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Two AF cases — and my changing view of AF

I receive many emails about AF. I don’t often answer them because it is bad practice to doctor without seeing the person. Recently, however, I received a note with more general questions. The sender suggested I could use the response as a blog post. The reason I am posting these two cases along with my response is that my views on AF are changing. I am in the process of putting these global thoughts on AF together as a more general update, but these cases are a start.

Here is the email from a reader: (a doctor).

Dear John,

What would you recommend?

My med school roommate and I are 69 years old and in good health, normal BMIs, non-smokers, social drinkers. We both exercise almost daily. He takes something for mild hypertension. I’m on no meds.

He has had 3 episodes of PAF in his life–one in 1984 and two in the last few months. They all converted spontaneously to NSR. His doctor worked him up fully including an echo. His heart is structurally sound and no clots were noted. He has been strongly advised to start taking Coumadin or Pradaxa.

I have also had 3 episodes–one at age 26 which reverted to sinus after one dose of quinidine (I am old) and two about 6 months ago a couple of days apart which disappeared in about 12 hours after a good night’s sleep. I did not see a doctor about this. I had a normal echo 10 months ago because a routine EKG done as part of a preop eval for shoulder surgery showed nonspecific changes and I didn’t have a previous EKG to compare it to.

I don’t know if you saw this ( It’s not much help.

What would you recommend if we were your patients?

Personally, I have seen so many complications with anticoagulation, especially Coumadin, that I am reluctant to take anything. I should mention that my father died of a stroke at age 76, but he was a heavy cigarette smoker all his life. He did not have A fib.

My response:

Sorry about the AF. (As an AF patient myself, I understand the frustration.)

A few things about treating AF.

First the complications:

The most important complication from AF is stroke—as it is often life-altering, or ending, the former is sometimes worse. The risk of stroke is surprisingly not related to the “amount” of AF a patient has. I often hear, from other physicians, that patients don’t have that much AF so stroke risk is low. There is evidence to support that this intuition is incorrect. Paroxysmal AF patients have as much risk as persistent AF patients.

The risk of stroke depends on the company AF keeps. We use the CHADS-VASC score, which considers the presence of CHF, HTN, AGE > 75 (2 points), Diabetes, Prior stroke/TIA (2 points), Vascular disease, Age >65  and Sex category (females  get 1 point).

Thus, your CHADS-VASC score is 1 and this confers a 1.3% annual stroke risk with no warfarin or other anticoagulants. The stroke risk on warfarin is not much lower — 0.5-6%, but the average risk of bleeding is in the range of 3%. Most guidelines, therefore, do not recommend anticoagulation. That’s a patient level decision though because there is a very small absolute risk reduction in stroke with anticoagulants. An important note is that there is no benefit from aspirin. And my view of the new anticoagulant drugs is that they are 99.3% similar in efficacy and safety but more than 100 times the cost.

Your friend’s risk score is higher because of hypertension. He gets a CHADSVASC of 2, which increases his annual stroke risk to 2.3-2.9% without drug and then 1% on warfarin. (Same 3% risk of bleeding.) His risk reduction is double yours, in the range of 1.5%—or a NNT of about 66. (A note on bleeding risk is that it’s not zero without warfarin; it’s about 1% in the general population but varies on other factors. Patients bleed without taking anticoagulants.)

Recall that almost all patients with bleeding leave the hospital the same person they came in as. That’s not often the case with strokes. ICH (intracranial hemorrhage) is the exception; thankfully, it is uncommon. A quick sidebar on ICH: the last two patients I saw with ICH probably had hemorrhagic transformation of ischemic stroke rather than a primary brain bleed. Meaning, if they had not had a stroke in the first place, they would not have bled into the brain.

Those are the odds that I quote. The risk of stroke and bleeding with different levels of CHADSVASC scores, on or off warfarin, come from population-level data, and have been confirmed in analyses of clinical trials.

Now onto the AF itself:

As for treating the episodes and having AF, it is now clear to me that AF is rarely a primary disease. Meaning, I think AF occurs because of perturbations of other health issues. This may sound pseudo-science-like but I think AF occurs when homeostasis of the mind, body or soul is disturbed. Think brain-heart connection via neural pathways. Poor sleep (?OSA), alcohol, stress, obesity, hypertension, caffeine, travel, worry. recent bronchitis, injury, surgery, etc are all common associated issues. And some individuals are clearly more susceptible than others, likely due to genetic variations in cell functions. Yes, of course, there are those patients who develop AF as a form of a focal tachycardia without any other health issues, a fluke if you will, but these are the small minority.

Research on the role of lifestyle and arrhythmia is beginning to show that AF may be unnecessary.

I like your treatments, which include prn (as needed) things. In your case, time and sleep–beautifully effective strategies for many medical problems. When I use anti-arrhythmic drugs, I often prescribe them as prn therapies so patients aren’t exposed to the drug on days they are not having the episodes. If a patient has one AF episode per month, that’s 29/30 days  she has no episodes. I find focusing on the positive is good for AF patients, as it sometimes helps them avoid over-treatment.

The problem (bias) I have, and other cardiologists too, is that we see a skewed population of AF patients. I, for one, see about 1 AF patient per year with a disabling stroke and a CHADSVASC of 0 or 1. We see the 1%, in other words.

