Flecainide and 1:1 Conduction Risk

My previous EP prescribed Flecainide 300mg PIP, which I used for 5+ years without any additional meds, but my current EP insists that patients taking Flecainide MUST take an AV nodal conduction-suppressing drug (ie.a beta-blocker or calcium channel blocker) to prevent atrial flutter with 1:1 conduction. This doesn’t bother me when only occasionally taking Flecainide (and thus taking Metoprolol along with it), but when on a daily dose, the other meds (Metoprolol and Diltiazem) lower by blood pressure and heart rate too much and make me feel tired, even at the lowest dosage. So for the past year or two, I’ve ignored his guidance and took 50mg of Flecainide nightly without any other drugs. I stopped Flecainide for a while, but am starting it again (50mg/nightly) and I’m have been pondering this topic again.

It seems atrial flutter with 1:1 conduction is a pretty rare problem. It seems to occur during exercise, particularly if a person in a arrhythmia reverts to NSR during exercise. One interesting thing was that in a retrospective study, in the patients who experienced atrial flutter with 1:1 conduction, they were all on anti-arrhythmia drugs, but half of them were also on a AV nodal conduction-suppressing drug which should have prevented the flutter - which makes me wonder how effective these drugs are at preventing the problem. Sadly, information seems to be sparse on this though.

My afib is vagal, which is why I take the 50mg Flecainide before bed, and taking a beta-blocker or calcium channel blocker then would seem to increase my chance of afib in the night. Also, by the time I’d exercise, chances are most of the Flecainide would be metabolized by then. Also, it seems that 1:1 conduction generally occurs after afib starts - at which point I’d take PIP of both Flecainide & Metoprolol. So overall, the downsides of the meds seem to outweigh the risks.

I don’t know if I’m just trying to rationalize this all to myself, so I’m curious other people’s thoughts:
- Do you take Flecainide without a beta-blocker or calcium channel blocker?
- Have any of you suffered from atrial flutter with 1:1 conduction?
- What are your thoughts on the general risk?

Thanks.



Edited 1 time(s). Last edit at 10/29/2018 08:29PM by MarkF786.

This is a subject near and dear to my heart (ha ha), and I've got a few thoughts about it, but I just don't have time right now. I've been exactly where you are now with this issue. Yes, I've experienced 1:1 flutter, but not due to flecainide. My heart was good at doing that all on its own. Yes, I've encountered that disagreement between EPs over adding an AV node blocker or not, and you raise a really good point about how half of those who experienced it were on a rate suppressor. I'll get back to this question ASAP.

1:1 conduction with flec is real - ask Shannon...

That being said - and this is where I come down. i don't have any solid evidence that what I do is correct. I've used 300 mg Flec PIP for 14 years without issue and without consuming a BB with it (none has every been prescribed). There was a time, about 6 years ago where I was consuming too much calcium and afib became more frequent. One week, I had 4 episodes in a row and a cardio suggested taking flec daily. Like you, my episodes were usually early morning, so I took my whole dose at night. I started at 300 mg/day and titrated down to 0 over a month while I added in ginger spice to act instead of the flec (I wrote this up here somewhere and it did work pretty well, but not 100%). After I realized my calcium error and corrected it, I went back to very infrequent episodes, so it has not been an issue.

On exercise, I always get prone or do little activlty till I convert when I use flec as PIP. Years ago, EP blogger Dr. John, mentioned doing that when he got afib and had to take flec, for exactly the reason you mention.

Also, I'm guessing, but have no evidence that a 50 mg dose would have a much lower probability of causing an issue than a 300 mg dose.

George

Great post Mark - a) The 5 years just carrying Flecanide to use if needed (and I know others do this, Pills In Pocket), is the ticket there just to "notice" when one has gone into Afib, "and that's good enough"? (I seem to be able to tell easily, and check with a finger pulsemeter pretty often, but that's the protocol?) and b), how does one know for sure, "My Afib is vagal"? Does vagal or not-vagal have different odds re: "it's persistent Afib"?

