I am a trauma surgeon and surgical intensivist who is very committed to exercise. Thus, my resting heart rate is in the 40s and can go into the 30s during sleep. I am 65 years old. I have been extensively tested and have NO heart disease.

I have Lone a fib with one episode in 1979, 1994, 2003, 2008, 2011 and at this moment.

The first three times I was electrically cardioverted and the last 2 times I have converted with the pill-in-the-pocket approach of 300mg of Flecanide by mouth

Today the flecanide has failed and I would appreciate any advise on what to do next.

My cardiologist wants to wait until Tuesday so that all the flecanide is out of my system. He wants me to take Rivaroxaban 20 mg starting tomorrow

Is there any opinions about whether this plan is a good one??

Std procedure is to anticoagulate for 3-4 weeks if you are in afib for > 48hours. So you might want to consider electro cardioversion before that window closes. I believe a TEE can substitute for the anti-coagulation.

I've used 300 mg flec on-demand for 10 years. There was one time I added another 100 mg after about 12 hours and I converted at about 20 hours. This was the 2nd time I used it. The first time, I converted a 2 1/2 month episode with 300 mg flec in 20 hours.

Subsequently I've converted in 1-4 hours with 300 mg flec. Currently I'm at one year post my last episode.

Once you convert, you may want to ask here about electrolyte repletion, especially magnesium & potassium.

Many of us true lone afibbers got here through the vehicle of chronic fitness, especially endurance exercise. I decided to moderate somewhat. I look at training from a minimum required dosage rather than more is better perspective. I am still very active, but I look at any endurance activity as having a cost rather than a benefit.

Good luck!

Thank you George, it is a great feeling not to be alone with this frustrating abnormality.

I declined to attend an evening event in NYC with my wife after the A.fib came on at 8:30 AM. She went to the event so I went to bed early (9PM) because I work 24 hours today in an ICU near our home. I awoke around 11:30 to urinate and was in normal sinus rhythm. I am so grateful.
I will look into Magnesium and Potassium supplements as a preventative strategy but it is maddening to develop a preventative strategy to something that has occurred 7 times in 35 years. Though, since 2008 it has occurred every three years.

I no longer do aerobic exercise. I only practice ashtanga based vinyasa yoga with an occasional mountain bike ride in the summer. However, my resting and sleeping heart rates are both very low.

How many times have u used the flecanide 300mg treatment? It seemed from your e-mail that your occurrences are more frequent then every three years.

Thank you again for your suggestion regarding potassium and magnesium

As I'm sure you are aware, afib tends to be a progressive illness. Once you know you've got the predisposition, it is wise to do all you can to halt or minimize that progression. Things like repletion of Mg++ & K+ tend to work much better early in progression.

In my case, my first episode came about 10 years ago as a delayed (several days) vagal trigger after a training run at altitude (14,000'). I was training for a race that gained 7,800' over 13 1/3 miles, topping out over 14,000'. During the first 2 months, I had episodes every 10-14 days lasting 6-9 hours. I could convert these with exercise. Then I had one that would not convert. This may have been a delayed vagal trigger to the race. The EP I ended up with suggested I stay out of rhythm as my afib HR was slow (70's). I suggested a "plan B" that included cardioverting the episode, then on-demand flec to convert future episodes coupled with electrolyte repletion to keep me in NSR. The EP bought off on the plan. Through trial and error, I created my repletion plan.

As to flec, I converted the 2 1/2 month episode in 20 hours, converted an episode a month later in 20 hours (with an extra 100 mg as mentioned). I think the cause of this episode may have been atrial stunning from the 2 1/2 month episode. I had two episodes a month apart about 3 months later. The first was clearly a vagal trigger to all day hard exercise (heavy pack, breaking trail through 3' of snow for five hours, then constructing a 3 person snow cave with the other two not helping much). This episode came on about midnight, while I was in the snow cave. I took the flec with some water from a half frozen water bottle. I always chew the flec to quicken the response. I converted in 25 minutes. I don't recall the trigger for the next episode, but it converted in about an hour with flec. After the second of these two episodes, I looked at my repletion protocol and realized I'd not been taking the 4 g/day of taurine powder that I had previously. I added this back in and did not have an episode for over two years. Over the next six years, I averaged about 1 episode per year, most converting in about an hour. Most of these were still triggered by vagal responses to hard exercise.

