way forward

[atrialfib]

it seems to me that i have PAF,stroke risk to cover apart from that,why do people take serious rhythm control drugs with serious side affects,why not just take rate control to keep it from going crazy with less side affects,does anyone agree.

[Hidden]

Rate control drugs do not work on me, in fact make me feel worse. Only rhythm control works and then only some of those drugs. Also, by controlling my rhythm, it seems to also slow my heart down. I suppose it stops struggling to keep up with my oxygen requirement or something like that, just guessing.

[Beancounter Volunteer]

Hi atrial fib

For some people rhythm control drugs work and they control the AF, and is you are PAF and get bad episodes, then controlling that is important of course.

Plus for those for whom ablation is either not advisable perhaps due to other medical conditions, or age or even longevity of the AF, then these can be a really useful tool.

Lastly not everyone gets the side effects, there are a number of people on here on Amiodarone (for example) without any serious side effects, and it controls their AF. And of course Flecanaide, is one of the most often prescribed drugs and that's rhythm control.

Horses for courses I think

Be well

Ian

[GivEmkeL]

Hi! I have had AF for several years, and tried rate control meds. Unfortunately, they did not work for me. I have been on rhythm control meds for almost three months, and have only had one episode of AF. Before switching, I was having several episodes a day. I will eventually opt for ablation, but I am waiting until after I am out of grad school. Best wishes! - KeL

[BobD Volunteer]

The flip side of that is my view which is why anybody would waste their time taking rate control drugs which don't stop the AF when a rhythm control drug may. There are a number of suitable such drugs and I am sure most people could find one which doesn't cause too many side effects. In fact most rate control drugs cause people a lot of problems such as tiredness, breathlessness and lack of energy (bisoprolol) whilst doing little to actually alleviate the symptoms. Of course we are all different.

Kel--- good call!

Bob

[CDreamer]

No I don't agree. I really didn't want to take ANY medications and didn't for many years, but then I failed to realize the risks of having AF. After finding this forum, the AFA and attending the patients day I started to consider the risks and benefits of a, doing nothing b. Listening to people on this forum and what the doctors and EP's I met and talked had to say as clinicians.

Then my AF got a whole lot worse and rate control on their own did nothing so although I didn't want to, I tried Flec and although it made me I'll the first few times I took it, I soon realized how effective it was. Stay completely debilitated for 3 days at a time, not being able to work or take a pill which relieved my AF in about 3 hours, no contest! After the first fewer times of taking I had no side effects and my GP monitored my bloods for signs of kidney damage so I felt quite secure.

I ended up taking 100 mg x 2 a day which controlled the AF completely for about 1 year, unfortunately AF overwhelmed the Flec's ability to control episodes, but luckily an ablation succeeded in blocking the rogue pathways so now I don't take anything,

[atrialfib]

did i get it wrong then,please tell me i did,i thought i read that rhythm control drugs can cause the heart to stop.

[Rellim296 in reply to atrialfib]

You might be right, atrialfib, but I've not heard about that. I took flecainide for three years, ending on 300mg a day for the last 8 months, without any big problems. I'm also on atenolol, but only 25mgs.

I did have side effects from the flecainide, and would have preferred a lower daily dose, adding more as a pill in the pocket whenever I had AF.

[rosyG in reply to atrialfib]

I wonder if you mean the studies where patients with heart problems had to stop anti arrhymic drugs?

They do test to make sure Flecanide is suitable for you i e no artery disease etc

[CDreamer in reply to atrialfib]

There is one drug which is called Sotalol which is a bit apidexris in that it is a bit of both which not only works on the atria but also affects the ventricles. It is the ventricles which keep you alive. Think of the atrias as the starting motor and the ventricles as the engine. As long as the engine keeps running you live.

Sotolol can in very rare cases affect the ventricles so that why it is trying to slow down the atrias, it sometimes also affects the ventricles whereas all of the other drugs only affect the atria. That is why I believe Sotolol is not recommended for AF patients by some EPs and indeed one leading EP in the UK would like to see it withdrawn.

Like ANY drug whilst it will relieve the symptoms most of the time it will always have the capacity to also cause symptoms so anti arrythmic drugs can, sometimes cause an arrythmia as well as stop or prevent them. As you will have seen from these posts, we all react very differently to these drugs and the old phrase one man's meat etc comes to mind.

There is a lot of confusion and it is difficult to know what to do and what will work for you and what not. I believe the recommendation is to take any anti arrythmic drug only under direct medical supervision for the first time so that any contraindication may quickly and safely be dealt with, this is certainly what happened to me.

[Beancounter Volunteer in reply to CDreamer]

Great post CDreamer

[CDreamer in reply to Beancounter]

My goodness, you must have been up early! Thanks.