Last question, are there others here who have managed to go just on daily Flecainide, no beta blocker like Metoprolol, and "you just watch it, catch it if there's an issue"? (and good question re: 1:1 etc). I'd love to drop Metoprolol, it's like a brick between my ears...

Thanks for the insight feedback, George and Carey (and I look forward to hearing further details from Carey!)

George, it's interesting what you write about calcium. It's something I've pondered in the past, but haven't taken action to correct in my own diet yet. I often strive to eat a low-carb diet, which leads me to eating milk products (like cheese and yogurt) - and would also increase my calcium intake. As a side-note, the other downside to a low-carb diet is potassium loss from the diuretic effect, another trigger for afib. My first afib episode was while on a very low carb diet, while also on hydrochlorothiazide, which in combination dramatically depleted my potassium (though my doctors all look at me like I’m crazy whenever I bring up the topic of potassium levels).

Maybe I should experiment with lowering my calcium - but it often feels like a tightrope, where I’m trying to fix one problem through diet or supplements (like losing weight), which then causes another problem (like afib). I come across this issue in many areas of health.

Another side-note on the calcium/magnesium balance, I’ve pondered if a high intake of magnesium through supplementation (like many of us here do) has a similar effect as a calcium channel blocker. I would think that calcium channel blockers decrease the ratio of calcium to magnesium in the cells - which would also happen by increasing the dietary intake of magnesium (or decreasing the intake of calcium). Similarly, both calcium channel blockers and magnesium slows the heart rate. Wikipedia has a reference to this idea, “Ionic calcium is antagonized by magnesium ions in the nervous system. Because of this, bioavailable supplements of magnesium may increase or enhance the effects of calcium channel blockade,” referring an article in the American Heart Journal, “Magnesium: Nature's Physiologic Calcium Blocker” This has been another point of justification for why I might not need an AV nodal conduction-suppressing drug.

I’ve read your previous mentions of using ginger instead of Flecainide and have experimented with it some, but hadn’t had great success - though I might not have taken large enough doses.

Mark

Hi Frank,

Yeah, the PIP method seems to only be a good option for people who are symptomatic (ie. they feel their afib). For me, I can immediately sense it, maybe because of many years of meditation practices, some which focus directly on the sensation of the heart. My father, on the other hand, was already in permanent afib by the time a doctor detected it, and he never noticed it.

People usually can determine if their afib is vagal or adrenergic based on the triggers. There’s a big grey area between the two, but one sure sign of vagal afib is that it occurs while sleeping (though you need to rule out sleep apnea first). For me, afib usually occurs sometime between 3-6 AM, and if I monitor my heart rate while asleep, usually my heart rate drops before the afib starts (thus I don’t want to take a drug that slows my heart rate more). My resting heart rate is about 60 bpm or less, though it’ll dip as low as 50 bpm while asleep.

Regarding you last question, I’m asking the same thing: who else manages their afib with only Flecainide, without a beta blocker. Regarding the safety, it seems like a personal decision we all have to make.

Mark

Mark,

I've been keto-adapted for 9 years. Only one afib episode that I can attribute to the naturisis of fasting. That was during my initial adaptation phase. For several nights I felt "hard" beats when I was going to bed. Thought it was lower potassium, so took copious quantities of it. Had a 3 AM episode. PIP flecainide converted me to 130 BPM. Very unusual - usual an 80 something BPM conversion. I immediately took a lot of extra magnesium. Fairly quickly, my rate dropped to the 80's quickly. This prompted me to up my already significant magnesium game.

On the calcium, I was going through a divorce six or so years ago. Being low carb, I thought I had a "free pass" on cheese. I was stress eating wheels of brie. My previously stellar afib control decreased materially. I thought it was divorce stress. Took me 15-18 months for me to go back a reread the literature on afib and calcium. Then I immediately quit the brie and my previously excellent afib control returned.