Then my wife wanted to separate and ultimately divorce after 34 years. My afib control dropped significantly during this time. I attributed this to stress. It got bad enough that I had 3am afib episodes 5 nights in a row. All converted with flec. At the suggestion of a cardio, I did try flec before I went to bed. This worked and after I added 1 tablespoon of powdered ginger spice to my pre-bed routine, I was able to titrate the flec to 0 over about a month. This worked reasonably well - I averaged I episode a month. When I looked at my situation, I was puzzled as I perceived my stress was decreasing as my afib episodes were increasing, over about a year. I tried to sort out what else it could be. I determined I'd added a lot of calcium into my diet, mainly stress eating cheese (I eat a low carb diet, so I could do so without other consequences). I eliminated the calcium and my control went back to excellent. It has now been a year since my last episode. I take no meds, ginger or anything except mag, potassium and taurine. I have mostly been successful avoiding the all day, very hard exercise triggers. A year and a half ago, when I had five nightly episodes in a row, I was ready to make an ablation appointment with Dr. Natale. Now, if my current situation continues, I see no need.

My repletion protocol is magnesium to bowel tolerance (which is very individual and mine happens to be very high - some reach bowel tolerance at a few hundred mg/day), currently about 4 g/day elemental mag as bicarbonate, glycinate, malate and chloride, 1-9g/day potassium as citrate and bicarbonate (for me, the mag is much more important than the pot, I take higher doses for the bicarb, not the K) and 4g/day of taurine. Jackie talks about her program here: <[www.afibbers.org]

George



Edited 2 time(s). Last edit at 05/25/2014 05:47PM by GeorgeN.

I never had a failure to convert with flec as a pip in about 50 doses over 5 years or so. I found that food in the stomach interfered with conversion time. On a relatively empty stomch I usually converted in an hour or two. A daytime Af attack after a full lunch took the flec pip 13 hrs to convert. When I first learned about flec as a pip strategy I misunderstood a posters comments about converting using the pip. I thought he said that flec tends to convert to nsr when the hr is high and that he raised his hr to aid the conversion. So I did the same and it worked every time. About an hour to an hour and a half after I took the met and flec, if I had not converted, I walked up and down the stairs until my hr reached about 185 bpm and the I would watch my hr monitor and bam back to nsr with a hr in the 60ies.
AS I SAID I MISUNDERSTOOD THE POSTERS COMMENTS. THIS PRACTICE MAY NOT BE WISE BUT IT WAS EFFECTIVE. Good luck! Dennis

Welcome to the board sbeckermd,

In addition to the excellent inputs from Geroge and Dennis, consider too taking a calcium channel blocker like Diltiazem or Verapamil if you are primarily a Vagal trigger afibber or add a beta blocker to your PIP protocol as well.. This is primarily to help prevent the dreaded pro-arrhythmic conversion tendency to a 1-to-1 flutter that a large Flec PIP can occasionally induce. But it make offer a little added value in converting to NSR, just from its rate reduction as well, in combination with the Flec PIP dose.

Shannon



Edited 1 time(s). Last edit at 05/25/2014 05:12PM by Shannon.

Shannon,

sbeckermd already has a slow heart beat (40-30 bpm), what effect do you think Diltiazem will have?
Ginger capsules may be safer. Ginger has a similar effect to that of verapamil.



Quote.

J Cardiovasc Pharmacol. 2005 Jan;45(1):74-80.    
Ginger lowers blood pressure through blockade of voltage-dependent calcium channels.     
Ghayur MN, Gilani AH.     
Ginger (Zingiber officinale Roscoe), a well-known spice plant, has been used traditionally in a wide variety of ailments including hypertension. We report here the cardiovascular effects of ginger under controlled experimental conditions. The crude extract of ginger (Zo.Cr) induced a dose-dependent (0.3-3 mg/kg) fall in the arterial blood pressure of anesthetized rats. In guinea pig paired atria, Zo.Cr exhibited a cardiodepressant activity on the rate and force of spontaneous contractions. In rabbit thoracic aorta preparation, Zo.Cr relaxed the phenylephrine-induced vascular contraction at a dose 10 times higher than that required against K (80 mM)-induced contraction. Ca channel-blocking (CC activity was confirmed when Zo.Cr shifted the Ca dose-response curves to the right similar to the effect of verapamil. It also inhibited the phenylephrine (1 muM) control peaks in normal-Ca and Ca-free solution, indicating that it acts at both the membrane-bound and the intracellular Ca channels. When tested in endothelium-intact rat aorta, it again relaxed the K-induced contraction at a dose 14 times less than that required for relaxing the PE-induced contraction. The vasodilator effect of Zo.Cr was endothelium-independent because it was not blocked by L-NAME (0.1 mM) or atropine (1 muM) and also was reproduced in the endothelium-denuded preparations at the same dose range. These data indicate that the blood pressure-lowering effect of ginger is mediated through blockade of voltage-dependent calcium channels.

