Flutter vs Fibrillation vs PACs

This is an "Afib" site and folks here are known as Afibbers. Flutter is another arrhythmia with its own special characteristics. Both involve errant electrical signals and circuits and both result in uncomfortable symptoms.

I have been diagnosed with both left afib and left flutter. Are there others here who have such a diagnosis or just a diagnosis of flutter. I assume all of the principles that are talked about apply equally well to the general case of arrhythmias.

The paper by Dr James Cox talks about "initiating events", usually a PAC, which then leads into "macro reentrant circuits", which carry on the arrhythmia unless it spontaneously stops. I realize that since starting my increased intake of potassium and experiencing a cessation of my afib episodes, I have been noticing "skipped beats" with no other symptoms, and the skipped beats stop after several minutes. This sounds like PACs from which re-entrant circuits are spawned but they can not continue, courtesy of the potassium and magnesium. Is this a reasonable model of what might be going on?

Thanks for your thoughts.

Ken

Ken - you may find that in time, as your magnesium becomes optimized so that the Na/K+ pumps can operate efficiently, your PACs also diminish providing that you have enough potassium on a continual basis. Only you will know what works in your body. Our guidelines are just generalizations; you have to do the experimenting and tweaking of dosing including timing of same. It should not matter if you have flutter or fibrillation. The goal is that tissue compliance status so that the refractory period is prolonged. Anything that alters that invites the onset of either arrhyhmia. Jackie

jackie: thanks to you and others for the continued support. I continue working my way towards a complete decision about surgery vs continued reliance on the electrolyte balancing. This group and a few individuals outside of it are my mainline support for information and comments on my many questions. It has been said in the past that I overanalyze things (the analysis paralysis syndrome). And yet this is so personal and impactful that I believe it deserves detailed scrutiny and consideration. I hope others here bear with my many questions.

I also appreciate that everyone is different and that numbers of the various ratios will be different for different circumstances and individuals. I do, however, assume the general principles stay constant and work for everyone, even though at somewhat different levels. I also assume that the principles work for people as they age, although of course they may need to alter the amounts given changes in their bodies.

One detail which is probably impossible to verify is whether the changes to the heart structures and tissues, etc. do not reach some sort of "threshold" after which no amount of electrolyte manipulations will work to suppress the errant signals.

Again, repeated thanks to you and others.

Ken

Ken - I can truly understand your cautionary research. It's far better to overdo it than be totally trusting and ignorant. You can get hurt that way. I know I certainly was trusting and was injured as a result in other medical areas; not for afib. With AF one, I really obsessed about learning all I could so that I didn't repeat any of my former mistakes.

You've had your share of medical procedures and it's good to go into another with a full understanding of what the downside may be versus coasting along 'as is' for a while. My motto is 'leave no stone unturned' when it comes to learning all there is about the procedure, the risks, the failures, and the consequences of same.

As for the threshhold area, one influencing factor would definitely be the cardiac fibrosis mentioned and referenced in CR #24 and following the advice to use the proteolytic enzymes to help clear out fibrotic tissue. The inflammation caused by elevated CRP would be another as well as making sure the other risk factors involved .... see the old post called Red Flags to Beat the Odds <[www.afibbers.org];

If all your markers mentioned in this post are in the low range, then you should have a better chance of having the nutritional approach be effective. They are all very important, and as Erling recently reminded us, the methylation factor involved that promotes elevated Homocysteine can be very influential in both overall health and heart <health.[www.afibbers.org];

The unfortunate thing is, most often, doctors don't routinely check these markers as a routine for preventive care.... and often argue when patients want them. Be insistent and get them done. It may be an extremely important finding for you.

Keep working on your research. There are still stones left to flip.

Jackie

Ken, please do not ever stop asking questions. You make me rethink the things i think i know, and i believe that to be a good thing. Certainly it is a thing i acutely enjoy.
PeggyM

Ken,

As long as you have healthy kidneys, from my way of thinking there is no reason not to experiment with Mg/K/taurine. The only way you'll know whether it all works for you is to try. If you've also had heart procedures, I'd be trying to work on my lifestyle to reduce the possibility of a repetition there. That could have benefits on both the plumbing and electrical heart issues.

