Enlightened Medical Management of Atrial Fibrillation, Part III: Flecainide for Chronic Suppression

As a practitioner of enlightened medical management of atrial fibrillation the skeptical cardiologist utilizes predominantly two antiarrhythmic drugs: amiodarone and flecainide.

As I outlined in Part I of this series, amiodarone is our most efficacious drug for maintenance of normal sinus rhythm (NSR) but requires close monitoring for long term side effects. It is also the safest antiarrhythmic drug (AAD) for patients with AF who have structural heart  disease.

The AAD I use in AF patients with normal hearts is flecainide.

Flecainide is a class IC AAD  which produces a potent and selective blockade of the cardiac fast inward sodium (Na+) current resulting in conduction slowing.

We don’t utilize flecainide (or any Type IC AAD) in patients with significant coronary artery disease or significantly depressed function of the left ventricle because of concerns about it increasing risk of more dangerous heart rhythms in such patients.

In patients with normal hearts, however, flecainide is very safe, extremely well-tolerated, and reasonably effective at maintaining NSR when combined with significant lifestyle modification.

I have scores of patients who have been maintained in NSR for years to decades with flecainide, therefore I think patients with normal hearts should undergo an adequate trial of this AAD before moving on to ablation.

Chronic Suppression of Atrial Fibrillation

A reader with atrial fibrillation recently submitted his case history which describes a typical scenario for a patient who would be a great candidate for long term flecainide therapy:

I am a 62 year old active male. I play (mostly) non-checking ice hockey 3 times a week and bicycle on off days and have a daily yoga practice. I suffer from Hashimoto’s disease and hypertension. Both are adequately managed with medication. I have been in persistent Afib for about a year, not sure about prior to that, but expect it was paroxysmal for awhile prior to diagnosis. There is no obvious cause. I was immediately put on Diltiazem and Eliquis. A month later I received a successful Cardioversion but at my follow-up a week later it was noted that the Afib had returned and is again persistent. I also had an echocardiogram that did not reveal any valve or muscle abnormalities. The advice at the time was to continue on the Dilt unless symptoms worsened. I was taken off the Eliquis due a risk factor of 1 and my desire to resume hockey. After about three months I noticed more fatigue, occasional dizziness, regular palpitations, etc. so got an appointment for another echo and to see an Electrophysiologist. The results of the echo indicate some structural changes since the last echo. Thus the EP recommended 3 choices: 1. continue with just the Dilt, 2. get a stress test and if OK then go back on Eliquis and add Flecainide for rhythm control and get another Cardioversion, or 3. get back on Eliquis and get an ablation and a Cardioversion. I’m not sure which option to choose. The difference in the two echos didn’t seem too extreme – how long can I go with option 1? Option 2 seems less risky but also less effective. Option 3 has the best results but is more risky. What will be the future of my hockey playing? With options 2 and 3 I;ll take a break while on Eliquis but once I turn 65 my risk will be 2 and I’ll probably be on Eliquis from then on. Can I chance option 1 for 3 years? I check my BP daily and use a KardiaMobile 6L to self-monitor.

The reader’s case history is similar to many of my patients.

He started with brief paroxysms of AF that were self-limiting (paroxysmal AF) but at some point, an episode began that was not self-limiting (persistent AF.)

At this point there are two major decisions for patient and physician: 1) Should a blood thinner be started to reduce the risk of stroke? and 2) Should the patient be left in AF (which generally means AF will be present lifelong , thus permanent- aka longstanding persistent AF) or should we attempt to restore and maintain SR?

I’ve reviewed the decision-making process for anticoagulation here.

The second decision is more complicated, controversial, and requires a good and unbiased conversation between physician and patient about options for maintenance of NSR.

In my post entitled “Why I Favor the Early Restoration and Maintenance of Sinus rhythm For Most Patients with Atrial Fibrillation” I laid out my rationale for trying to restore and maintain SR for most patients. In this 62 year old otherwise very healthy and active individual I would strongly favor a very aggressive approach to maintaining SR.