[Thomps95]

I have paroxysmal AF and both rate and rhythm control tablets work well to prevent episodes. However, if I take rate control drugs regularly (e.g., atenolol) then I end up feeling tired and unmotivated. I now take a rhythm control tablet (50 mg flecainide twice a day) and it works well. But you are correct: there are some serious side effects of flecainide: in extremely rare instances with a large dose the heart can stop, and it can cause a rapid heart response. For this reason some doctors suggest combining rhythm control with rate control - but I've decided to go with just rhythm control, and take rate control only on occasion - for example if I plan to play sport or have a big night out.

[Hidden]

I am not medically trained at all, except with sheep!!! But just from experience rhythm control drugs can cause irregular heart beat. Some (if not all, don't know?) say so on the label. I was put on Flecainide and although it seems to work for most people, it gave me palpitations so we stopped it immediately. I was asked not to try and get used to it, but to stop straight away.

When I was in a coronary ward, the cardio explained to me that giving rhythm control drugs was like cooking. They try one, didn't work, so they try another. It was the third or fourth one that worked for me. Only the one caused palpitations though, the others just didn't do enough or had side-effects we didn't like.

We're all different and what works for one person may not work for the next. Also, what worked on me 10 years ago does not work so well now. So I've been changed over to another drug which so far is working and no side-effects I can detect.

Koll

[meadfoot]

I took rate control alone which worked for three years then needed a rhythm control drug too. So far so good. I hate taking big gun drugs but I hate my dreadful AF attacks more. Currently on an ablation list.

We can all only do what we can do and hope and pray new and hopefully improved treatments come along over time.

In the interim we just have to carry on regardless I guess.

Be well.

Dee.

[Finvola]

I took a rate control drug only for 5 months (Bisoprolol) and it did nothing for my AF or other arrhythmias but made me tired, unable to walk any distance and slightly unbalanced (mentally and physically). Once I started rhythm control (Flecainide) 3 months ago and had the Bisoprolol reduced, my arrhythmias stopped and I have a fairly normal life at the moment.

Regarding the seriousness of anti-arrhythmic drugs - I agree with you and starting them was, for me, an ordeal. But, uncontrolled AF/tachycardia was a much, much worse option.

One of the effects of these drugs is that they MAY cause other arrhythmias, including serious tachycardias which is perhaps what you are referring to in causing the heart to stop. That is why patients starting antiarrhythmics are closely monitored, especially at the outset to ensure there are no unwanted health problems with their use.

It's a matter of each of us choosing how we want to live and cope with the condition we have - weighing the risks and benefits of the various therapies as best we can.

[CDreamer in reply to Finvola]

Very well put.

[Rellim296 in reply to Finvola]

I found flecainide wonderful when I first took it almost four years ago and had no problems of any sort. I don't feel I was closely monitored nor assessed. However, after a couple of years the AF was creeping in again. I didn't notice the side effects (like numb feet) until the start of last year and I still have them although I stopped taking flecainide in July which was four months after an ablation. I think the sensation is beginning to be slightly less intense and less extensive. I am really pleased to have stopped taking a significant dose of flecainide and would be unwilling to go back to taking so much, partly because when you are not far off the maximum dose it gives you little scope to zap any AF when it strikes.

[EngMac]

I find it interesting to read the different experiences. I was put on antiarrhythmics and the prescribing EP doctor went on vacation for a month. I had problems with the drugs and no other doctor would hazard an opinion or suggest a change. You would think maybe doctors should have back-up. I stopped the drugs on my own and don't take any drugs right now. If I avoid triggers, I don't have AF. For now that seems like the best approach for me and the prescribing doctor did not disagree. Daaa!!

[Hidden]

Yes, bigleg, we're not that much different from cattle or sheep. Mag deficiency as you clearly know is extremely important. Without it either a sheep or cow it'll eventually be lethal. And magnesium is unique. It's the only mineral/nutrient that can lock itself up in the soil. Usually too much of one thing can lock up another, so it doesn't get through to the animal, but with magnesium, too much of itself can lock it up. It's a weird one. I wouldn't want too much or too little.

The basis of all animal health is simply a good, appropriate/natural diet. i.e. feed what they were designed to eat. Very few problems then (he says confidently whilst dealing with an outbreak of pneumonia out in the fields!).

K

[Bagrat]

I'm on flecainide which works well.Have always been on 100mgs BD after the first week. Take warfarin but no rate control as pulse 48 on bisoprolol and no alternatives offered. "Close monitoring" has been me asking for an ECG in July after two years since an episode so no monitoring. GP said ECG "OK". No doubt I will have to ask again soon in spite of leaving the AFA info on flecainide at the surgery to be scanned into my notes.