My diet continues to be keto. I eat in a 2 hour window daily. For the last 4 years, it is more "ovo-pegan," hence my fat sources are mostly monos - olive, macadamia and avocado oil. My animal protein is shell fish, white fish & eggs. On the veggie side, no grains, legumes, nightshades or seeded veggies and almost no fruit except avocados.. It is also carbier than many keto diets - average carbs around 125 g/day with a range of 80-180. Even with this, my morning serum betahydroxybuterate is normally between 0.5 and 2.0 mmol/L, when I sample. I do relatively frequent extended fasts: 5-7 days. On these, my blood sugar drops in a couple of days into the 50's (mg/dL) and ketones are in the 4-7 range. One time, I ran my glucose down to 31 (ketones around 6) and went to the gym and set some PR's on some lifts. None of this caused any electrolyte disturbance that would precipitate afib.

When I did a two week diet monitoring experiment with a gram scale and putting all the info into cronometer.com, my calcium intake was around 600 mg/day. I did a DEXA scan a year ago and my T Score was 0.3 (meaning my bone density was 0.3 standard deviations > than the mean of a 30 year old male, I was 62 at the time).

Thank you Mark for bringing up the "area, the option", of riding on just rhythm control (Flecainide etc) and the concept of dropping / reducing the beta blocker (and I know we are all on our own / we are responsible for risks we take). Great insight with your posts above. GeorgeN it's amazing how "technical" and in-depth the grasp is and how helpful the data is, people like you, Carey etc, much appreciated.

PS, one piece of advice I saw on earlier threads re: "going without meds, then Pills in Pocket if you go into Afib", was advice about taking the beta blocker (Metoprolol etc) a touch before the Flecainide, to bring the rate down / then rhythm control. That would speak a bit to the danger asked about with the initial posting question.



Edited 1 time(s). Last edit at 10/30/2018 05:11PM by FrankInFlorida.

Hello Mark - I'm late in joining in but I wanted to comment to you about the magnesium/calcium topic. It's well established that magnesium is difficult to get in optimal amounts from food alone without heroics; therefore, typically afibbers do benefit significantly by regular use of Mg supplements and some forms are more effective than others. It's very important to reduce intake of calcium-containing foods as it's easy to overload with dietary calcium... (by comparison to the food Mg). Additionally, in many afibbers, it's observed that it often takes several months or longer to reach the optimal intracellular levels that stabilize the heart.

In my history and, while I was taking supplemental magnesium daily, I was having periodic AF that was increasing in regularity over a span of 8 years. I was also taking flecainide and metoprolol 'on demand' or PIP which worked better for me than the daily use because the metoprolol made me too sluggish. However, eventually, when the afib increased in frequency, I did have a consult with Dr. Natale and was given a date 6 months out for the procedure. That motivated me to try one last time to stop the AF recurrence.

I hadn't yet had the intracellular electrolyte test (ExaTest) and when the results came in, I learned I was low in magnesium... even though I thought I had been using enough. And the potassium was also slightly low. As I have reported... it took about 3 months to start notice a difference, but the AF events diminished and I coasted along without using any of the meds and I was considering cancelling my procedure date... but didn't because of a change in insurance coverage so I kept the date and all went well.

I'm just mentioning this because so many afibbers either don't get enough magnesium regularly or calcium overpowers what they do get ...plus the potassium factor can be highly influential in both directions. And... also very important, there are numerous lifestyle habits that may seem innocuous but in the presence of the tendency to develop arrhythmia, the status of some of the core electrolytes may need to be formally assessed as well as making the lifestyle changes that are known contributors.

Jackie

Wow, George… you’ve got your diet down to a science, and you have strong discipline to be able to do extended fasts like that. I’ve at best done only single day fasts, but maybe you’ll inspire me to take if further. BTW, do you recommend any good books on ketogenic diets?

Yeah, it’s during the induction phase of ketosis where I’ve run into electrolyte imbalances (and thus afib). I’ve been off low-carb / high-protein for year or so, but I need to start again.

You mentioned getting prone during an afib episode; do you literally mean lying prone?

