This and That

Happy New Year fibbers,

While I’ve been reading the BB posts I’ve continued to experiment and contemplate the LAF mystery. I’ve seen many posts touting the ablation approach. I’m sure many of you will agree that this route is most tantalizing. However, this post will hopefully encourage some of you with a prominent vagal component to persist in your search for a medical (v. surgical) solution.

After diligent experimentation with disopyramide (Norpace, Rythmodan) I have found that it will eliminate not only my AF but also my PACs. My life is no longer dominated by avoiding free gluatamtes (MSG), late and/or large meals, sitting down or reclining after exercise, etc. It has been almost two months since my last episode, the longest AF interval since I started keeping a diary (three years). I have found that if I take 125mg q3h (with an extra 125mg at 5PM) and then 250mg at bedtime (around 9PM for this old fart), all is right with the world.

I just returned from a trip to NY with my family and indulged in ALL at risk behaviors without so much as a disconcerting PAC. So I encourage many of you to try this wonderful med. My regimen totals a gram per day. The PDR recommends 600-800mg per day for adults. The side effects are mainly dry mouth, constipation, decreased urine flow and blurred vision. It also has a negative inotropic effect, which means that cardiac output doesn’t respond as well on demand. While there is no shortness of breath, there is increased burning in your muscles during physical activity. But I can still easily run 4 miles in under 30 minutes. But talk to your cardiologist.

I noticed during my initial regimen (lower dose) of disopyramide that I sometimes went into tachycardia. This tachycardia might or might not transit to AF (brief periods). The shortened atrial refractory period (AERP) and dispersion of this refractoriness caused by increased vagal tone presumably allowed reentry throughout the atria, resulting in 6 or more wavelets of Moe (critical mass for AF). Lower blood levels of disopyramide might limit this dispersion and reentry might then occur only near the PVs, where the PACs originate. Perhaps slightly higher levels are eliminating not only reentry around the PVs but also the triggering PACs.

Once a week or so I can detect a flurry of 3 or 4 fast beats but no PACs. I know they still occur from my S810 Polar monitor. My 24 hour Holter monitor done some months ago revealed over 30 such brief episodes of supraventricular tachycardia (without AF).

Reentrant Tachycardia in Pulmonary Veins of Patients with Paroxysmal Atrial Fibrillation
[www.ncbi.nlm.nih.gov]

Electrophysiological and Electrocardiographic Characteristics of Focal Atrial Tachycardia Originating From the Pulmonary Veins
[www.ncbi.nlm.nih.gov]

Although most of my AF episodes undoubtedly are triggered by PACs, I know that a sudden sprint can also trigger AF. I just don’t do much sprinting these days.

Since AF can often be induced in dogs after fast pacing (creates more dispersion of refractoriness) and since sympathetic tone can also cause shortening of the AERP (as well as increased automaticity), perhaps this is the main mechanism at work in adrenergic AF. In fact there is a very recent article on “The Emergence of Aldosterone As a Cardiac Toxin” at
[www.medscape.com]
that states that not only are there aldosterone receptors in the heart but also that it is produced in the heart (as well as the adrenals). Not only is aldosterone produced as a result of physical or emotional stress it also causes oxidative stress and inflammation in the heart. So the inflammation and oxidative damage caused by stress might parallel that caused by prolonged physical activity in VMAFers (see pp 137-138 in Hans’ book).

There have been quite a few posts recently on sleep apnea and LAF. I know that in the past there have been times when sleeping on my back that I have noticed my breathing to be more audible (I hesitate to say the S word). This never happens if my head is turned to the side. Obviously my soft palate and uvula become more relaxed as sleep approaches and gravity combines to slightly obstruct the air passage. This is more of a problem in the obese because the these tissues are bulkier. Since being on disopyramide, this never happens. My mouth is much drier because my salivary glands are not secreting as much mucin (disopyramide blocks M3 muscarinic receptors in salivary glands). These tissues are less bulky.

Could obstructive sleep apnea be just another manifestation of increased vagal tone? This may not be so far fetched in view of the fact that diabetes is virtually unknown amongst LAFers, whereas many complain of hypoglycemia (please see Hans’ survey). Secretion of hepatic insulin sensitizing substance (HISS) is also controlled by the parasympathetic nervous system via M1 muscarinic receptors. Disopyramide works in VMAF because it blocks M2 muscarinic receptors in the heart critical in establishing vagal tone.

Incidentally I finally had my intracellular Mg levels repeated. A year ago after 6 weeks of waller water it was 34.3 meq/liter and a year later after continuous daily Mg supplementation of 500-1000mg it was 34.6 meq/liter. Rather disheartening. However, my leg cramps present for years have over the last few months completely disappeared. My sleep is also much improved. But I have no doubt that my entry for the past two months into the land of the AF free is due to disopyramide.

