Why I Favor The Early Restoration and Maintenance of Sinus Rhythm In Most Patients With Atrial Fibrillation

When your heart stops beating synchronously and goes into atrial fibrillation all sorts of bad things begin happening. The normal mechanisms for controlling how fast your heart is beating are lost and in most individuals the rate accelerates inappropriately. The strength of the atria’s pumping force and the normal precise synchronization of the upper and lower chambers  deteriorates.
You might logically conclude then, that all efforts should be focused on converting the rhythm back to normal,  for in the normal rhythm the heart can go back to beating regularly, efficiently  and synchronously the way nature intended.
Maintenance of this normal (sinus) rhythm (NSR), presumably, will eliminate the high risk of clot formation and stroke associated with atrial fibrillation (AF) , prevent heart failure, and prolong life.
AF is abnormal. the thinking goes, and normality is the state in which we were born and to which we should seek to return.

Is Normal Sinus Rhythm Superior to Atrial Fibrillation?

It would be hard to find a cardiologist who doesn’t believe that patients are better off in NSR than AF but the more difficult question and more clinically relevant question is “if your heart has gone into atrial fibrillation will you do better in the long run with a strategy of trying to convert the rhythm back to normal and keep it there (which involves medications (anti-arrhythmic drugs) and/or procedures) versus just controlling the heart rate and letting the atria fibrillate to their heart’s content.
Unfortunately, studies that have compared the  strategy of maintaining NSR (rhythm control) with leaving the heart to fibrillate have not shown a benefit in preventing stroke or death in the patients randomized to rhythm control
To quote the 2016 European Society of Cardiology  guidelines on AF

Although many clinicians believe that maintaining sinus rhythm can improve outcomes in AF patients, all trials that have compared rhythm control and rate control to rate control alone (with appropriate anticoagulation) have resulted in neutral outcomes.

(see references for this below)
However, findings from these studies can only be applied to the population studied, thus younger patients without structural heart disease and patients over age 80, who combined constitute up to 50% of the AF group were not represented in these comparison studies.
The elderly are more dependent on normal atrial function for maintenance of cardiac output and are more likely to have issues with anticoagulation, thus they may benefit more from maintenance of NSR than the young.
In addition, much of the morbidity and mortality in these trials was related to failure to anticoagulate patients who were in NSR. The stroke risk persists in this group, we have learned, because they may not recognize when AF occurs. Therefore, most authorities recommend lifelong  anticoagulation for those who have had  AF and have significant risk factors for stroke whether or not they have documented episodes of AF.
These and other  reasons for the  failure of the so-called rhythm strategy have long been debated but most experts blame it on the absence of a safe and effective method for maintaining NSR: the drugs  and procedures (catheter ablations) we have used create their own problems and don’t always work.

Why Then, Do I And Most Cardiologists Recommend Efforts To Maintain Normal Sinus Rhythm?

This is a question almost no AF patients ask. It is quite easy for a treating cardiologist to invoke the “normality” of NSR and the dangers of AF and most AF patients require no more justification. But they really should demand a compelling rationale.

For those who feel badly in AF despite treatment with medications to keep the heart rate normal cardiologists can justify the efforts because we are making patients feel better

The ESC guideline summarizes this as follows

For now, rhythm control therapy is indicated to improve symptoms in AF patients who remain symptomatic on adequate rate control therapy.