Jackie, thanks for the feedback. I’ve been supplementing with magnesium, potassium, and taurine since around the time my afib first started about six years (shortly after, I found this website). I’m currently taking 600-700mg of magnesium a day (depending on the brand I’m using), though indeed that may not be ‘enough’. I haven’t estimated my calcium intake though; it’s something I should look into. I do suspect though that a person taking a substantial amount of magnesium for many years would be less at risk than the average person (with high calcium / low magnesium intake) for 1:1 conduction - but again, maybe I’m just rationalizing my decision.

Quote
GeorgeN


My diet continues to be keto. I eat in a 2 hour window daily. For the last 4 years, it is more "ovo-pegan," hence my fat sources are mostly monos - olive, macadamia and avocado oil. My animal protein is shell fish, white fish & eggs. On the veggie side, no grains, legumes, nightshades or seeded veggies and almost no fruit except avocados..

.

g

Doubtfull that very many people can eat the way you do, but what do you mean that you eat in a 2 hour window daily, do you eat every 2 hours? I believe that grains, legumes which the Med. diet says is good for you is what I follow I ate a lot of tomatoes in Aug., sept. and Oct., I had one AF episode in Aug. I hope people don't follow your diet, I think it is bad, but what do I know.

Liz

Quote
MarkF786
Wow, George… you’ve got your diet down to a science, and you have strong discipline to be able to do extended fasts like that. I’ve at best done only single day fasts, but maybe you’ll inspire me to take if further. BTW, do you recommend any good books on ketogenic diets??

As adapted as I am, the fasts really aren't bad. I always have plenty of ketones on board to feed the brain. Going through adaptation wasn't fun, but I've not had to do that twice.

Turns out I have a genetic risk for AlzD (ApoE4). My mother (no idea of her genetics) had dementia/AlzD (not sure which as doc said don't bother to test). I organized her care during the last 8 or so years of her life. After testing, I determined to see if I could mitigate the risk. I consult with Steven Gundry in Palm Springs CA. He's been testing for this allele for ~17 years, and has had good success clinically keeping patients with it from experiencing the heart and AlzD consequences of having it. My diet is somewhat modified because of these genetics. It is not high protein. Links to labs and transcripts of 7 consults are posted here, along with other links <[www.apoe4.info] It was my experience being succesful keeping afib mostly in remission that motivated me to see if I could ward off or postpone AlzD. Who knows? So far so good. I'm also acquainted with Dr. Dale Bredesen, author of The End of Alzheimers <[www.apoe4.info] Bredesen just published these results on 100 patients <[www.omicsonline.org]

My 30,000' view on ApoE4 is a) it is very good at inflammation, this is an attribute in an acute setting and a detriment chronically; b) it is good at surviving deprivation, this is a detriment in an environment of excess (the first world). Hence I try to impose some deprivation in my life. Even things like cold. It was 40 degrees and snowing today. I wore shorts, a short sleeve shirt and sandals to work. I commonly take 20 minute baths in 49-60 deg F water (temperature varies with tap water temperature seasonally). I will ski or takes hikes in the winter in only shorts. Plus the fasting.

Quote

Yeah, it’s during the induction phase of ketosis where I’ve run into electrolyte imbalances (and thus afib). I’ve been off low-carb / high-protein for year or so, but I need to start again.

You mentioned getting prone during an afib episode; do you literally mean lying prone

Yes, lying prone.

Just a small point, George. Since lying prone means lying on your front do you, in fact, mean lying supine. lying on your back?

Quote
Elizabeth

Doubtful that very many people can eat the way you do, but what do you mean that you eat in a 2 hour window daily, do you eat every 2 hours? I believe that grains, legumes which the Med. diet says is good for you is what I follow I ate a lot of tomatoes in Aug., sept. and Oct., I had one AF episode in Aug. I hope people don't follow your diet, I think it is bad, but what do I know.

Hi Liz,

I mean that I water fast 22 hours/day and then eat in a 2 hour window.