PC v55

Great news PC that you've found something that works. I do hope that it continues. I'm still going strong after 12 months with my pacemaker (atrial pacing only at 70bpm) and Verapamil (180mgs SR). Life is so much better not having to worry about all those triggers! Best wishes for an AF-free 2004! Rod V54 in sunny Tasmania.

Hi PC,

I have been on norpace 2 years this Jan 15 and I have not missed a beat since I started on the medication. I still take mg, fish oils. co q10 and many other supplements but the norpace has totaly changed my life. I have no bad side effect except dry mouth.

The only question I have is can this realy last or will I wake up one day and the medication will have lost its effectiveness. It may sound strange but I make many life decisions thinking I will go back to the daily attacks.

My doctor says it can last for the long term but I alway think that would be to good to be true.

Glad to hear that norpace has work as well for you, have a great new year and enjoy life with no afibb.

kevin

PC,

125 mg q3h? What is q3h?

John,

q3h means every 3 hours.

This is a physical q3h reminder to me that I'm

1) lucky that my health problems are presently limited to just LAF

2) lucky to have such an effective med to address it.

PC

PS I could easily have given up on disopyramide at the recommended daily dosage and moved on to something else. We're all different and must pick our own path toward improvement.

"Do not go where the path may lead, go instead where there is no path and leave a trail."
- Ralph Waldo Emerson

PC,

Happy new year to you too. Good to hear from you again here on the board..... and good to know that your by now finely-tuned Norpace regimen is working so well for you. Most encouraging for a vagal AFr like myself (last three episodes - during last 15 months - commencing at 3am and self-converting at 6-7am) to know that another strategy (i.e. your own) is waiting in the wings should my episodes increase in frequency during the coming years.

Since having had the last 2 of the aforementioned 3 episodes just 3 weeks apart (Oct 11 and Nov 1 2003), I've introduced 400mg cimetidine at bedtime to both help with nocturnal GERD and also to offset increased nocturnal vagal tone by virtue of its antihistamine effect. So far so good....... no more AF and less palpitations if awake during my 3 am vulnerable time...... although I do not particularly wish to stay on the cimtidine indefinately.

Cheers,

Mike F.

Oh yeah PC........... MANY HAPPY RETURNS TOO!!

PC,


Do you consume alcohol? If yes, was alcohol a trigger for you before
starting Norpace? If yes, does the Norpace allow you drink without
going into Afib?

PC,

It's good to hear that you're doing so well on dyso. Hope you enjoyed your holiday in NY and I wanted to wish you a Happy New Year.

Richard

Glad to hear about your success, PC!

I've had similar success with sotalol, but I may be more adrenergic.

When on dyso and a calcium channel blocker, I had a lot of PACs (I guess) and weekly AF. At the same time I was using a supplement containing naringenin (citrus bioflavonoid) which probably increased the calcium blocker blood levels, perhaps spoiling the therapeutic effect.

-will

Jon,

Never been much of an alcoholic, so I don't really know if that would be a trigger.

If any of your episodes are typically vagal in origin, I'd give Norpace a whirl. Unlike flecainide (Tambocor), it's relatively innocuous. Any drop in PACs while on it would probably be an indicator of its efficacy for LAF.

PC

PC,

Have you ever been on flecainide ? If yes, how did it work for you - compared to disopyramide ? Would you say - as my EP does - that diso is a far "weaker" drug than flec - so it would not make much sense to change over if flecainide starts loosing effect ? Currently I'm on flecainide on demand (200mg at onset) - but the intervals between my bouts are getting shorter and shorter ...

Gert, V57

Gert,

Your cardiologist seems a bit confused or at least inexperienced on this point.

Flecainide is a much more dangerous drug. Many MDs will not initiate therapy without hospitalizing the patient in advance to cover themselves, at least medicolegally. Disopyramide is less dangerous but has decidedly stronger vagolytic properties.

My experience with flecainide parallels yours. I too took 200 mg on demand with initially very good results. It cut the duration of my episodes from 18/20 hours to 4/5 hours. However, after a few months the episodes began to increase in frequency to the point where they were occurring every 36 hours. So I went to a maintenance dose without improvement and dropped the drug entirely. My episode duration returned to its former level but episode frequency also dropped off and returned to its previous level.

If you decide to try disopyramide, it is very important to maintain steady blood levels. Otherwise you'll get breakthrough episodes during the troughs (most notably in the early AM). You'll develop good feel for this from the dry mouth and decrease in urinary stream. Don't be afraid to gradually increase your intake from the 600-800mg adult recommended dosage and to take the drug more frequently to achieve the therapeutic target.