However, there are important limitations to letting symptoms guide our approach.
For one, symptoms are in the mind of the patient and cannot be measured objectively. For another, the symptoms a patient experience could be from something other than AF.
You might think that we can objectively verify that symptoms are due to atrial fibrillation if they resolve after converting the patient to sinus rhythm but symptoms can be heavily influenced by the patient’s perception that something has been done to fix them. This placebo effect is well-known from clinical trials of medications but may be even more prominent after procedures.
It is not uncommon for me to perform a cardioversion on a patient , see the patient in follow-up in AF and have them tell me how tremendous they have felt since the cardioversion.
The difficulty of objective symptom measurement is one of many factors contributing to  a tremendous variability in how cardiologists approach rhythm control  for AF.
Some cardiologists have concluded that maintaining SR is rarely worth the trouble and they add rate controlling medications and anticoagulants and see the patient back once a year. Let’s call these NSR Nihilists
On the other end of the spectrum, cardiologists who are true believers in the value of NSR run their patients through multiple anti-arrhythmic drugs, cardioversions and ablations to achieve that goal. When this is done excessively such cardiologists become NSR Overtreaters.
I put myself somewhere in between the Nihilists and the Overtreaters and consider myself a rational NSR advocate or enthusiast but one who has a very clear understanding of the dangers of over treatment and who recognizes that many patients have done well for decades in permanent AF.
Recording and observation of symptoms depends heavily  on the recorder and observer: the Nihilists are loath to find symptoms attributable to AF whereas the Overtreater may see any and all symptoms as due to AF.
Like other areas in life and medicine we have to look closely at hidden motivations and conflicts of interest to fully understand variations in behavior.
If one were to analyze the financial benefit from testing and procedures to treating cardiologists I have no doubt that the Overtreaters are getting a lot more than the Nihilists.
In an ideal world, cardiologists would not benefit more financially based on what procedures they recommend be performed on their patients but this is not the reality.

Reasons For NSR Maintenance Beyond Symptoms

 I’ve mentioned two solid reasons for aggressively trying to maintain NSR in a previous post:

A second group of patients, I think, benefits the most from maintaining sinus rhythm (rhythm control strategy): patients who develop heart failure when they go into AF.
These patients may not even know they are in AF because they don’t feel the typical symptoms initially.  After a few days or weeks or months of being in afib silently, however, they develop shortness of breath, weakness and leg  swelling – classic signs of heart failure.
When we look at the heart of such a patient by echocardiography, we often find one of two things causing the heart failure: a weakening of the heart muscle (cardiomyopathy) or significant leakage/backflow from the mitral valve (mitral regurgitation). Following cardioversion and maintenance of SR for weeks to months, the heart muscle strengthens back to normal and/or the mitral regurgitation improves dramatically and the heart failure resolves.

The 2014 ACC guidelines for management of AF admit the lack of randomized trials supporting maintenance of NSR but cite several factors that would “favor attempts at rhythm control” with which I generally agree. These are:

  • difficulty in achieving adequate rate control,
  • younger patient age,
  • tachycardia-mediated cardiomyopathy,
  • first episode of AF,
  • AF precipitated by an acute illness
  • patient preference.

If, after discussion of the options, a patient decides they prefer no attempts at maintaining NSR,  I try to make them aware that AF begets AF. The longer they stay in AF the larger and more diseased their atria become and the harder it is to stay in NSR with any techniques. In other words, this not a decision that can easily be reversed a few years from now if they start feeling poorly.
The ACC guidelines put it this way:

AF progresses from paroxysmal to persistent in many patients and subsequently results in electrical and structural remodeling that becomes irreversible with time . For this reason, acceptance of AF as permanent in a patient may render future rhythm-control therapies less effective. This may be more relevant for a younger patient who wishes to remain a candidate for future developments in rhythm-control therapies. Early intervention with a rhythm-control strategy to prevent progression of AF may be beneficial.

Many of the factors cited for leaning toward NSR maintenance are, of course, soft and vague.  One doctor’s young patient is another doctor’s old patient. The definition of adequate rate control is unclear. What qualifies as an acute illness?

