GREAT post! The only 2 points I'd add would be: i) to reemphasize what you've said in previous columns - namely that one very valid approach for certain patients (esp. older ones with longterm AFib) is rate control with aticoagulation and not even thinking about rhythm control; and ii) that a 6th reason to consider antiarrhythmic drugs is because the patient asks for this (perhaps because they are not yet ready to have an ablation procedure). In a sense - that's another way to "buy time".

 Again - GREAT post - and  I think you covered the key points extremely well (and in proper perspective). 

First, thanks very much indeed for your articles and blog.  As a 70-yar old lone AF patient in the UK I find them helpful, clear and entertaining.  I realise that you can't comment on my personal case.  I am seeking your general opinion on the effect of AF medications on the patient's capacity to exercise.

At 5'9" and 116lbs I run, walk and train with weights, don't drink or smoke and eat an obsessively healthy diet.  My problem is that I am currently taking a 5mg beta blocker as a pill in the pocket.  I am not sure if that helps curtail my AF episodes, but I AM sure that the beta blockers hold down my HR so that it is hard for me to do aerobic exercise for the two days following an attack.  Thus each AF episode costs me 3 days of exercise.  If I DON'T take the beta blockers the attack may or may not last longer (they are so variable it is impossible to judge) but I only lose 2 days - one for the attack, one to recover and the 3rd I'm OK.  

As you are an advocate for exercise, please could you tell me whether a different pill in the pocket (eg Flecainide) might have a less negative effect on my sporting life than beta blockers?  It has been suggested that I take Dronedarone regularly, as my AF is linked to my digestive problems. Is this known to affect exercise capacity?  I am sure you will appreciate how important these questions are for me. Thank you.

One aspect I have seen unfortunately too little recognition of, even today, is that when it comes to AF drugs, one class - Beta blockers - is not always very good for one class of AF sufferers - vagal - especially symptomatic ones.  I was "fortunate enough" to suffer from asthma and for that reason have never been prescribed Beta blockers, but my AF was/is clearly strongly vagally mediated, as is the case for many fit, active people including sportspersons.  Other AF drugs I have had also slow the heart and made my AF worse, though flecainide seems to be OK for me. 

But my heart sinks every time I see someone saying "I can't run/walk/hike/bike any more since I was prescribed beta blockers". Especially as it is often followed up by "and they don't convert me back to sinus, either". Nope, they're probably taking you further away from sinus.

Now, I know there are other reasons why Beta Blockers are considered, but each time they are considered, make sure the sufferer is not vagal, and even if the vagal/adrenergic balance is not clear (as it often isn't), if they're a sportsperson then give htem the benefit of the doubt and find somethign that doesn't slow their rate.

Thanks, once again, for sharing your knowledge and insight.

From one with parox Afib... on regular flecainide and toprol, who still has episodes every now and then... no discernible patterns of course... When there is an episode, it feels like a near death situation, especially with low BP from extra toprol, flecainide and aspirin.  In the midst of those situations, ablation would be a welcomed option.  Once it reverts, after minutes or hours or days... life is fine again... why mess with ablation.  So the big dilemma is "what to do next?"  Try to live under the black cloud of parox Afib or go have an ablation and "hope" that it eliminates the problem(s) and doesn't introduce any new ones.  Flip a coin?  OK, it's heads... so it's time to go have an ablation.  I'll let you know if it was the right decision for me.  There's only a 3-4 week delay between decision and the actual procedure.  How many people back away at the last minute?  Will I?

Excellent piece and timely for me.  I was relatively AF free on a set of medications for 3.5 years.  Late June went to AF and would not convert with medication.  Had a cardioversion and remained on same medication for 32 days and went to artial flutter.  Additional doses of same medication unsuccessful and required cardioversion on 1 August. My cardiologist referred me to the EP to discuss options.  The EP increased the doses of Rythmol from 325 to 425 mg twice daily. He discussed dofetilide, flutter ablation and AF ablation as a path to pursue. 

I have a "tough" time grasping the impact of AF.  First medical issue that hasn't been able to be fixed with medicine, stitches or replacement.  The uncertainty of the next episode is difficult to deal with and determine how much I want to stretch the limits of exercise.  

I sincerelt appreciate your articles and blog.