Enlightened Use of Flecainide To Suppress Atrial Fibrillation


Let’s take the example of Ralph,  a 63-year-old man who I saw first 5 years ago.  At that time he was admitted to the hospital with a prolonged episodes of weakness and rapid heartbeat.  Atrial fibrillation with a high heart rate (rapid ventricular response) was the cause and after starting a blood thinner and slowing his heart rate with intravenous diltiazem we proceeded to electrical cardioversion (ECV).

The cardioversion was successful in converting him back to normal sinus rhythm and he was discharged on oral diltiazem and a blood thinner.

Diltiazem is not an anti-arrhythmic drug and has not been proven to lower the risk of recurrent atrial fibrillation but is used in this situation to slow the patient’s heart rate should atrial fibrillation recur. I tell patients that after a first ECV without adding an AAD it is highly likely that AF will recur but we can’t predict if that will be in 5 days or 5 years. Given this possibility of no recurrent AF for years I generally don’t start an AAD with first ECV.

I highly recommend to all my AF patients the acquisition and use of a mobile Kardia ECG device to monitor their heart rhythm. The Kardia (or Apple Watch if the patient has one) is particularly useful pre and post ECV to alert us to the development of AF.

Ralph noted his heart rate had increased about 7 days after the ECV and his newly acquired Kardia ECG device confirmed AF as the cause.

At this point, we had another patient-physician discussion about the value of maintaining NSR and the therapeutic options. Given the early recurrence of the AF,  just repeating the ECV makes little sense. If he had maintained NSR for 5 years just repeating the ECV would be a reasonable option.

To increase our chances of maintaining NSR I started flecainide 50 mg twice daily. Flecainide can be started as an outpatient (as opposed to sotalol or dofetilide which require 72 hours of monitoring in hospital) and it often converts the patient’s rhythm back to NSR without the need for an ECV.  In addition, flecainide as a generic is cheap and at low dosages extremely well-tolerated without significant side effects.

The starting dosage of 50 mg is low but one of my guiding principles for Enlightened Medical Management of AF (EMMOAF) is to use the lowest effective dosage of AAD possible in order to minimize adverse effects.

After 5 days on flecainide, an ECG showed normal  QRS and QT intervals but AF persisted and we performed another ECV. After this ECV, the patient remained in NSR for 2 weeks but again noted high heart rates and AF had recurred.  Following another discussion I had him increase the flecainide to 100 mg twice daily.

Some patients, again, will convert to NSR upon an increase of the flecainide from 50 to 100 mg twice daily, but Ralph remained in AF and we performed a third ECV.

By this time he had acquired a Kardia device and was able to monitor his rhythm. The higher dosage of flecainide was the dosage that worked for him as he maintained NSR after the ECV and has maintained NSR for 5 years since.

I have scores of patients who have a similar path to Ralphs’s with successful maintenance of NSR on flecainide for many years. Some of them converted without an ECV and some, like Ralph, required 3 ECVs.

If AF recurs after a prolonged period of maintenance of NSR with flecainide, the choices are

  • -Leave in AF and control the rate
  • -Leave flecainide at current dosage and repeat ECV
  • -Increase the dosage of flecainide (which may or may not convert rhythm on its own) and repeat ECV at higher dosage.

Enlightened management of these patients who are maintaining NSR on flecainide over many years requires periodic visits (I recommend every 6 months) with an enlightened cardiologist to assess for

  •  any signs or symptoms of structural heart disease
  •  any evidence of proarrhythmia or electrical conduction abnormalities
  •  significant QRS prolongation, ischemia or arrhythmias during exercise stress
  • proper concomitant use of dromotropic (rate-slowing) drugs such as beta-blockers or diltiazem.
  • appropriate use of blood thinners to reduce the risk of stroke or systemic embolism.

When utilized in the manner I’ve described, flecainide usage results in prolonged maintenance of NSR at an extremely low risk of adverse effects in most patients who have structurally normal hearts.

Its effectiveness is greatly increased by patient attention to the eight lifestyle factors that increase the risk of AF and I emphasize these factors to all my patients on a regular basis.

Flecainidingly Yours,

-ACP

N.B. I’ve answered my readers question as to which option I would recommend if he were my patient but not some of his other good questions. Those will be discussed in Part IV of this series. And later I’ll discuss the pros and cons of other AADs for AF.

