The skeptical cardiologist has just updated his page on atrial fibrillation. I’ve updated the sections on medical management of AF and on AF ablation and included the relevant sections at the end of this post.
I’ve had a lot of reader AF questions by emails and comments and I’ve addressed three that are likely of general interest below
Beta-blockers, Sotalol, and Exercise
A half year ago I experienced atrial fibrillation (at 57), with a heart rate of around 100 beats per minute while resting. Sotalol (2x40mg/day) didn’t fix it, but a cardioversion did and I stayed on the same amount of Sotalol. I have discussed the usage of Flecainide with my cardiologist. He described the risk of flutter, as I am quite active in sports (swimming, running and cycling), and would only prescribe it with an additional bètablocker. I was satisfied with that explanation. Last week I was allowed to stop with the Sotalol, but needed a cardioversion within 10 days. Now back on the same amount of Sotalol (no Eliquis, as the cardioversion was within 24 hours and my risk for a stroke is low).
Question: is Flecainide without a bètablocker an option? I quite liked being ableto run the last week without the effect of Sotalol.
Since my first experience with atrial fibrillation I have reduced the intensity and durations of my workouts, as I favor being healthy above athletic performance
Sotalol is an antiarrhythmic drug that has beta-blocking properties and which must be started in the hospital under ECG monitoring for 72 hours in order to monitor for QT prolongation and possible ventricular tachycardia.
I’ve written about flecainide for suppression of AF here and emphasized that concomitant use of a rate slowing drug (beta-blocker or calcium channel blocker) is highly recommended.
I’ve been thinking a lot about beta-blockers and exercise performance in the last year and will post soon on that topic.
I think the reader is wise to cut back on “the intensity and durations” of his workouts as there is evidence that excessive exercise is associated with AF and a higher cardiovascular risk compared to moderate exercise.
A review of the mechanisms for AF with exercise contains this graphic
and another review on the management of AF in athletes contains this table on treatment
To the comments on catheter ablation, I would add that the risk of complications includes pulmonary vein stenosis which can lead to markedly reduce functional capacity and that there is a good chance of needing multiple procedures if lifestyle isn’t moderated. Any discussion of ablation should mention the possibility of death from esophageal-atrial fistula.
Ablation versus flecainide in Masters Bicyclist
I was diagnosed with AFIB in June and had a successful cardioversion in September. I am on 50mg of Flecainide twice per day. I am still in rhythm.
Long term if I am able to stay in rhythm, would you recommend staying on the Flecainide or going off of the Flecainide and having an ablation if the AFIB comes back..
I am 73, was training fairly hard as a masters bicyclist but have cut way back on that. Also, I was diagnosed with sleep apnea and have addressed that.
Basically, do you see an advantage for ablation over a successful cardioversion plus flecainide?
As indicated here I am a huge advocate of AFibbers doing everything in their power to modify lifestyle to reduce or suppress recurrent AF. I congratulate this reader on addressing the overexercise factor and the sleep apnea.
For many patients following weight loss, reduction of alcohol, modifying exercise and addressing sleep apnea SR can be maintained without drugs or ablation.
My approach to patients who are successfully maintaining SR on low doses of flecainide without side effects (which is the norm for flecainide) is to continue the drug unless the patient wants to stop it. If so, we warn them that stopping flecainide does increase chances of AF recurrence but that if AF recurs we can easily deal with it.
If AF recurs off flecainide quickly I typically advise resumption of flecainide over ablation but always mention the patient has this option.
If AF recurs late (>6 months or so) off flecainide, a repeat CV without flecainide is reasonable with close attention to lifestyle factors that may have contributed to recurrence.
Long Term Implications of Holiday Heart: Alcohol and AF
My usually extremely healthy husband who has been battling a nagging cough, had a brief episode of A fib on Wednesday morning after having 7 beers, cough syrup w/ codeine, and inadequate water the night before. ER doctor stated that heart was strong, echo revealed no regurgitation by any valves, no bloodwork evidence of heart attack. He had no shortness of breath, pain, nausea, etc. He has exercised strenuously all of his life (nationally ranked swimmer age 12-25, now weight training + cardio 3-4x/week). His slight HTN is well-controlled by rxs. He has no lipid profile concerns. Question to you: Any chance that this episode was a one-time thing assuming he is mindful of alcohol’s/dehydration’s role in arrhythmia issues? We were in the midst of trying to secure lower cost health insurance when this occurred. Now he will be saddled with “pre-existing” A-fib which will kick him out of all but ACA, which is not affordable for us. And more importantly, we hate the thought of life-long meds which may not be necessary and possibly harmful. It seems that you are the only one who has a fresh perspective on these issues. Thanks so much!!