My Approach to Maintenance of NSR

I favor a more aggressive approach to maintenance of NSR. I justify this because in my experience with meticulous attention to detail and with close monitoring of patients on anti-arrhythmic drugs I have observed that most patients do better in the long run with NSR Than AF.
Over thirty years of managing patients with AF and comparing those who are left to permanently be in AF versus those who maintain NSR  I see substantial differences. Let me cite two case examples to buttress my argument.
A 75-year-old man with permanent atrial fibrillation came under my care after his cardiologist retired. He had been in AF with rate well controlled and on anticoagulation since 2008. He is active without any symptoms.
He had an echocardiogram in 2008 with the new onset of AF and it showed a normal sized left and right atria and no valvular problems.
Over 10 years,  however, the size of both his atria have dramatically increased. His current echo shows severe enlargement of his left atrium (LA volume index=72 cm3/M2) and right atrium (RA area=26 cm2). He has developed significant leakage (regurgitation)  from both his mitral and tricuspid valves.
This is the norm for most patients who have been in AF for a long time.
The larger the left atrium gets over time, the more dysfunctional it becomes and the more likely clots are to form in the LA appendage. Although anticoagulation dramatically reduces the formation of LA clots, patients frequently have to come off anticoagulation for surgeries, spine injections, bleeding and other issues.
Would you rather have a left atrium that has been maintained in NSR or one that is massively enlarged and dysfunctional if you have to stop your anticoagulation?
The other exam example is of a 74 year old man whose AF was detected at the time of a colonoscopy. When I saw him he was without symptoms with normal lab and cardiac testing. We attempted one cardioversion without anti-arrhythmic drugs and within two weeks he reverted back AF. He elected not to start any anti-arrhythmic drugs and repeat the cardioversion and was doing fine when I saw him 6 months later.
However, shortly after that visit he ended up in severe heart failure with severe left ventricular  dysfunction and severe mitral regurgitation at an outside hospital. This time he agreed with a more aggressive approach to maintenance of SR and after prolonged amiodarone loading and a repeat cardioversion he has maintained SR for 6 months. The function of his left ventricle has improved to near normal (LVEF has increased to 49%) and there is no significant leakage from his mitral valve.
Whereas, most patients who feel fine in AF and elect to stay in it do well there is an unpredictable but significant number who despite adequate rate control develop cardiomyopathy and valvular regurgitation with resulting heart failure.

Medical Maintenance of SR

Yes, I’m convinced that patients can safely and effectively be maintained in SR with medical therapy and the occasional cardioversion.
I try not to fall in the camp of Overtreaters but consider myself a Rational Normal Sinus Rhythm Enthusiast and Advocate.
In my practice when atrial fibrillation reaches a point that requires addition of an anti-arrhythmic medication  I predominantly utilize two such drugs: amiodarone and flecainide.
Patients with structurally  normal hearts do well with flecainide and those with structural heart disease (heart failure, left ventricular hypertrophy, or significant coronary artery disease ) do well with amiodarone when they are monitored closely by a cardiologist with extensive experience using the drugs.
I’ll talk about each of these options  as well as cardiac ablation in detail in subsequent posts.
Antifibrillatorily Yours,
Six studies showing no difference in outcomes between rhythm and rate control strategies.


18 thoughts on “Why I Favor The Early Restoration and Maintenance of Sinus Rhythm In Most Patients With Atrial Fibrillation”

  1. Actually I did ask and he answered, though not directly and a bit evasively:
    “Michael I do not have access to exact data on this as we do not have such a database at this time. I can tell you that we are a high volume center for AF ablation and I am a high volume operator for AF ablation. I do not wish to give you an estimate since you are interested in specific numbers. Cleveland Clinic in Ohio where I worked previously keeps extensive data on their volumes and complication rates and I would imagine that we are in line with this data.”
    He sent a link to a graph of data from 2014 – 2018 and the numbers of ablation are 772, 863, 935, 960, & 1120 respectively. So they’ve increased but I don’t know how that compares nationally nor the percentage of these that were successful, needed repeats, etc.
    More googling I guess. He is on the Cardio team at Main’s largest hospital.

