Hi. I was diagnosed with aphib and flutter with rapid ventricular response a month ago. My doctor did an ablation of my right atrium to prevent organized flutter yesterday. He put me on flecainide and Cardizem to control aphib with RVR. Today an episode that lasted a few minutes, then stopped. Any idea if this is normal? I am on a 30 day event monitor, but don't know how to get info from the monitor on what is going on. Just push the button to send data to the company.



Edited 2 time(s). Last edit at 08/03/2017 07:40AM by Michael777.

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Jon E. Block et al
Although evidence is scant, the effectiveness of right and left atrial ablations appears to be independent and additive with respect to AF episode reduction.

Article on right atrial ablation and aphib. Many people are helped by this safer of the 2 ablation procedures. There is typically a 3 month or so healing period after ablation, with gradual improvement throughout the period.

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Michael777
Today an episode that lasted a few minutes, then stopped. Any idea if this is normal?

Yes, that's perfectly normal following an ablation. Short periods of arrhythmias during the "blanking period" after an ablation are expected and shouldn't be cause for concern. (The "blanking period" is the two months following your ablation.) Congratulations on your apparently successful ablation. :-)

Welcome Michael777,

Your experiences with what appears to have been a CTI (Cavo-tricuspid-Isthmus Flutter) are normal, though most often a successful CTI Flutter has little to no recurrence. Also, the article you posted promoted some questionable ideas. Firstly, typical right atrial flutter is not the same thing as AFIB ( and just to get you started on the right foot the acronym is spelled 'AFIB' rather than 'Aphib' though they both are phonetically the same and easy to mix up.

CTI or typical right atrial flutter almost invariably eventually leads to AFIB triggering in the left and often right atria alike and often acts as a kind of canary in the coal mine signally and almost certain progression over time to full blown AFIB too. From what you have described, at least there is no indication that you had any AFIB ablation at all as yet, but instead it seems you had a typical CTI Flutter ablation which is the easiest kind of ablation for sur. However it does NOT reduce AFIB either in the left or right atria .. it addresses CTI right atrial flutter specifically.

Keep searching through our forum archives as well as our 141 issues of The AFIB Report that has been on sabbatical since last August and you will make quick progress in your understanding of this lousy condition and how best to put it in the rear view mirror.

You can lock the AFIB genie back in its bottle for the long haul as well by following both our life style risk factor reduction recommendation and nutritional repletion protocols, most often in combination with an 'expert AFIB ablation process' with a highly experienced operator.

Enjoy your exploration here and many experienced afibbers will be glad to help!

Cheers!
Shannon



Edited 1 time(s). Last edit at 08/05/2017 06:22PM by Shannon.

Thank you Carey. Yes they have been short. A few seconds to a few minutes.

Thank you Shannon. It was indeed an anti-flutter ablation. The flecainide started coordinated flutter with RVR which lasted 23 hours, so doctor did the ablation. Flecainide and Cardizem are prescribed to prevent AFIB with RVR.

Yes, the anti-arrhythmic drugs can often have the unfortunate side-effect of promoting flutter. What's good for disorganized conduction in the left atrium is not good for somewhat organized conduction in the right.

Thanks wolfpack.

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American Family Physician
Pharmacologic agents are effective in converting atrial fibrillation to sinus rhythm in about 40 percent of treated patients.

A 2002 article for physicians. Meds seem to work okay for some people.

They do.

The question, rather, is "how well" and for "how long"? The answer will vary, depending on the patient.

I wonder why such varying results?

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Michael777
I wonder why such varying results?

Because this condition sucks! ;-) And based on my limited knowledge none of the drugs are really targeting the cause of AFIB (If you can find two EP's who agree on that). It's just a lucky coincidence they sort of work for some.

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Fibrillator
And based on my limited knowledge none of the drugs are really targeting the cause of AFIB (If you can find two EP's who agree on that). It's just a lucky coincidence they sort of work for some.

All the antiarrhythmics work by altering aspects of the action potential of cardiac cells. The action potential is just the cycle a muscle cell goes through of charging, firing, and then recharging. For example, some of the drugs widen the refractory period. The refractory period is right after the cell fires and can't fire again until it's fully recharged. So if you widen the refractory period, an errant afib impulse is more likely to encounter heart tissue that doesn't respond, thus breaking the cycle and terminating the arrhythmia.

So what that means is the drug slows your heart cells down by a tiny amount, just milliseconds, and hopefully that's enough to interrupt the reentrant signals of afib and flutter. As you might imagine, those few milliseconds might work for one heart but not another; hence, the hit or miss nature of these drugs.

Note that none of the gobbledygook above has much to do with what causes afib, so you're exactly correct that the drugs don't target the cause of afib.

Now if only we fully understood what the cause of afib actually is....



Edited 1 time(s). Last edit at 08/10/2017 08:16PM by Carey.

Quote
Carey

And based on my limited knowledge none of the drugs are really targeting the cause of AFIB (If you can find two EP's who agree on that). It's just a lucky coincidence they sort of work for some.

All the antiarrhythmics work by altering aspects of the action potential of cardiac cells. The action potential is just the cycle a muscle cell goes through of charging, firing, and then recharging. For example, some of the drugs widen the refractory period. The refractory period is right after the cell fires and can't fire again until it's fully recharged. So if you widen the refractory period, an errant afib impulse is more likely to encounter heart tissue that doesn't respond, thus breaking the cycle and terminating the arrhythmia.