 

Excellent article. I am fairly new to Afib. Had Afib, had a cardioversion and then went into V-Tach. I am 69 years old and was very active walking, exercising and on the treadmill.   I am Afib free for 2 months but have a fear of being active again. Took Amioderone 600mg. for a month and now take 200 mg. My cardiologist tells me to stop the Amioderone but I still have the fear of going out of rythem if I do. After i had V-Tach I had an ICD put in but I am also looking into having ablation . 

 I appreciate any thoughts or sugestions.

 

As a patient of occasional a-fib, and a person very sensitive to medications, I prefer this 'wait and see' approach, or as I like to call it, 'wait and investigate'. For others in a similar situation, I believe doctors could encourage patients to explore the root cause or what may trigger these episodes, rather than offer only meds with potentially serious side effects and/or ablation, which is not without it's own dangers. 

I suspect it may have been blood pressure meds that triggered my a-fib in the first place.  Through a plant-based low sodium diet, I was able to completely stop the bp meds. I've further learned that my a-fib is induced by sulfates and food additives, particularly flavor enhancers (MSG, etc).  There is research pointing to the correlation between heart arrythmias and the mountain of preservatives and chemicals in the American diet: Why not explore these possibilities as well? Astonishingly, I have yet to find a cardiologist to suggest this. I've been frustrated and confused by pressure to immediately begin anti-arrhythmic drugs and/or schedule an ablation.

I appreciate the honesty of this informative article.

It should be recommended that patients with poor diets or who are on acid blocking therapy be sure they are not magnesium depleted as determined by serum or RBC magnesium studies.  Oral magnesium is cheap, almost impossible to overdose if taken orally (providing normal kidney function) and wonderful for A Fib.  Acid blockers such as Proton Pump Inhibitors and H2 receptor blockers all decrease magnesium absorption.

Taurine 1-2 grams three times daily can also be used for adrenaline sensitive patients and has been shown to decrease PACs and PVCs. 

 

What about Vernakalant? It isn't approved in the US yet though.

I read this article and feel a little nervous for myself in regards to my medication. I am 55 years old, female, a school teacher and in otherwise good health. I believe I started to have AFib/Flutter in my early 30's but was always told I had anxiety and was treated with xanax. I became increasingly frustrated with my Dr's diagnosis so finally sought out a cardiologist who monitored me several times to finally get what was happening. I underwent an  Afib/Flutter ablation in February of 2010. I continue to take Flecainide 100 two times a day and a 10 mg Zebeta. I tried to go off of the meds a few months after the ablation but found that I felt more comfortable staying on them. I have had only a couple of AFib episodes since the ablation but am scared to death of them when they happen. My life is 95% better since the ablation but the procedure not a walk in the park so I really am not excited to have a "touch up." I think this article is very informative but it has left me questioning the continuation of my meds the way they are. They do provide peace of mind for me.

I liked your article very much as it gave he options and your thinking behind those options.

I am slightly concerned about all the comments of those people who say they are vagal.  Do you believe in the vagal mediated afib?

When I first got mine, I always went into afib at night or possibly late afternoon.  Vagal, right?  Unfortunately I was the wrong age, sex, and weight for it.  They checked out apnea, treatment of which did in fact cause the afib to occur more during the afternoon.

Almost all afib meds drove my blood pressure low, enough so they would discontinue use and it was always a worry, but I also found that when they drove the heart rate too low when I was not in afib; I actually could tell when I was going to go into afib soon.   My body would feel peculiar and I would welcome the afib to get me over it.

I would be interested in your opinions about vagal afib, etc.

 

 

 

Thanks for a very interesting article, with which I agree as best as I can with my own experience knowledge.

I have just had my 4th electrocardioversion in 7 and a half years! I am a paroxysmal AF68 year old woman, with no other health problems.

I have been using a regime of Sotalol 2x40 mg-day during this time.  From my understanding and reading of your article, I can assume that the sotalol is nearly as a prophylaxis as when I do have an AF episode, additional such medication does not revert the condition.  Nor, have I ever self converted back into sinus rhythm.

I believe I am fortunate to have a plan which works, ie. ambulance, hospital and cardioversion asap.

Would the readers here think that I should just continue as is, or venture into another medication etcetc?

I have never suffered with hypertension.  I am overweight, but relatively fit. The sotalol keeps my heart rate on the low side, but it makes me tired sooner from every day activities etc.

It would be nice to hear other view points. thanks for this opportunity.