N.B.2.  For more detailed information on flecainide I recommend this 2015 review in the World Journal of Cardiology

If you are prescribing or taking flecainide it is important to be aware of the CAST trial

(Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324:781–788. [PubMed] [])

 

a seminal study which showed that Type I C AADs are dangerous in patients who have had a myocardial infarction and reduced heart function.

“The publication of the Cardiac Arrhythmia Suppression Trial (CAST) study in 1989, which was designed to investigate the efficacy of class I antiarrhythmic agents moricizine, encainide or flecainide in patients after myocardial infarction with reduced ejection fraction and frequent ventricular ectopic beats, resulted in a major revision of the role of these antiarrhythmic drugs. Thus, while flecainide suppressed ventricular ectopy in those patients, a threefold increase of arrhythmic death was recorded compared to placebo[]. Based on CAST results, flecainide nowadays is not recommended for patients with structural heart disease and coronary artery disease. However, it is recommended as one of the first line therapies for pharmacological conversion as well as maintenance of sinus rhythm in patients with atrial fibrillation and/or supraventricular tachycardias without structural heart disease”

 

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19 thoughts on “Enlightened Medical Management of Atrial Fibrillation, Part III: Flecainide for Chronic Suppression”

  1. Hi Dr. P, I hope your feeling better and recovering from Covid, we have seen a slight uptick on the unit of covid + pts, they get their 5 day course of IV remdesivir with some optiflow and bounce right back. Glad to see your symptoms weren’t too serious, especially with the beautiful weather the last few days, hopefully you got a chance to be outside.

    I was reading about Class IC Na blockers (I remember your thorough enjoyment of the nuances of VW classifications 🙂 specifically flecainide and wanted to revist your blog post. I read a passage about how flecainide when used as a standalone for AFib that it can have a problematic effect on ventricular rate by converting AFib to flutter and then slowing it down just enough to allow for 1:1 AV conduction,which can lead to high ventricular rates. I just noticed how you included for effective mgmt of Afib that in conjunction with flecainide a negative dromotropic agent like a dilt or BB must be included. Is this the reason why dilt or BBs are used with flecainide or are there other reasons?

    IIRC diltiazem also has negative inotropic properties along with all BBs, which could be problematic for HF pts w/ afib in the perfusion department, with those pts I assume flecainide is off the table, but is amiodarone still a possibility, since it doesn’t have much of a negative inotropic effect?

    Reply
    • Christian,
      Thank you. Gradually returning to normal but still fatigued and short breath.
      You are correct. The only reason for adding dromotropic agents is what you described.
      and flecainide not indicated for heart failure patients,
      Amiodarone is great for heart failure patients as it is very effective and doesn’t worsen heart failure or lower bp significantly. it also slows the rate should a breakthrough afib episode occur
      dr p

      Reply
  2. A half year ago I experienced atrial fibrillation (at 57), with a heartrate 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 cardiologis. 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

    Reply
    • Joop,
      I can’t provide individual medical advice but as time permits I will include this in an updated post on medical management of atrial fibrillation with my thoughts.
      Dr. P

      Reply
    • Three months back I (72 yr old male, Chad score 1) began having a high rate of ectopics (8-10,000 a day) most of which were PVCs confirmed by a Zio patch. This increase was a vast worsening of my more normal 0-1000 PVCs a day. Two weeks into the new pattern I had my first afib episode of three minutes duration. This paroxysmal pattern continued, expanding twice to an hour’s duration over the next two months. Finally I saw a cardiologist and we agreed on a trial of Flecainide. Like a miracle it shut down the ectopics to absolute zero. Or I can’t feel them or catch a single one on my Kardia ‘Kard’ (Haha, Dr P.)

      General question concerning those of us who are flecainide success stories and are otherwise healthy: might it perhaps be more ‘enlightened’ to conscientiously monitor ecg and in the absence of ANY ectopic activity repeat the Zio patch with an eye to stopping the blood thinner. My cardiologist isn’t a fan. Perhaps I need to find a new doc. But wondering what your general thoughts are.

      Love the blog. I sincerely hope you keep at it. Hugely informative. Thanks.