On the grains & etc, as noted my genetics are proinflammatory. My doc tests a lot of inflammatory markers (various cytokines among others). I try to optimize them. Since an infant, I've had autoimmune issues. For many years had frequent itchy roof of mouth as well as itchy rectum. Assume inflammation was throughout my digestive tract. Prior to starting my current program, I was starting to get rheumatoid arthritis symptoms in my hands. Within several weeks of initiating this program, all these symptoms disappeared. Additionally, I've had nasal congestion since an infant. This has reduced 80%, My wife shares my ApoE4 genetics. Several years ago, she'd gone off plan for two meals several weeks before our blood draw for the labs. She showed a response like a celiac, even though she does not have celiac genetics. I'm sure the sensitivity is very individual. Just like many can run marathons or frequent century bike rides without having an afib isse, I know that I cannot.

George

Quote
Sam
Just a small point, George. Since lying prone means lying on your front do you, in fact, mean lying supine. lying on your back?

Actually, my approach is to remain relatively inactive and still before conversion, generally flat whether on front or back. When I read Dr. John's post, I believe this is what he meant, too. I will move around if I need to, but I don't exercise.

Hi George - I certainly respect and honor your strict discipline that is working very well for you. Given the genetic history you've elaborated for us, it certainly makes sense. The grain and lectin issue is definitely something that is apparently very detrimental for most individuals and I appreciate your sharing. The experts you've consulted are certainly on the cutting edge of advanced protocols in this area. I'm glad you are continuing to maintain your Afib free life and certainly protecting your brain from the genetics.
Best to you,
Jackie

Quote
MarkF786
It seems atrial flutter with 1:1 conduction is a pretty rare problem. It seems to occur during exercise, particularly if a person in a arrhythmia reverts to NSR during exercise. One interesting thing was that in a retrospective study, in the patients who experienced atrial flutter with 1:1 conduction, they were all on anti-arrhythmia drugs, but half of them were also on a AV nodal conduction-suppressing drug which should have prevented the flutter - which makes me wonder how effective these drugs are at preventing the problem. Sadly, information seems to be sparse on this though.

Yes, information on it is sparse, presumably because it's a rare phenomenon. My first go with flutter was 5 days after my first ablation. I was cardioverted out of it, and then my EP put me on flecainide and metoprolol for the remainder of the blanking period. I soon learned how much I despise beta blockers and asked to stop it, but he was adamant that flecainide without it was dangerous. That was when I first learned about 1:1 conduction. But then I saw people on forums saying they were taking flecainide without an AV blocking drug. I asked my EP about that, and he said some EPs were ignorant of the risk, while others simply thought it was too rare to worry about. He continued to insist that I take it and put it in stark terms: "You could die."

Roll the clock forward 4 years. I undergo another ablation with a different, more highly qualified EP. Everything seemed fine until my follow-up visit one month later. While I was in his waiting room I realized I had a very fast rate. I figured flutter at my usual ~150 bpm. But when they got me in a room and put a pulse ox on me, it said 230 bpm. Holy crap. The NP quickly got an ECG hooked up and sure enough, I was clocking along at 230-240, and it eventually rose to 250. (Side note: every nurse, PA, student and resident in building came in to look at the guy with a HR of 250 who was sitting there talking and smiling in no distress. I was the day's freak show.)

So here comes the point of the story. My EP gave me 100 mg of metoprolol and told me to just lie down and relax. He came back an hour later and the monitor still said 240-250, so he gave me another 100 mg of metoprolol. An hour later, I was pegged squarely at 250. The metoprolol was completely ineffective. It didn't slow my rate one single beat per minute. He said, and I quote, "You have an unusually healthy AV node, probably in the top 5% of the population. What you could use is a little heart disease to slow it down."

So this is when I learned that flutter is often immune to AV node blocking agents. It is for me. Never again did I allow anyone to give me metoprolol because all that 200 mg did to me that day was kick the chair out from under my BP. A BP of 50/nothing combined with a HR of 250 turned me into a gray, sweating, puking mess that had to be emergently cardioverted.

