/2 inch to 1 inch! Pretty small thing to be such a problem!

I am on the 4th floor at work. The floors are 24 steps, so it is 98 steps. When I walk up I am not out of breath but my boss and someone who is a gym rat both tell me they are out of breath by the 3rd floor... I walked up with the gym rat guy and he could just about talk. He has had a stress test too, so I know he was evaluated.

96 I mean

Petey: It amazing to put the actual size in perspective! That IS a very small place for all the trouble it causes. Regarding the rate medication you are taking, Bystolic, do you take it only once a day (time released) or do you have to take it twice or more a day? I promise, this is my last question...for today. Just kidding :) Seriously, I very much appreciated you entertaining my questions today. The funny thing is, even though I have had AF for well over a year now, I never entertained the notion that I would have to manage it, rather than cure it, so much of my research hours went into ablation rather than treatments/management/living with AF. Thanks again.

Wondering what your experience with ablation has been. I am considering an ablation procedure this spring and would appreciate hearing from someone who has gone through the procedure.

Once a day (at night 7 pm). 10 mg. You want your BP low at night and you will sleep better and be more acive in the day with that schedule.

CarBomb2012- I have had two pulmonary vein isolation ablations. Some individuals have good results after 1 ablation, but most of the time, 2 are needed. I was given the odds of 70% cure rate with 1 procedure, 85-90% cure rate with a second ablation. There a quite a few people on this support group that have had great success after 2 procedures and I hope you hear from some of them. I have atypical areas within my heart driving AF (areas other than the pulmonary vein area which is said to account for 95% of AF). these atypical areas were not ablated in the 2 procedures I had. I am an atypical case and probably not the best person for a good example :) I require additional ablations and have elected not to have further ablations at this time and try other medications. I told myself I would try 2 and I do not regret trying. I believe in the procedure because it is a chance to get off medications and for many people, it is life changing. Please feel free to private message me if you have any questions.