This AF episode was clearly triggered by alcohol and testing as described indicates no structural heart disease. It could be a one time thing but in general when AF occurs under a particular trigger it tends to recur at some point down the line even without the specific trigger.
For patients with structurally normal hearts and one episode of AF clearly triggered by excess alcohol (so-called holiday heart) my approach is to emphasize lifestyle modification. I don’t start antiarrhythmic drugs for first episode and definitely wouldn’t look at ablation. I would have long discussion with patient on stroke risk and I would recommend they obtain a Kardia ECG monitor or an Apple Watch to monitor their rhythm.
It’s also possible this is another case of overexercise and exercise modification may be in order.
and here is the excerpt from my updated AF page:
Posts About Treatment Of Atrial Fibrillation
How Obesity Causes Atrial Fibrillation in Fat Sheep and how Losing Weight can reduce the recurrence of atrial fibrillation.
Eight Lifestyle Changes to Prevent Atrial Fibrillation
Drug Therapy: Rate Control and Anticoagulation
Foxglove Equipoise. When William Withering began treating patients suffering from dropsy in 1775 with various preparations of the foxglove plant he wasn’t sure if he would help or hurt them. After 240 years of treatment, we are still unsure if the drug obtained from foxglove is useful.
Should Digoxin Still Be Used in Atrial Fibrillation? Recent studies suggest that we should not.
Why Does the TV Tell Me Xarelto Is A BAD Drug? Anticoagulant drugs that prevent the bad clots that cause stroke also increase bleeding risk. A bleeding complication is not a valid reason to sue the manufacturer. The lawsuit are strictly a money-making tactic for sleazy lawyers.
Drug Therapy: Antiarrhythmic Drugs for Maintenance of Sinus Rhythm
If lifestyle changes alone can’t control atrial fibrillation, I am an advocate of enlightened use of medications (antiarrhythmic medications or AADs) that can safely restore and maintain the normal sinus rhythm long term.
The most recent study supporting drug therapy for suppressing atrial fibrillation, EAST-NET AF
My three-part series on “enlightened medical management of AF”:
Part I: Amiodarone. Kardia and Cardioversions
Part II: The Pill in Pocket Approach
Part III: Flecainide for Chronic AF Suppression
Cardioversion and Ablation
We can shock (cardiovert) the heart back to normal rhythm with little risk and very high success rate when performed by experienced and enlightened cardiologists. Keeping the rhythm normal after successful cardioversion is a bigger challenge (see above) and when medications and lifestyle changes fail an invasive procedure (ablation) is an option for some patients. Ablation should not be considered a cure for AF as recurrence is common and successfull ablation has not been shown to lower stroke risk thus anticoagulants are still recommended lifelong after the procedure.
Cardioversion: How Many Times Can You Shock The Heart?
Ablation: Cautionary Words From Dr. John Mandrola and The Wisdom of a Team Approach
Catheter Ablation of Atrial Fibrillation: Will it Reduce Your Risk of Death, Serious Bleeding or Stroke?
Ablation For Atrial Fibrillation: One Patient’s Experience
What Happens If You Go Into Atrial Fibrillation On A Cruise?
Apple watch versus Kardia to monitor atrial fibrillation from home: A case study
30 thoughts on “Atrial Fibrillation Page Updated: New Questions on Exercise, Ablation, and Medications Answered”
AFib and Covid. I believe I had Covid shortly before I had AFib. though no diagnosis was made until nearly a year later.
From this article it can be seen that AFib is the second most likely cardiology issue as linked to Covid.
This article does afib risk is substantially increased post COVID. Much more common in those hospitalized than not.
Would stents after MI with EF > 50% and stressed test passed contraindicate use of Flecainide and use of Tikosyn instead? Currently on metoprolol. AF burden has increase from .3 to 1.2 this year.