After 8 years of paroxysmal AF and 6 drugs, including ones mentioned favorably above, my very symptomatic episodes were becoming more frequent and lasting longer, up to a week with shorter respites. Three ablations in 2011 (male, 69 yrs old, strong heart) accompanied by 4 cardioverts + a pacemaker did the job. (Ablations pain free...worst part anesthesia hangover for few days.)  After a couple months of healing in the heart, of which I had no sensation, the AF did not recur. It's been 6 months now and I exercise regularly and enjoy 2 glasses of wine daily.

Fleckanide 100 2x daily + metoprol 100mg (also for BP ) but will reconsider with MD after this excellent blog post. At least will supplement magnesium. Pacemaker keeps HR ar 72 vs historic norm of 50ish (good genes + years running)  

Quality of life dramatically improved!  Would do it again if necessary but realize damage potential to heart fron multi- ablations. I think "fried" is the word I've heard. Life is good!

Dear Dr.

I was shocked to learn about dofetillide.  Never heard of it??

If it is such a wonderful drug, how come it is not more commonly used???

I am 73 with persistent A-fib.

Thanks,

Wendell williams

WW,

The reason why dofetilide isn't that well known or commonly used is because it is a complex medicine that has to be used carefully and only by experts. The medicine must be initiated in the hospital over 3 days. The prescribing doctor has to have completed a special course on the drug. It is cleared by the kidneys and has numerous drug-drug interactions. Finally, it is a potent QT-prolonger. 

But yet, AF doctors, especially AF ablationists, use a lot of tikosyn. As I wrote, the drug sometimes works like magic.

I would not and should not give medical advice over the internet. When AF patients write to me with their AF story, I answer with the same response: You should discuss your case with your doctor--and it's okay to seek out numrous opinions. Two things are true about AF therapy: In many cases, there is often a couple different ways to treat the disease, and two, knowledge and expertise about AF treatment varies considerably in the cardiology community.

JMM 

Dear Dr.,

I have been very impressed reading your blog ;and your answering me on a Saturday nite put the icing on the cake.

I wish you lived in the S.F. Bay area (I live in Sonoma). If and when I get ready for ablation you can be sure I will chose you.

Sincerely,

Wendell H. Williams

Former Democratic Nominee

U.S. Congress (Calif)

  

Thank you Dr. John Mandrola for interesting article. As a 59 years old cardiologist with paroxysmal AF, I would like to share some ideas with you and your readers, and I hope to read your comments on them:  

1.       Most, if not all, my paroxysms started in the night and awaked me because of severe palpitation, chest discomfort and sweating. I discovered that lying in the left side was the trigger of AF episode, and after avoiding that position I became free of any episodes during the last two years. I searched the literature for positional AF, but I didn’t find enough information!

2.       During AF paroxysm, I took 40 mg and sometimes 80 mg of propranolol to relieve the symptoms, and it partially works. The rhythm – thank God- converted spontaneously to sinus in no more than five hours. So, prescribing beta blockers during the attack which converted spontaneously seems advisable.

3.       I tried beta blockers as a prophylaxis – before I discovered my positional trigger for AF- but it doesn’t work, nor was ACE inhibitor or statin.

4.       When the paper of pill-in-the pocket approach was published, I prescribed them to some of my patients; but as I have risk factors for coronary artery disease (rich family history, hypercholesterolemia, age, sex) I felt it could be dangerous to try taking class Ic antiarrhythmic medication!

5.       One of my colleagues told me that his paroxysmal AF was disappeared after using proton pump inhibitor for potential gastro-esophageal reflux.

6.       The last, but not the least, point I like to mention is that keeping patients of AF in sinus rhythm should be our goal, and we should try all the tricks we learned to do that. Although the studies say that controlling ventricular response of AF or converting AF to sinus rhythm will have the same mortality percentage, quality of life is very important. And if you experienced an episode of AF you can tell the difference between normal sinus rhythm and abnormal AF rhythm!   

The pill in the pocket approach is useful, however can you clarify a couple things:  When this was reported in NEJM, there is clearly a description in Methods that these patients were all treated in a monitored setting, prior to being given a Rx for outpatient use.  I think that is often ignored.  Do you use this only on those whose first use of propafenone or flecainide is in the hospital or ER? 

Detection and treatment of sleep apnea is underappreciated as an adjunct to prevent recurrences of afib.  How much do you push to add ACE inhibitors and statins, both of which have been shown to decrease the likelihood of recurrence of afib?