So what that means is the drug slows your heart cells down by a tiny amount, just milliseconds, and hopefully that's enough to interrupt the reentrant signals of afib and flutter. As you might imagine, those few milliseconds might work for one heart but not another; hence, the hit or miss nature of these drugs.

Note that none of the gobbledygook above has much to do with what causes afib, so you're exactly correct that the drugs don't target the cause of afib.

Now if only we fully understood what the cause of afib actually is....

In a nutshell, the vast majority of the anti-arrhythmic drugs either work to sequester potassium in the cells or otherwise prevent the influx of sodium. Given that the sum of sodium and potassium ions in intracellular fliud is supposed to remain constant, this seems like a basic problem to solve. Eat less sodium and its helper ion calcium and eat more potassium and its helper ion magnesium!

And, if that doesn't work - add an expert ablation procedure to the mix!



Edited 2 time(s). Last edit at 08/10/2017 09:47PM by wolfpack.

I hope they figure it out soon.

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Dr. John Mandrola
In the short-term, I use temporizing measures to relieve AF symptoms: drugs for rate control, anticoagulants for stroke prevention, and maybe even cardioversion with or without anti-arrhythmic drugs. The key is that these treatments are temporary. We aren’t shocking or medicating an AF patient with the idea that this is the fix; we are doing those things to buy time for risk factor management to work. And it does. I’ve seen it work.

Meds buy time for lifestyle changes like achieving the proper weight..

Wolf:

"In a nutshell, the vast majority of the anti-arrhythmic drugs either work to sequester potassium in the cells or otherwise prevent the influx of sodium. Given that the sum of sodium and potassium ions in intracellular fliud is supposed to remain constant, this seems like a basic problem to solve. Eat less sodium and its helper ion calcium and eat more potassium and its helper ion magnesium! "

Funny the guy that has controlled his AF (GeorgeN) eats salt, my holistic doctor tells me to eat more salt. I get AF in the evening while relaxing or sometimes by putting pressure on my upper stomach or the back area, but not in the daytime. Do you think my salt/potassium levels are more in synch in the daytime. I know people that put a lot of salt on their foods and no AF.

I wonder what Dr. Natalie believes is the cause of AF in some of us.

Liz

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Elizabeth
Wolf:

"In a nutshell, the vast majority of the anti-arrhythmic drugs either work to sequester potassium in the cells or otherwise prevent the influx of sodium. Given that the sum of sodium and potassium ions in intracellular fliud is supposed to remain constant, this seems like a basic problem to solve. Eat less sodium and its helper ion calcium and eat more potassium and its helper ion magnesium! "

Funny the guy that has controlled his AF (GeorgeN) eats salt, my holistic doctor tells me to eat more salt. I get AF in the evening while relaxing or sometimes by putting pressure on my upper stomach or the back area, but not in the daytime. Do you think my salt/potassium levels are more in synch in the daytime. I know people that put a lot of salt on their foods and no AF.

I wonder what Dr. Natalie believes is the cause of AF in some of us.

Liz

Liz,

That type of AF sounds vagally-mediated. Mine was quite similar, and I didn't really correlate AF episodes with food intake of any sort. It was just like "ok - it's 8PM, time for a-fib!" with me.

My comments regarding the supplementation with mag and K are really more based on my post-ablation experience with PACs and my efforts to squash them forever. I didn't really supplement that much while in AF, since it was such a short time between my initial diagnosis and ablation (4 months). I just took the propafenone and dealt with the breakthroughs. Beta blockers were a mess, I stopped them when I changed cardiologists. Betas often make vagal AFers worse, and that was for sure the case with me.

I don't know what causes AF but my guess would be electrolyte imbalance in the cardiac cells to upset the electrical potentials, some degree of atrial stretch to upset the electrical lengths and then all topped off with a central nervous system imbalance that "fires" too many impulses at the atria via either the parasympathetic (vagal) system or sympathetic (adrenergic - adrenaline) system. The first bits are the "bullet in the chamber" and that last bit is the "trigger".

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wolfpack
I don't know what causes AF

I don't either but the thinking seems to be turning toward an atrial cardiomyopathy we simply don't understand yet. In other words, those of us who were told we have "lone afib" because we have afib but no structural heart disease may have been told wrong. It may be that our heart disease simply wasn't recognized. I think it's very likely that in a few years the term "lone afib" may be considered obsolete and wrong.

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Europace
...electrical remodelling in AF can be reversed in some patients if SR is maintained from an early stage, suggesting that prompt recognition and management of AF is critical.

Reversing remodeling is good.

Yes Carey you are right!,

I did a report on the likely demise of the 'Lone AFIB' diagnostic descriptor in a past issue of The AFIB Report about 1.5 to 2 years ago with the advent of more subtle distinctions of subclinical cardiomyopathy in the early days being the likely culprit behind most early AFIB after all!!

I even removed 'Lone AFIB' from the title of this website!

Take care, Shannon

PS let's chat soon before your adventure to Tejas!

Shannon,

Where can I find that report? I'd love to read it.

Thanks.
Elaine