[EngMac]

Hi Bagrat. I have pasted the contents of a study that could interest you assuming that you have not seen it. I think bisoprolol influences rate, thus a beta-blocker. Maybe you can get off this drug so your heart rate would increase a bit. You may feel better. Just something to ask.

Most vagal afibbers receive wrong medication

MAASTRICHT, THE NETHERLANDS. There is still widespread denial among North American cardiologists as to the existence of vagally-mediated AF (atrial fibrillation) and a pronounced tendency to treat all AF patients the same. Hopefully, this will now change with the publication of the results of the Euro Heart Study. This study involved over 5000 AF patients treated in 182 hospitals in 25 different countries.

A total of 1517 of the patients experienced paroxysmal (intermittent) afib and was studied in detail. Among this group, 42% (640 patients) had a distinct, physician-verified, autonomic pattern as far as triggering an episode was concerned. Another 35% reported no clear trigger patterns, while in the remaining 23%; the physician did not verify the presence of triggers. The authors of the study classified the trigger pattern as vagal if episodes occurred after a meal or during the night, and as adrenergic if initiated by exercise or emotional stress. Afibbers with no clear trigger pattern were classified as mixed.

Sixteen percent of the group had lone AF defined as afib without the presence of hypertension, coronary artery disease, or heart failure. Somewhat surprisingly, the researchers found no difference in the incidence of heart disease among vagal and adrenergic afibbers. Among the group with clearly defined trigger patterns, 18% were classified as vagal, 46% as adrenergic, and the remaining 36% as mixed. (NOTE: The distribution in our most recent LAF survey was 30% vagal, 6% adrenergic, and 64% mixed).

The major conclusions reached from the study are as follows:

•Exercise and emotional stress were the most common triggers followed by electrolyte imbalances, and alcohol and caffeine consumption.

•The majority (72%) of vagal afibbers received non-recommended drugs (beta-blockers, sotalol, digoxin or propafenone) – 57% were prescribed beta-blockers or sotalol.

•Vagal afibbers who were prescribed non-recommended drugs were more likely to progress to persistent or permanent AF than were vagal afibbers prescribed recommended drugs (primarily flecainide). After 1 year of follow-up, 19% of vagal afibbers prescribed non-recommended drugs had developed persistent or permanent afib as compared to 0% in the group prescribed correct drugs.

•Among adrenergic afibbers, 20% did not receive the medication recommended in the 2006 ACC/AHS/ESC Guidelines for the Management of Atrial Fibrillation. However, there was no indication that the type of medication affected progression to persistent or permanent in this group.

•Quality of care would appear to vary considerably between the regions in Europe. In the Mediterranean region 41% of patients received the recommended treatment as compared to 20% in Central Europe, and only 19% in Western Europe. Similarly, in the Mediterranean region physicians verified the presence of triggers in 75% of cases as compared to 79% in Central Europe and only 46% in Western Europe. Editor’s comment: It would seem that afib care in Western Europe is substandard, but probably no worse than in North America.

•The authors point out that beta-blockers are often given in conjunction with class 1C antiarrhythmics (flecainide and propafenone) in order to prevent 1:1 conduction in the case of atrial flutter induced by the class 1C drug. They suggest that verapamil and diltiazem could be used as safer alternatives.

The authors conclude, “Physicians do not seem to choose rhythm or rate control medication based upon autonomic trigger pattern of AF. However, the role of autonomic influences should be taken into consideration in order to achieve an optimal management of the disease as non-recommended treatment may result in aggravation of the arrhythmia.”

de Vos, CB, et al. Autonomic trigger patterns and anti-arrhythmic treatment of paroxysmal atrial fibrillation: data from the Euro Heart Survey. European Heart Journal, Vol. 29, 2008, pp. 632-39

Editor’s comment: Although not specifically directed at lone AF, this new European study is clearly a landmark and emphasizes the importance of determining trigger pattern (vagal, adrenergic or mixed) before prescribing medication for paroxysmal afibbers. It is interesting that our first LAF Survey (February 2001) revealed that 50% of vagal afibbers had been prescribed non-recommended drugs. This resulted in an average afib burden (# of episodes times their duration) more than twice as high than the burden among vagal afibbers taking flecainide or disopyramide. As far as propafenone (Rythmol) is concerned, the situation may not be as clear-cut as suggested in the Euro Heart Study. Some vagal afibbers have found this drug quite useful. Some fairly recent research have found that the degree of beta-blocking effect exhibited by propafenone depends markedly on how fast it is metabolized, so this may explain why it works for some vagal afibbers, while it is contraindicated in most others.