George

Ken and others,

Elevated homocysteine (HCY) is the primary cause of arteriosclerosis, not cholesterol. The reason doctors don't often know this, and tell us, is that they're not told. Dangerous anti-cholesterol 'statins" are a multi-billion (dollar, yen, pound, franc, krone, whatever) money making machine. Homocysteine is easily controlled with non-patentable, inexpensive vitamins B6, B12, and folic acid*. Additional methylators are advised**. A strong case can be made for elevated homocysteine being causal in afib by causing micro-plaques in the arterial capillary beds of atrial muscle, with necrosis causing discontinuance and disarrangement of electrical signals from the sinus node.

See:

*The Homocysteine Revolution, by Kilmer McCulley, MD
[www.spacedoc.net]
[www.nytimes.com]
[www.lef.org]

**Methyl Magic, by Craig Cooney, PhD
[www.uams.edu]
[www.lef.org]
[www.lef.org]
[www.lef.org] (this article has a graph showing serum HCY levels vs. vascular disease risk)

[www.afibbers.org]

You guys are really great! I really mean that.

I had three bouts of plugged coronary arteries, about 10 years apart, and each caused by gradual let down in doing all of the right things diet and exercise wise. Amazing that the same syndrome (dumb syndrome) caught me three times. After successful application of fish oil, antioxidents, and other supportive vitamins after the second round of plugups, I let myself get caught in the "immune fallacy", ie, all of those pills will magically ward off any further blockage so it is ok to eat the bad stuff. Wrong! I have said that if it happens a fourth time (for the same dumb reason), I will shoot myself -- no, no just kidding. Now I have afib to keep me occupied.

I find it interesting that Dr James Cox outlines the ablation lines he believes can stop all afib circuits and one of them (at the "ismuth") lies right over the circumflex coronary artery and can't be executed unless the surgeon uses HIFU (High Intensity Focused Ultrasound) to create an ablation line "behind" the artery without harming the artery. How is that for rolling the dice.

Sorry for the digression. The above experiences have me well tuned in to arterial inflammation and the importance of the proper amounts of antiox and vitamins and fish oil (krill oil anyone?). The electrolyte balance science revealed to me via searches for help in afib has been new learning (to add to my stores of other info from the CAD front).

Anyway, getting closer to a decision. Have a meeting with my cardio (my plumber) tomorrow and will ask him his opinion, but quite frankly, I may know more about these electrical issues and especially the electrolyte connection than he does. But it will be interesting.

Thanks for comments. And Erling, thanks for the articles. You are a walking reference room for sure.

Ken

Ken, two thoughts:

1. Afib does not necessarily require an errant electrical signal to be initiated or sustained. In my opinion, what it does require is for the atrial muscle tissue to be non-compliant with normal sinus-node signals. Such non-compliance is, in my opinion, the root cause of all afib, and can be caused in various ways. It is this non-compliance that makes the muscle tissue vulnerable to errant signals. This logically means that it is impossible for PV ablations to ever be 100% effective -- in my opinion.

Logically, this is why I no longer have afib. With 82 years of 'oxidative stress' to my PVs, I can only imagine the degree of electrical chaos that is now bombarding my atria. It is my firm theory that my atria were 'fixed' by years of Mg supplementation, after having been 'damaged' by years of Mg deficiency (NSR, 8 years and counting).

2. How can it be that only the left atrium fibrillates, 'left afib' as you say?

Erling

Erling:

I will have to reread some of my sources, but I remember the "circuits" being described differently for the right and left atria. An initiating signal from the left pulmonary veins could be expected to create circuits that remain in the left atria. Maybe.

Question for you: in your eight years of maintaining NSR with electrolyte balance, have you concluded how "wide" is the proper "zone" of electrolyte intake needed to maintain the NSR? I ask this because yesterday, I altered the pattern of my potassium and Mg intake (due to unusual scheduling issues that changed my day). I do not measure precisely the amounts (three doses of Mg Citrate, spaced, two to three bananas, med size, half cup of yogurt -- these are the extent of my measurements).

Something changed because last night, I went into afib and am still in it this morning. So much for my "record" of three + weeks of complete NSR.

If anything will help me decide to proceed with the TTM Maze procedure, it will be finding that electrolyte intake will have to be more "precise" than I am able to or desireous of achieving.

Do you have any thoughts about how "precise" one has to manage electrolyte intake? How "precise" do you have to be?