I buy my disopyramide (Rythmodan) from Canada 250mg SR. The tabs are scored and can easily be broken into two. The below website sells this for about $69 US for 100 tabs. At a gram a day (my dosage) this translates to about $1K per year. I looked for a quite awhile and this was the lowest.

[www.rx-counter.com]

I have no doubt that a new K channel blocking drug more specific for M2 muscarinic receptors in the heart will be soon available. But I'm also quite sure that it will very expensive.

PC v55

PC,

I have been using flecainide on demand (as mentioned on this board). It works beautifully for me. My
episodes always start at night (totally vagal). I take the flec at onset
and then in the morning and I convert like clockwork in 12-14 from onset.

Questions:

1. what is your overall view of taking antiarrhythmics prn?

2. Is flecainide less likely to lose efficacy if used this way?

3. My EP originally recommended Norpace when the flecainide was causing
increased AF frequency with daily use. I opted to use the flec prn rather than start taking a new drug daily.

4. Do you think disopyramide would work well prn. If so, maybe I should
consider switching given that flec. does pose danger, although I have
used it successfully on demand. I get episodes about once every
two to three weeks, a level of frequency that my EP is not concerned about
as long as I convert fairly quickly.

PC,

just noted that you mentioned in above post that you started on demand.
sorry.

Kerry,

I think most cardiologists would agree that flecainide is better than disopyramide in converting an episode already in progress. However, disopyramide is particularly good at preventing the start of an episode.

If flecainide works for you, I wouldn't rock the boat. I think its main danger is at the start of therapy, i.e., idiosyncratic reaction, especially in those with subclinical CV disease.

My view of antiarrhythmics is whatever works. The less required the better.

PC

You guys are great. My cardio suggested I go from toprol to amiderone, a very strong medicine with really bad long-term side effects with just inter-mittent afib WITHOUT recommending or even telling me about all of the other medication I've heard about on this board. PC, as a physician, wouldn't it be prudent to try less powerful meds first?

Also, can we assume that the supplements, diets, etc. suggested by this board didn't help in your case and that's why you are on the med route?

Are you aware of any long term negative effects of Norpace like amiderone?

Anyways, always to happy to hear of people that have solutions - gives me hope.

Gregg,

You have no idea how frequently, even now, digitalis and amiodarone are prescribed as first line meds for LAF, vagal or otherwise.

I know of no long term negative effects of disopyramide. If you hear of any, please let us know.

I think it's important to separate the many excellent suggestions for general health that are posted repeatedly on this BB from those that specifically apply to our own personal flavor of LAF. Discussions of insulin and sugar, paleo diet, etc., are great but have had no lasting or discernible impact on my LAF.

My problem is hypoglycemia, not diabetes. Just because two out of three Americans are overweight or obese doesn't mean that I have that problem. So I pick and choose what to pursue.

While it may be physical/emotional stress for many, it's vagal tone for me. I don't think that one should be sentenced to a life of denial of certain foods, dining out, sex, etc., in order to avoid an episode. The problem for me is much more deep seated than that. It's mostly genetic, but has probably been potentiated by oxidative damage in the left atrium. Prolonged dietary shortfall (Mg, vitamins C, E, B, etc.) was probably the straw that broke the camel's back. Since the latter is more easily rectified and this in turn seems to result in some improvement, we give it undeserved emphasis (MHO).

For my money, meds or ablation hold the only real hope for us LAFers. Some have used diet (Fran)and supplements (Erling) to surmount the problem, but this is clearly the exception and not the rule. Perhaps the more important point is that LAF is small potatos in the general scheme of human disease. Proper diet and judicious supplementation clearly are great weapons in delaying disease and death in general.

PC

PC,

Your personal experiences re disopyramide give me at least some hope for an option "after flecainide". My EP said there would be nothing but amiodaron, which I wouldn't take by no means and tikosyn which I fear also. Thank you for your info.

Gert

Gregg,

Ditto mate to your sentiments. Thank God for this board (and Hans and all contributees of course).

First time AF saw me in a (UK) hospital setting (May 2002) I was given digoxin and 'threatened' with amiodrone (no WAY was I gonna take it) if the digoxin didn't 'work' within 24 hrs................ I converted in 20 hrs........ despite the digoxin!! (I'm for sure a vagal AFr). All other episodes WITHOUT the 'help' of digoxin (or any other meds either contiuous or on-demand) have lasted between 3 and 5 hrs (early am and self-converting). And as for amiodrone? SURELY this a med of last resort......... NOT first resort!!!!

Jeez.

Mike F.

Gert,

Statements from a physician, even an EP, on LAF must be taken with a grain of salt. As an MD, I can speak with great authority on our shortcomings and need to appear to know it all. We are masters at the "often wrong but never in doubt" mentality. Like a captain of his ship the MD must project confidence. We do our best but are far from perfect. Listen to what they have to say but don't take it as gospel.