    • Interesting. I like that you recorded his answer in detail.
      I find it remarkable that EPs don’t have this data. I guarantee you the hospital where he works has information on significant complications.
      And it would be pretty easy for EPs to count up their annual volume. And also very easy to follow up on patients to see if they are having any AFIB.
      Clearly he has an idea of what a “high volume” operator is. Is it 50 per year, 100 per year 250 per year?
      The data link must have been for Cleveland Clinic which is not relevant to his post-training clinical practice volume.

  2. Oh, forgot to mention, my EP did a fellowship at the Cleveland Clinic which I’m told is fairly respectable and has done many ablations.

    • What would be nice information to get would be validated statistics on the success rate and complication rate of your EP’s ablations along with precise and validated number of procedures. You should ask for that and let me know the response.
      In my experience these sort of data are impossible to get.

  3. I don’t exactly recall your preference so I’ll go back and re-read your posts.
    I was told “some changes” were noted. From the report:
    1. Normal left ventricular cavity size, mild left ventricular hypertrophy, and normal global systolic function, calculated ejection fraction by 3D imaging of 56%
    2. Bi-atrial enlargement
    3. Dilated proximal ascending aorta (4.2 cm)
    4. Mild aortic insufficiency

  4. Flecainide: Failure; then success.
    Flecainide failed to control my AF in 2012, so I opted for a cryoablation. That fixed the AF, but less than a year later I got a second ablation for atrial flutter (Is flutter iatrogenic?). Then a bit more than a year saw my third ablation for atrial tachycardia. Then two Summers ago I experienced sustained atrial tachy 1:1 to ventricles of 230 BPM. Dofetilide seemed to control it at the low dose for more than a year. Then more tachy this Fall, failure of high dose dofetilide and return of the tachy the day after what seemed a good cardioversion. So, then, my fourth ablation.
    Well, was quite a bit. Not over yet.
    My electrophysiologist agreed that it was discouraging when I yet again showed arrhythmia on my EKG weeks after that fourth ablation. This time it was many PACs, quite a few PVCs, and short runs of Atrial tachycardia. Not as debilitating as sustained tachy, but serious enough for concern.
    Flecainide seems to have fixed me up nicely, in combination with verapamil. The last two months have been quite normal – no insomnia due to my heart jumping around while I’m trying to sleep.
    As my EP pointed out, a drug that failed once might well work nicely in the same patient under different circumstances.
    I’ve been on apixaban and losartan through all of this.
    All this was done with a successful high-volume EP at a high-volume hospital.
    Enlighteningly yours, 🙂

    • All this flecainide discussion is definitely moving my flecainide post to the top of the queue. I’m sure EPs don’t feel the afib ablations create flutter as the origin of the two abnormal rhythms is in totally separate locations, however…… it seems to me I’ve only seen pesky atrial tachycardias emerge after ablations. Flecainide is a good premature beat killer.

  5. 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.

    • If you have read my posts on medical management of AFIB and my posts on ablation you likely know what I favor.
      What was the structural change on the echocardiogram?
      I have been planning on post on flecainide as part of my series on “enlightened medical management of AFIB” and your case would be a perfect starting point.

  6. Very interesting topic. I am 82 years old and have been living with AF for 10 years. Until recently I have managed to stay in NSR by having a cardioversion each time i went into AF. Over the years I had about 15 cardioversions as well as two ablation procedures. However last January I went into AF twice in 6 weeks and my cardiologist advised me to give up on trying to maintain NSR and accept that I will be in permanent AF. I can live with that (hopefully) but he also prescribed a beta blocker to limit my pulse rate . The result is a fairly severe impact on my mobility. Climbing a flight of stairs is now like climbing Mt Everest…well not quite but I am not going up two at a time. After reading this article I am going to lean on my cardio to try and get me back on NSR even if it means a cardioversion every few weeks. My local hospital does them in Emerg and the trunaround time is about 3 hours.


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