I meant to mention above but forgot, bowel preps severely deplete the body of fluids and electrolytes. That in itself can sometimes trigger arrhythmias. That is one reason gastroenterologists typically recommend an abundance of both fluid and electrolyte replacement when prepping. (Gatorade and the like). Perhaps that was his trigger. It’s happened to me. My cardiologist said the majority of his arrhythmia patients have some level of dehydration that only exacerbates their problems..
yes I guessed that the fluid and electrolyte situation probably was the trigger, even though he was very compliant with the Gatorade etc it can only do so much. But of course afib once triggered doesn’t revert right away when the trigger resolves, and he wound up in it for 3 days and (thank God) spontaneously converted yesterday. I don’t know what that means for the long run of staying out of afib — his cardiologist is assuming it meant that the flecainide isn’t working because it didn’t overcome the trigger event
My personal experience age 49 : had to be cardio verted as digitoxin made LAF worse- small amounts of alcohol triggered LAF ( 2-3 days later), research shows alcohol depletes magnesium levels in the body, magnesium is most dense in the heart.. I simply cut alcohol and ate pumpkin seeds for magnesium. Age 62 zero Heart issues.
We have been going through the afib odyssey for a while now; my husband is currently post-ablation and on daily flecainide and had a recurrance of afib/aflutter during bowel prep for a colonoscopy/endoscopy for anemia at the two month post ablation mark. His cardiologist decided that the ablation/flecainide is not holding him and wants to proceed to Tikosyn with an implanted pacemaker as backup for possible bradycardia. He also found out during the procedure that he has GAVE in his stomach, and the cardiologist also thinks he should have the Watchman implanted so that he can get off of Xarelto (which he’s off of at the moment anyway till the gastric bleeding/anemia is sorted out). The pacemaker (and Watchman) is a huge step medically for us; do you have any experience with Tikosyn?
You may want to consider proceeding with caution in regards to the Watchman device. It’s not a panacea to prevent clots forming in the left atrial appendage. Clots have been shown to develop on the Watchman device itself. Here’s the abstract to the evidence that supports that. You may want to print this out and have your husband’s cardiologist comment on it. https://pubmed.ncbi.nlm.nih.gov/29622159/
There are some first-line treatments for GAVE (Gastric Antral Vascular Ectasia) to consider which may potentially allow him to stay on anti-coagulation therapy. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547119/
I guess it comes down to a Risk vs. Reward type judgement. Just my two cents worth.
John is correct as I’ve had lots of patients go into afib with colonoscopy prep which lowers potassium levels. I don’t necessarily see that as a failure of the flecainide. I am also very cautious about recommending the Watchman.
I have never recommended a pacemaker for “possible bradycardia” related to initiating tikosyn.
Tikosyn should be initiated on a monitor in the hospital for 72 hours to monitor QT and rhythm and if there is significant bradycardia that is causing symptoms then I would consider a pacemaker.
Studies show tikosyn is about as effective as flecainide at preventing atrial fibrillation recurrence.
Please correct me if I am wrong, but as I understand it, an enlarged left atrium could be considered both a cause and a result of AFIB. I have paroxysmal AFIB and a severely enlarged left atrium (48 ml/m2 left atrial volume index), likely due to both the years of AFIB and many decades of high intensity aerobic running and cycling.
I have read Dr. Mandrola’s book and have been “detraining” for 2 months now by cutting back on both intensity and duration. Is there reliable evidence that several months of detraining can result in reversal of atrial enlargement as point #6 suggests in this article in JACC?
https://www.acc.org/latest-in-cardiology/articles/2018/11/06/05/58/atrial-enlargement-in-the-athletes-heart. My local cardiologist is excellent but he admittedly is not up to speed on detraining and the potential for reversal f atrial e large the.
My echo is otherwise unremarkable. Of course, I manage my other risks factors extremely close (BP, blood sugar, BMI, sleep quality, nutrition, lipids, thyroid, etc.). I also take daily metropolol and flecainide (pill-in-the-pocket).
Thanks for the great blog and post, along with any details on detraining.
You are correct. An enlarged left atrium is both a risk factor for afib and a consequence of prolonged duration of afib.
You asked: Is there reliable evidence that several months of detraining can result in reversal of atrial enlargement as point #6 suggests in this article in JACC?
To answer that fully I would have to pull up the entire JASE article you reference and look at any original research in detail.
If time allows I will do that and write a post on the topic. Until then, I can tell you that i generally agree with the statement that within 3-4 months of training cessation, all cardiac chambers in the athlete typically revert back to normal size..
I would also say that I have always felt that changes in chamber size in most athletes reflects a physiologic adaptation to CV training and slower heart rates. In other words, the changes are not pathologic and are easily reversed.
You seem to be suggesting that there is an overlap between athletic enlargement of the atria and pathological enlargement that leads to arrhythmia –– AF. Neither John’s link above nor the original article it refers to make that sort of connection, that I can see. The problem they examine is the difficulty in differentiating between the two.