In general, assuming full disclosure, I would take the consensus advice from this BB over that of any cardiologist. They oftentimes don't have the time to properly and exhaustively investigate the matter and usually only the patient has the required motivation for that. The latter includes every poster/patient on this BB.

PC v55

Hi PC ,

I agree with "All" of what has beenposted here. I sent this to a guy in a cycling forum as an answer to his post. (Hope Han's not minding pushing his site?)

Hi Mark, I have attached my record of Cycling forums etc and note I have made/copied from www.afibbers.org/forum I have had VLAF for some eighteen months now and have found afibbers invaluable. ( I am on afibbers as David s if you see a post from such a person)

I first was sent to a "heart specialist hospital" emergency room via my GP which I agree with. The hospital put me on amiodarone and a minerals drip that lasted all night in ICU until I went into NSR. Then the cardio (after waiting a month!) put me on Lanoxin and a beta block that bloody near killed me-turned me into a Zombie. Talk about one med suits all, with no cardio follow up. He said "go see your GP if a problem arises"!

I got another referral to a different hospital and cardio he said "The meds they put me on because I had no underlying heart disease was pro-arrhythmic!" He put me "on demand Flecainide" 100 mg at onset, which works well for me. But, I ride VLAF (I am vagal type LAF) out now -it only lasts for half to two hours.

This mind you is after much research into LAF via the net but mainly afibbers.org. You want to find out that you have no heart "faults", what supplements might help, and weather you are vagal or adrenergic afibber to help in diagnosing-customising a regime to stave off, or at least manage your afib.

Keep up the good work all you well read afibers. all the best for 04
stay well and safe. In 32 deg sun will be 35 on wednesday! David s

Just discovered this bulletin board. I have had atrial fib since 1999 - at first 2 episodes (2 wks apart) I was converted by ER physician. Then hospitalized and assigned a cardiologist. She was involved in a study and asked if I would consent to take part. Knowing nothing, I consented. I was put on Cordarone (amiodarone) supplied by the study group. I was given NO information on the drug and no printed literature and no warnings of possible side effects. I also was put on the usual Coumadin. I had no further episodes and was tested every 6 months (tests that were not explained to me). In Feb. of 2002 I began experiencing strange symptoms --hard chills, tremors, weakness, fatigue, shortness of breath, etc. I went to ER several times and they gave no definitive explanation. I was placed in hospital and saw, among others, my pulmonary specialist. After being released from the hospital, he called me at home and said that in reviewing my chart, he noted that my heart rate had dropped to 40 and suggested that I call my cardiologist. My cardiologist was out of town. In desperation, I talked to her nurse who saw me and gave me a heart monitor to wear for a couple of days. My heart rate was still very low. The cardiologist returned and said I needed a pacemaker. This was done a week later.

Things were okay for a while or at least no worse.

In the spring of 2003 I began having symptoms again. Again, my cardiologist was out of town - her nurse mentioned a possible thyroid problem. First I had heard of this. My internist was out on medical leave and not available. I then began to do research on my own via the Internet, on A-Fib and amiodarone. It was there I learned what devastating affects amiodarone can cause. When my cardiologist returned to her office, I tried to discuss the medication with her. She was totally uncooperative and said there was no other treatment available, except a new medication that, if I should miss a dose, would required hospitaliztion for 72 hrs each incident. Her attitude was negative and impatient. I left her office in tears. I spoke then to the nurse practitioner who was filling in for my primary physician. She suggested getting a second opinion as did my pulmonary specialist. I received some names from them and made an appointment with one of them.

This period was concurrent with a study that had come out about amiodarone which apparently said it was not the only game in town. Did not my cardiologist know of this study? Hmm!

After talking with the new physician, he said other treatments were available and put me on Tiazac 120 mg. I did okay until this month (Jan., '04). I went into atrial fib again. Hospitalization followed and Med was changed to Atenalol which I could not tolerate since it exacerbated my lung problems. I was also given Digitek, Zetia, Lipitor and Spironolactone. I was already taking Zesteretic and Coumadin. They next tried Verapamil which also did not control the A-fib. I am now awaiting an ablation procedure within next 2 weeks.

Apparently the amiodarone was effective in controlling my A-fib, but its destructiveness overrode its value. I would never take it again, ever! I feel my original cardiologist was neglectful and arrogant in not properly informing me about amiodarone. She appeared to be more interested in having guinea pigs for her study.

No one ever really questioned my lifestyle and habits in the course of my treatments for A-fib.

I have now, for 2 years, been devastated by these events. I can only hope that the combination of my pacemaker and the ablation procedure will help to alleviate my A-fib problems. I am 76 yrs old and would like to have a little quality life for what time I have left.

That's my story.