Finally, what were the causes of your 8 hours out of 50,000+ where you apparently experienced afib.

Thanks,

Ken

Hi Ken,

To answer one of your first questions--yes, I have also been diagnosed with atrial flutter. Initially, I was diagnosed with right atrial flutter and left atrial afib. I had an ablation for the flutter and have been on antiarrhythmics for the last two years to control the afib; however, even with potassium/magnesium supplementation, exercise, good nutrition, etc., my episodes got progressively worse. A few weeks ago, I started showing signs of heart failure (fluid accumulating in lower limbs and torso) and then three weeks ago I ended up collapsing and my EP did emergency ablation on my right atrium.

During that ablation, they discovered that I had flutter in my left atrium as well, and that it only LOOKED like lone afib because my flutter degenerates to afib before I return to sinus rhythm. In another week, they are going to have a team of EPs go in and do a left atrial ablation to hopefully fix the remaining electrical issues.

I mention this because I think that the "threshold" you mention is probably unique to each person. I am young and have no cardiovascular disease or major structural defects in my heart, so on paper I look like a perfect candidate for nutritional intervention/supplementation to prevent these arrhythmias. Unfortunately, nutritional changes just weren't enough to keep the problem from progressing in my case.

I hope that info helps a little... Thanks, Kelly

Kelly: thanks for sharing. I REALIZE everyone is different. But your experience suggests that supplementation and electrolyte balance may not work for everyone, in spite of various success stories.

My last night's bout of afib has subsided, and yet I am more confident than ever in going forward with my TTM in Sept. Decision is made. Time to reserve a hotel room in Columbus, and a spot for our Golden in the kennel.

Ken

Erling:

You asked:

"2. How can it be that only the left atrium fibrillates, 'left afib' as you say? "

I offer you this from Dr James Cox, "Surgical Management of Atrial Fibrillation", Texas Heart Institute, 2004:

"The left atrium can sustain the relatively smaller macro-reentrant circuits that are characteristic of atrial fibrillation, because the refractory periods are shorter there. The right atrium, which has relatively longer refractory periods, is probably not capable of sustaining atrial fibrillation by itself, unless it is pathologically enlarged. Therefore, the treatment of atrial fibrillation can be focused on the left atrium in the knowledge that fibrillation will not recur if macro-reentry can be prevented by the placement of certain critical lesions there. The right atrium, which is capable of sustaining only atrial flutter, can then be treated ...... " (rest omitted as it deals with ablation lesion placement).

This may answer your question at least in part.

Ken

Ken, if you use the Mg citrate for a Mg supplement, likely you will reach bowel tolerance long before you can reach Mg repletion. Mg glycinate is a better choice because more of it is absorbed, leaving less of it in the bowel to attract water to itself and give you diarrhea. Mg citrate is used for bowel cleanouts prior to medical procedures for this reason.
PeggyM

Ken,

Thanks for clearing that up. It's always good to learn something new!
I would never have thought that there would be a difference in refractory periods.

Erling

Ken and others,

Elevated homocysteine is the primary cause of arteriosclerosis, not cholesterol. The reason doctors don't often know this, and tell us, is that they're not told. Dangerous anti-cholesterol 'statins" are a multi-billion (dollar, yen, pound, franc, whatever) money making machine. Homocysteine is easily controlled with non-patentable, inexpensive vitamins B6, B12, and folic acid. A strong case can be made for elevated homocysteine being causal in afib by causing micro-plaques in the arterial capillary beds of atrial muscle, with necrosis causing discontinuance and disarrangement of electrical signals from the sinus node.

See:

The Homocysteine Revolution, by Kilmer McCulley, MD
[www.spacedoc.net]
[www.nytimes.com]
[www.lef.org]

Methyl Magic, by Craig Cooney, PhD
[www.uams.edu]
[www.lef.org]
[www.lef.org]
[www.lef.org] (this article shows the desirable HCY level)>

[www.afibbers.org]
===============================================

Ken,

You wrote:

> I will have to reread some of my sources, but I remember the "circuits" being described differently for the right and left atria. An initiating signal from the left pulmonary veins could be expected to create circuits that remain in the left atria. Maybe.