DOES a strictly athletically enhanced left atrial volume make it prone to arrhythmia?
I gotta wonder if I might have avoided my first ablation for AF by simply becoming a couch potato for four months or so.
I wonder this not only to tease my 20/20 hindsight, but to inform my children. My father, my sister and I have had AF.
Will you be looking into the current knowledge of genetic causes?
It is not clear if a left atrium enlarged due to athletic training makes the heart prone to arrhythmia/atrial fibrillation. The left atrial enlargement may just be a marker of training and not be causally related to atrial fibrillation.
You are correct that the article John referenced doesn’t weigh in on this issue and in general that article is fairly useless.
Here’s a better one written by Mark Estes ….https://www.sciencedirect.com/science/article/pii/S2405500X17305261 which notes
” Although echocardiographic studies showed that left atrial dilatation occurs in up to 20% of athletes, this finding was not associated with an increase in AF prevalence in younger athletes 46, 47. In contrast, physical activity, height, and left atrial size were noted to be independent risk factors for lone AF in middle-aged healthy individuals (24″
A point which most non-echocardiographers probably don’t appreciate is that left atrial volume index is a very operator-dependent measurement. I see serial echos on patients where the LAVI goes from severely enlarged to normal and vice versa without any qualitative change in its size or any clinically meaningful change that would have caused the change in LA size. Unless you are in a research study where a core laboratory is insuring consistent measurement standards , atrial size may be inaccurate and any changes noted from one study to another may be due to different operators/measurements/recording views.
Uh . . . genetic causes? In the future, yeah??
Definitely a genetic component for some.
I have several patients who have a twin with almost an identical afib history.
I will be very interested when you write your thoughts on beta-blockers and exercise performance. Near and dear to me…
Still working, learning and researching on this topic but this 2007 paper found that beta-blockers despite lowering peak heart rate don’t impair the benefits of exercise.
“Mean training heart rate was significantly lower in the patients on beta-blockers (97.2±7.7 vs 118.3±7.5/min, P<0.001). Lactate-based aerobic endurance training evokes comparable cardiovascular benefits in the presence and absence of beta-blockade including a marked improvement of endothelial function. In the present study, target training heart rate with beta-blockers is about 18% lower than without.”
Remind me what other questions you had in this area?
I’m 73. I had a successful cardioversion about four months ago. I have been on 50 mg Flecainide and 5 mg Eliquis ever since. Eleven days ago I went off of the Flecainide. I monitor for Afib twice per day with my Kardia. Is it safe to go off of the Eliquis as long as my Kardia shows that I am not in Afib? I still bicycle extensively (though not as far or as intensely as prior to Afib), so I am thinking I should balance the risk posed by Eliquis in the event of a serious bicycle accident vs the ongoing risk of a blood clot. My current CHAD score is 1.
For AF patients in the subset with no known heart disease (old term “lone” AF), is their a survival difference between rate and rhythm control?
I am a 72-year-old family physician. I began having intermittent atrial fib over 30 years ago and I underwent cardio version twice. I then went several decades in NSR. About 7 years ago I had atrial flutter and underwent a successful ablation. A year later I started having intermittent atrial fib again. I tried all the usual meds but they didn’t prevent the episodes. I finally underwent a 5 hour ablation procedure by Dr. Silver of Lahey in Boston. Since then I have remained in NSR. I have chosen to only take ASA 81 mg daily rather than a stronger anticoagulant. So far, so good.
Thanks for sharing your afib/flutter journey. It is similar to many others I’ve witnessed and illustrates how variable the presentation and long term course can be.
Recurrence of afib after ablation for flutter is very common in my experience. Recurrence of afib after afib ablation, unfortunately, is also common but I hope you don’t experience that.
If you do go back into afib, as I’m sure you know, you will be at risk of stroke and aspirin will have little effect on reducing that risk.
Hopefully you can monitor for recurrence closely with devices like Apple Watch or kardia and have a NOAC ready to take upon noting recurrent AF. Although in the past you may have known immediately when you went out of rhythm, sometimes the ablation procedure and/or meds changes the feel and/or rate of your afib making it less noticeable.
What defines moderate exercise? How is “extreme” exercise different?
I have a history of four ablations for AF, flutter and two different atrial tachycardias respectively. I’m now maintaining normal sinus quite well on flecainide . . . and very little exercise. Fear of more tachycardias due to exercise (Or, read “hard work” here.) has me out of shape.