      Reply
      • Peter,
        Flecainide is definitely a great PVC killer. I’m presuming that it was utilized in you because you have a structurally normal heart (normal echo and no evidence for CAD)
        If you were my patient I would definitely be open to the approach you have described for your afib.
        I have been meaning to write about pill in the pocket approach to anticoagulation. With your permission, I may anonymously use your comment as a launching pad.
        dr. p

        Reply
        • Yes, structurally normal heart, no evidence of CAD. Feel free to use post, and of course edit for clarity, brevity. Thanks for the speedy response, Dr Pearson.

          Reply
  3. I have been on the other Na channel blocker (propafenone sr) for 6 years, non-stop and have not had any AF during that time. I started Rx immediately with the first episode. I also take Bystolic and a few other poisons for HTN. Any thoughts on Propafenone as the Na channel blocker of choice?
    Thanks

    Reply
  4. I really enjoy these kinds of posts. I don’t have AF, but the clinical insights and walk through of clinical decision making our fascinating. It has also given me more information to do more research on, so much to learn!

    Reply
    • Unfortunately not as I just manufactured that term rather than delve deeply into my quite unscientific justification. Apple Watch tells me my Max VO2 (something i promise to write about soon) is 51 various reliable sources tell us is good for individuals much lower than me

      “The average sedentary (inactive) male achieves a VO2 max of about 35 to 40 mL/kg/min, and the average sedentary female scores approximately 27 to 30 mL/kg/min.
      Elite male runners have shown VO2 maxes of up to 85 mL/kg/min, and elite female runners have scored up to 77 mL/kg/min.
      A good VO2 max for a 25-year-old male is 42.5-46.4 mL/kg/min, while a good value for a 25-year-old female is 33.0-36.9 mL/kg/min.”

      Is the Apple Watch Max Vo2 accurate. Probably not.
      Does VO2 predict risk of COVID-19? Hard to say.
      What we need is a biological immunologic age calculator and I haven’t come across one of those.

      Reply
  5. Flecainide is now my go-to med. I’ve been on the smallest dose for about six months following my somewhat successful fourth ablation. That ablation stopped the sustained almost-200 BPM atrial tachycardia I was experiencing. Good. But. I was then still experiencing many PACs and short runs of atrial tachy. On flecainide I’m in perfectly normal sinus rhythm.

    Two things:
    My doc put me on verapamil as well, saying they would work together.
    What’s the rationale with that – slowing heart rate as with dilt?
    Rhythm if fine, but, whew, the old energy and stamina ain’t what they used to be. ‘Course that’s to be expected with hypertension meds in general, but I’m wondering if that combo is particularly enervating.
    Just theoretically, naturally. 🙂

    Reply
    • Verapamil is a rate-slowing calcium-channel blocker like diltiazem. I tend to use diltiazem preferentialy over verapamil. Mostly because I see less side effects with dilt. Verapamil also has more negative inotropic properties so preferred in patients with hypertrophic cardiomyopathy.
      The combo raises chances of low energy Side effect.
      Options are try lower dosage verapamil, try diltiazem, switch to beta-blocker. If side effects on standard beta-blocker try nebivolol.

      Reply
  6. ACP did a fine job in his discussion. An high Mg++ (90% organic unprocessed whole foods vegan wi optional wild caught fish 3 X a week) diet would be a freebie that increases retention of sinus rhythm & reduces needs for meds altogether. Plus a trial of the supplement hawthorn is safe and somewhat effective. Personally, I prefer starting wi a beta blocker but exactly as ACP recommends, begin wi quite low dose as that might be effective, The non-generic Bystolic-nebivolol because of its lowest incidence of side effects is my drug of choice. HRS, MD, FACC

    Reply
    • Anecdotal evidence:
      You just described in detail my diet of the last decade, prior to my 1st ablation. A very good diet –– tor so it seems at this point. Don’t forget, it was gotten wrong from the 50s till recent years.
      The good diet still did my afib, flutter, and atrial tachycardia no good. You gotta look at the particular body being fed, as well.

      Reply
    • That’s great!. But in my experience the vast majority of AFIB ablation patients redevelop afib down the line. Flecainide is a very useful drug for those folks as well.
      Hopefully, the damage done to the atrium by the ablation doesn’t result in more pesky atrial arrhythmias (like atrial tachycardia) which might be more difficult to control.

      Reply

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