I've never been able to find numbers on what percentage of people with flutter are immune to rate control, but I've read that it's common. So the imperative some EPs feel about combining beta blockers with flecainide isn't the guarantee some think it is. In my case, taking metoprolol with flecainide all those months was utterly useless and wouldn't have done me a bit of good. But there's no way to know that in advance, so a conservative EP is still going to insist on it. After all, I was lucky that I only hit 250. Others have gone over 300 and nobody's going to be able to withstand that. Cardiovascular collapse and v-tach are almost certain at rates like that.

Quote
Carey
A BP of 50/nothing combined with a HR of 250 turned me into a gray, sweating, puking mess that had to be emergently cardioverted.

That was the only option? Glad it worked.

Quote
jpeters
That was the only option? Glad it worked.

Yes, cardioversions were my only option for months. There was no other way to stop or slow the flutter. I became a well known frequent flyer at the local ER. After a while they knew I would refuse anything other than propofol and electricity so they quit even suggesting it.

And then, thanks to information I found in the archives here, I learned that I could chemically cardiovert myself with potassium chloride. I subsequently learned I could use potassium to actually prevent the flutter as well. I spent the next two years managing it successfully with potassium and potassium-sparing drugs that my EP prescribed. It took some effort to convince him because taking potassium with potassium-sparing drugs is a big medical no-no, but I did my due diligence, provided him with proof that I could monitor my potassium levels, and he came around and supported me.

Carey, now it makes sense why metoprolol did nothing much (reduced HR by 10 to15 ppm) for me when i was went to ER 3 years ago. They kept me in for 5 days without much success using beta blockers (and one dose of digoxin).

I think the sotolol had more of an effect and now the atenolol with flec definitely has an effect. Too much so i think?
Liz did give me a heads up on atenolol. I've cut back from 50mg 2x/day and 100mg of flec 2x/day (i've converted in the meantime) to 25mg atenolol and 50mg of flec 2x/day.
My concern and question (feedback please) is that my HR is in the low 40s in the morning and yesterday after slow exercising for 50 min and working up only light perspiration my HR only got to 55.

After having read the flutter/flec relationship i wonder if cutting the atenolol to 25mg 1x/day with the flec is a good/safe idea? In other words, how much beta blocker is commonly recommended when taking flec? (not seeing the cardiologist for another 2 weeks) I know there are exceptions like Carey.

Quote
Joe

I think the sotolol had more of an effect and now the atenolol with flec definitely has an effect. Too much so i think?
Liz did give me a heads up on atenolol. I've cut back from 50mg 2x/day and 100mg of flec 2x/day (i've converted in the meantime) to 25mg atenolol and 50mg of flec 2x/day.
My concern and question (feedback please) is that my HR is in the low 40s in the morning and yesterday after slow exercising for 50 min and working up only light perspiration my HR only got to 55.

After having read the flutter/flec relationship i wonder if cutting the atenolol to 25mg 1x/day with the flec is a good/safe idea? In other words, how much beta blocker is commonly recommended when taking flec?

I'm not a doc and the following is how I would likely approach it in your shoes. Doesn't mean its right.

Every person's biology reacts differently. The half life of flec is listed as 12 to 27 hours. Half life of atenolol is 6 to 7 hours. So it might make more sense to do 12.5 mg atenolol with each flec dose (using a pill cutter if needed). My approach was to take all my flec at night as that is my risk time. Then I'm going to bed and I'm on the bed, so less risk from the flec (at least as I fathom it). Going on this theory, I might only take the atenolol at a 25 or less dose in the morning, Which it sounds like you are doing;

Good luck!

George

George's suggestion makes sense. I can't think of anything better because, like he said, everyone is different. Until you've actually experienced 1:1 conduction and you know how your body reacts, I would stick with the conservative advice and have at least some rate limiter on board.

Thank you George and Carey! I'll reduce the atenolol a little more and see.
I've also read that Propranolol has the ability to to decrease T3 and increase rT3 production. My T3 is on the low end of the scale.
(Greg Kelly. Peripheral Metabolism of Thyroid Hormones: A Review. Altern Med Rev 2004; 5(4): 306-333)
Presumably Atenolol is having the same effect - both being beta-blockers?