So, the fairly strenuous exercise I used to do to keep toned for the hard work I do seems to have caused past arrhythmias.
However, if I do any of that hard work now that I’m out of shape – the scary PACs and PVCs come back.
Can you talk about exercise specifics? Heart rate monitoring?
Interval training seems to be the hot idea now. A bad idea for us arrhythmiacs?
No opinions on interval training??
sadly, altho cardioversion is easy and effective, it is not always easily available. My husband has pretty much always(in 4 years) had to wait a week (even when presenting to the ER) because “afib is not life threatening ” and because cardiologists will schedule cardioversion on an outpatient basis — multiple days out if you’re really lucky, over a week if you’re not — don’t go into afib on the weekend! Now, that is 100 times worse with every hospital filled with covid. He self-converted back when it started; eventually had to have ECV with recurrent episodes because although he used flecainide as pill in a pocket, it only worked once and then not at all. After that, even though they put him on ascending doses of flec and beta blockers as a daily med, he went into afib sooner and sooner (9 months apart then 6 mo then 2…). He was finally convinced to go for ablation because they told him other drugs were unlikely to work and the flecainide was clearly no longer suppressing afib (he is extremely symptomatic with afib) and now we are working our way through the ablation recovery time and hoping afib does not recur. They left him on a beta blocker + flecainide afterwards until realizing that his heart was just too slow (kept sinking to the 40’s) so dropped the beta blocker and then had to cut back on the flec as well in order to get a livable heart rate. He hopes that after ablation there will be some opportunities for exercise without triggering afib; the past couple years he’s been pretty much unable between the side effects of the meds and the recurrence of afib. We’re hoping to get something closer to the semi-active life style we had before afib entered the picture. Since he doesn’t drink or smoke, controls hypertension and sleep apnea since before afib, the only life style alteration he has left is the exercise piece. The doc told him that ablation is “no cure” but it could put him “back up the descending slope” long enough to let him get back into exercise, at least for a while.
Thank you for this most enlightening article. I now fully appreciate the need to not overdo exercise. Pushed too hard in my early 70s resulting in Afib. Cardio version twice and appropriate medication along with less intensity has worked so far into my mid seventies.
Several years ago, with my cardiologist’s ok, I went on the pill-in-a-pocket approach. All was fine until I visited my son’s family at Christmas, traveling by train. The morning after I returned, I had an appointment with movers to consolidate 2 units. They had just finished loading their truck from the first unit when I suddenly felt very lightheaded and nauseous. I used my Apple watch and Kardia band to verify I was in AF. Unfortunately, I was too lightheaded to drive, the young movers had no clue, so I had to let them call 911. This resulted in an ambulance drive to a Kaiser hospital (after the EMTs decided my life wasn’t in danger) over 20 miles away. Big bill! It turned out I was in the every early stages of flu I picked up on the train – also experienced lack of sleep. The ER doc was about to arrange a cardioversion when I said, “Wait! My cardiologist told me a 200mg dose of flecainide would probably work.” She checked with cardiology, and gave me the med instead. An hour or so later, I was discharged. So… my suggestion is for those opting for pill-in-a-pocket, be sure you have your pills with you at all times (I didn’t), and rethink before taking a trip away from home, especially if you might be in an area with poor medical facilities or if you are staying with family or friends who might be very inconvenienced hauling you to a hospital. One other thing: I seem to run into trouble only on weekends or late at night when whoever is on duty (advice nurse, MDs nurse consults, etc.) is too busy to scour my medical record thoroughly. This has, inevitably resulted in my being sent to ER – something of a nuisance as well as an expense and usually unnecessary as matters have turned out.
I was hopeful that you might respond to my earlier question about 2xd 5mg Eliquis for paroxysmal afib rather than taking anticoagulant ONLY when I go into Afib along with the 30mg Diltiazem (not ER). I am 81 with CAD (thoroughly stented) and have had only 2 episodes of afib in the past 16 months and converted each time with the 30mg DILT. I regularly take 240mg DILT ER and 50mg metoprolol. The occurrences of afib have been dramatically reduced on this med management routine.
What you are describing is what I term “pill in the pocket” anticoagulation. It’s an approach I have employed with select patients and was hoping to write about in detail soon.
When we have employed this approach it is very important that the patient has the capability of self-monitoring with either Kardia or Apple Watch. Electrophysiologists like to insert implantable loop recorders for this purpose, something else I’ll be discussing.