> Question for you: in your eight years of maintaining NSR with electrolyte balance, have you concluded how "wide" is the proper "zone" of electrolyte intake needed to maintain the NSR? I ask this because yesterday, I altered the pattern of my potassium and Mg intake (due to unusual scheduling issues that changed my day). I do not measure precisely the amounts (three doses of Mg Citrate, spaced, two to three bananas, med size, half cup of yogurt -- these are the extent of my measurements).

Reply: Over time, my atria became essentially invulnerable to fibrillation, so "electrolyte balance" is not an issue for me. "Sufficiency" is of course, as it is for everyone. One needs to think of each electrolyte separately. As a general rule for most afibbers:

-- magnesium is limited only by how much one can handle, and for most it's "bowel tolerance".

-- Potassium, all sources, should be at the top of the RDA, high on the serum level range, and at least 4 times that of sodium - critical!.

-- Calcium should ideally not exceed magnesium.

-- About chloride and phosphorus I have nothing useful to say, except:

-- The "Exatest interpretation guide" is a "must" resource for all of the above:<[www.afibbers.org];

>Something changed because last night, I went into afib and am still in it this morning. So much for my "record" of three + weeks of complete NSR.

If anything will help me decide to proceed with the TTM Maze procedure, it will be finding that electrolyte intake will have to be more "precise" than I am able to or desireous of achieving.

Do you have any thoughts about how "precise" one has to manage electrolyte intake? How "precise" do you have to be?

Reply: "Precision" was never an issue for me, and shouldn't be for you either. SApplements/electrolytes are foods, and unlike drugs, they are not toxic. But, you have the same special need for maximum magnesium and vitamin B6 that I had when starting out, to maximize Mg dependent enzymes. Important to- learn about orally consumed enzymes, so perhaps you could consult with Jackie, she's the enzyme wizard. You have known plaque/ calcification in the cardiac arteries, which could mean that the root cause of your afib is some degree of "degenerative change" within the atrial musculature, such as fibrosis, calcification, possible plaque in the arteries/ arterioles/ capillaries feeding the muscles, or anything else that can mess up signaling between the muscle cells. Specific enzymes might conceivably be your way to NSR.

>Finally, what were the causes of your 8 hours out of 50,000+ where you apparently experienced afib.

Reply: I believe it was George N. that said that. I stopped keeping a logs year ago. The few minor breakthroughs I've had were all caused by potassium shortfall/low K:Na ratio/shortened ARP, and were easily corrected with additional potassium. Adequate potassium intake is a critical, continues requirement for everyone.

Erling

Ken,

"Finally, what were the causes of your 8 hours out of 50,000+ where you apparently experienced afib."

Here is a history from the end of my 2.5 month persistent afib episode in Nov. 2004. In addition to the 8 one-hour episodes, it includes a 20 hour episode one month after converting the 2.5 month episode. I'm assuming atrial stunning was still operative, hence the 20 hour conversion. All subsequent episodes converted in an hour or less with PIP flecainide. Quick summary - either stopping one or more supplements, and/or heavy exercise are the primary cause except for the last, which was electrolyte depletion from dietary change (ketogenic diet initiation). The answer has always been adding more magnesium. I currently take > 2 grams/day elemental in the forms of glycinate, chloride and bicarbonate.

<[www.afibbers.org];

George

Wow, what a group of helpful people. Great replies to a bunch of my questions. (Only glad I was able to give a little back in terms of right vs left atrial flutter/fib.)

Peggy: thanks for the (re)clarification on the Mg Glycinate. I am off to order some right after this.

Erling: I hear you on homocysteine. My copious intake of antioxs and Vit-C, Fish Oil, over the years have, I think, been consistent with trying to keep inflamation down.

I guess "precision" was not the right word, but it seems there are so many variables, for me in my circumstance, that relying on electrolyte intake to control/prevent my afib symptoms will be more than I want to do.

I have transitioned across my "hesitant zone" and am comfortable going forward with my TTM procedure (have hotel reservations, etc). This does not mean I will ignore electrolyte balance but that defense will be on top of the ablation lines Dr Sirak will lay down.

George: I read the referenced other reply you wrote and am amazed you can recall all of that detail from memory (no logs indeed). Brain and memory function working well in your case. I can not find my car keys three minutes after laying them down and have been known to search for my glasses even though they were on my head. :-( I hear you about Mg.

Many thanks folks.

Ken

Ken'

You say: "I hear you on homocysteine. My copious intake of antioxs and Vit-C, Fish Oil, over the years have, I think, been consistent with trying to keep inflamation down."