With 6 episodes in 35 years my focus is on prevention rather than treatment

Colindo. Pre ablation my night time hr was low 40ies even falling to high 30ies. Even with this rate the MD's insisted on the bb before the flec for fear of the 1 to 1 conduction that Shannon mentioned. I don't recall my hr going lower as a result of taking the one time bb followed by the flec. Dennis

Colindo , The calcium channel blocker is preferred generally over a BB in a FLec PIP combo for folks with preexisting bradycardia, even fitness induced brady. I'm surprised Dennis' Cardio did not give him either Verapamil or Diltiazem rather than a BB with his low resting night time HR as well to go along with his Flec PIP, unless he has some other contraindications for calcium channel blocker? They tend to be less suppressive of resting HR than a comparable dose of BB in most cases. There are exceptions, but that is the rule of thumb and is why I mentioned that first to Sbeckermd who, from his report so far, I would hazard to guess is more clearly vagal rather than adrenergic though perhaps after a good number of years of even sporadic episodes may well be moving toward a mixed bag of vagal and adrenergic influences on his triggering.

As I've recounted in the past, I did have a 1 to 1 pro-arrhythmic flutter episode form a Flec PIP dose while living in Holland, which also coincided with my flipping from 16 years of steadily increasing paroxysmal AFIB, to persistent AFIB, and I can assure you, you do not want to experience 1-to-1 flutter if you can at all avoid it!

Cheers!
Shannon

Sbeckermd,

Speaking of prevention, you mentioned you are very committed to exercise. Chronic fitness or overexercising can be contributory factors to episodes of atrial fibrillation...likely were in my case. Don't know how much you exercise but might review your patterns and if excessive consider cutting back some.

Welcome, Dr.Becker... In addition to the good advice you’ve received thus far… also it would be important for you to pursue the comments on the exercise factor. There are past posts about oxidative stress/free radical damage from exercise causing cardiac fibrosis as well as magnesium deficiency causing cardiac fibrosis. That buildup interferes with the electrical conduction pathways.

Most afibbers are deficient in magnesium. Heavy exercisers are found to be deficient in magnesium along with a tendency for low levels of potassium....often offset as well by too much sodium.

Stress depletes magnesium quickly…. I’m sure your experiences as a trauma surgeon are not without stress. And and exercise, while important, is a stressor, itself.

Electrolytes must be optimal and in the proper functionl ratios. There are numerous posts about using intracellular testing of all electrolytes so you can evaluate the results of your dietary intake of the critical nutrients required to maintain NSR. Check the info at www.Exatest.com. Order the test for yourself.

The experience of many, myself included, is that we have to do heroics with electrolyte supplementation to keep those intracellular levels in the proper ratios to maintain NSR. Serum values are not reflective of IC levels so the Exatest becomes an extremely useful assessment.

This will be a great start for your recovery program.

Healthy regards,
Jackie

Thank you Jackie

My exercise is 3-4 75 minute yoga classes per week since 2007. I no longer participate in strenuous aerobic exercise.
The change in my exercise pattern resulted from a concern regarding my joint longevity if I continued running, boot camp classes etc. Seems like this change was good for my heart as well.

I am presently half retired, which means that I work 8 days per month. The most recent attack occurred at the end of 8 days with no work so work stress is probably not the factor it was years ago.
However, this lessened work schedule allows me much more time to care for our two acre property on the waterfront in NJ. The day leading to the last a fib onset was filled with moving 15-20 wheelbarrow loads of dirt from one location to another. Looking back, I was surely dehydrated and there could have been electrolyte depletion

From now on, when I engage in strenuous yard work I will strictly adhere to hydration and I am going to start a regimen of daily magnesium intake.

This blog has been very helpful to me because I have been made aware of other people who have this malady and have used PIP for many more conversions then I. My fear of these attacks every three years is not converting back to NSR with PIP. The life of a permanent a fibber with anticoagulation and rate control medicine would be a major, major insult to my quality of life.