I say that if you had read the links to Drs. Kilmer McCulley and Craig Cooney on homocysteine (HCY) that were provided at the top, you'd know that antioxidants, vitamin C, and fish oil won't detoxify it. If you and I had been paying attention to this 11 years ago when the science was already fully mature, reported in the two books, and the protocol proven fully effective, you would likely have avoided stents, possibly a-fib. I would certainly have avoided carotid artery surgery and its surgically-induced - iatrogenic - stroke and its consequences, from which 7 months later I am still recovering.

To properly reduce serum homocysteine to safe levels requires vitamins B6, B12, folic acid, choline and inositol, minerals zinc and selenium, fish oil, plus the nutraceutical trimethylglycine (TMG). See Dr. Cooney's book Methyl Magic.

Everyone should have their serum homocysteine (HCY) measured, a standard test. Just be certain that it's to be done properly: if I recall correctly, the sample must be centrifuged and frozen at once in order for the results to be accurate. Please read the article 'A Lethal Misconception' [www.lef.org] Scroll down about halfway, see and understand the graph showing HCY level vs. arterial disease risk. This is very important!

Erling

Just to give an idea of a nutritional supplement designed specifically to manage HCY... here's the ingredient list of that from Designs for Health...
You can look for similar ingredients but be sure the form of each nutrient is the same so you get optimal results.

Homocysteine Supreme (TM)

Vitamin B2 (as Riboflavin-5-Phosphate) 50 mg.
Vitamin B6 (as Pyridoxine Hydrochloride 40 mg;(Pyridoxal-5-Phosphate 10 mg) 50 mg
Folates - (NatureFolate blend) 2 mg
Folinic Acid (as 5-Formyl tetrahydrofolate) 400 mcg
Vitamin B12 (as Methylcobalamin) 1000 mcg
Zinc (as Zinc Chelazome®Bis-Glycinate Chelate) 5 mg
Magnesium (as Magnesium Chelazome®Bis-Glycinate Chelate) 10 mg
Trimethylglycine (TMG) 500 mg
Choline 100 mg
Serine 100 mg
N-Acetyl-Cysteine (NAC) 100 mg
Take 2 capsules daily with meals.

This product contains synergistic nutrients including the proprietary NatureFolate (TM) blend of active isomer naturally-occurring folates known to facilitate the efficient metabolism of homocysteine. Homocysteine Supreme allows the homocysteine pathway which begins with methionine, to produce its necessary and important end-products, including the sulfur-containing amino acids taurine and cysteine and the neurotransmitters, norepinephrine and dopamine. Any block in this pathway can cause homocysteine to elevate.

Patients with homocysteine levels above 7 maybe in need of intervention with Homocysteine Supreme. Patients with a family history of early heart attacks or depression are prime candidates for such interventions as are patients with MTHFR enzyme abnormality.

I have a pdf product data sheet describing the action of the supplements needed to combat elevated HCY...if you'd like a copy, please email me.

Jackie

Excellent, Jackie, so thank you!

This is such a vital, and relevant, topic that I do believe it should be continued at the top, as it will soon disappear from view. In fact, even though methylation was a CR session previously (#20, '03 -'04) it now needs to be updated and amplified as a single science topic, and the place to that is in the Conference Room. Perhaps Hans will agree. Otherwise, we should take it to the top with instructions to stay 'on-topic' and not commandeer the thread with other issues and digressive comments. At least its life will be extended a bit.

Erling

Erling,

If you can give me a title for the subject you wish to discuss in the conference room and provide the lead-in posting I'll be happy to set it up.

Hans

Hello Hans,

That's good. The more I think about this topic the more significant it seems. I've been searching the web on and off for a scholarly article to describe specifically a causative connection between methylation and cardiac arrhythmia, which of course is obvious, probably too obvious for such a paper. Indirectly, of course, the literature is plentiful and clear: DNA methylation -> gene expression -> protein formation -> cells' channels and pumps -> electrolyte flux, etc. Perhaps the way in which a session could work is to present a limited open-ended case and have the participants find and contribute supportive documentation. Well, of course that's what a CR session is all about anyway. Googling DNA methylation just now produced 918,000 results, so there's plenty of information to work with. I'll be thinking about how to write this for a while yet.

Best wishes!

Erling