I never “strongly advise” low-risk patients to do anything. Instead, I strongly advise them their statistics. People feel differently about NNTs of > 50 or 100.

Another bias of mine: I have little fear of warfarin. If my AF came back, I would get a home monitor and never have an INR out of range. We now do pacemaker and ICD surgery (and AF ablation with transeptal heart puncture) with patients fully anti-coagulated. There was even a NEJM study showing lower complications with device surgery when patients were left on warfarin.

I realize the anticoagulation viewpoint of other MDs is different from mine.

Hope this helps.


27 replies on “Two AF cases — and my changing view of AF”

It’s the tendency of untreated paroxysmal AF to eventually progress to persistent.
It seems that successful antiarrhythmic drug treatment may not help if Dr J. S. Steinberg, in HRC News is correct: “Switching to AAD may do little more than give the AF time to worsen.”

Clots don’t form simply as a result of blood stagnation. There are endocardial and blood chemistry changes with AF that support clotting and stroke.


There are research articles that happily conclude that a successful ablation (How do you define that??) puts you in the CHADSCVASC category of people who never had AF.

Why would you not get an ablation right away… or as “upstream” as is feasible?

Dr. John: A few questions. And comments.

Comments: 1) I believe that there are many more people with afib than the statistics capture. Since many have silent afib, the only way you would know they have afib is if they have a stroke or you happen to capture the afib in a routine examination. That would tend to lower the stroke risk numbers (in theory). 2) I have met and corresponded with many people with afib. Although some have hypertension, are overweight, drink, or have some of the other risk associations, none of them are extreme examples of any of the risk factors you mention. That’s why I am not sure the “afib may be unnecessary” theory works. There should be more obese people with afib (1/3 in the US are considered obese). 2/3s in the US are overweight. I think there is an unknown reason why certain people with the same risk factors get afib and others don’t. I hear many people (50%+?) with afib also have OSA (many times caused by jaw abnormalities and aging versus weight) seems to hold some clues. Maybe genetics.

Questions: 1) Since very few people ever have an MRI to detect silent strokes, how can anyone discount that a large portion of those with afib don’t also have silent strokes… infarcts that could lead to dementia and that should give a point using CHA2DS2Vasc? Maybe those “low risk” patients that have strokes already had silent strokes. And how do we know that the anticoagulants aren’t effective in reducing silent strokes? 2) On the other end of the spectrum- debilitating and fatal strokes- I’m wondering if they have broken out absolute risk (separately) for debilitating and fatal strokes for a person with a CHA2DS2Vasc of 1, since many have “identified” silent strokes or strokes that result in minor disability that patients recover fully or partially from (I care about those also, but the debilitating or fatal stroke data would really influence my decisions). 3) Is there data on the ability of anticoagulants to lessen the severity of strokes? In other words, are most low risk patient strokes on anticoagulation less severe?

As an afib patient, the things I care most about are 1) fatal or major debilitating strokes (while I don’t want any stroke, being unable to move about/talk, being a vegetable, or dying get most of my attention), 2) Silent strokes that, over time, might wind up as some type of dementia, and 3) Not having a brain bleed caused by an anticoagulant, particularly Coumadin/Warfarin, that is known for causing the most. I get the part that 1% have “bleeds” without anticoagulants, and 3% have bleeds with anticoagulants, but those numbers don’t tell the whole story. The severity and the location of the bleeds matter just as much. I’m taking Pradaxa and fewer brain bleeds (as well as convenience/slightly better stroke prevention) trump cost (It’s only $10 a month with the savings card BI has, along with my health plan).

Thanks for the article. It helps me focus on my big questions and priorities.

… oh and, of the 1% that DO have strokes with a CHA2DS2Vasc score of 1, have they studied those patients? I’m assuming they are talking about risk if not anti-coagulated, right?

Hey, wait a minute, the Framingham Study said that a man age 65-69 has an 11% chance of a stroke in 10 years. That’s a little over 1% per year. If that person had afib and no other stroke risk factors, it seems little or none of the risk comes from afib. If that person was on anticoagulation, there risk would be cut in half (.5-.6% risk/your stats). So the 65 year old male with afib (CHA2DS2Vasc score 1 for age) has less risk for stroke than non-afibbers that age if he is anti-coagulated? His anti-coagulated bleed risk is not 3% either (as compared to the 1% not anti-coagulated) using the HAS BLED scoring system (if no other factors):

“HAS-BLED Score is 1. Patients with this score are considered to have an INTERMEDIATE risk of bleeding. The 1 year estimated risk of bleeding on oral anticoagulants is 1.02 – 1.5%.”

Small chance for a stroke. Small increase in bleed risk (most of which is not serious). $10. Sounds good to me since I absolutely don’t want a stroke or a brain bleed. Also- sounds like I’m playing with very small numbers that will change when I’m 75 and/or I get more risk factors.

I took Xarelto for 30 days after cryo. During that time, my EP strongly suggested I stay off my mountain bike. He was concerned about falls and a brain bleed. If your afib returns and you go on warfarin, would you continue to race cross and mountain bike? How much does a person have to quit doing while on these drugs?

GOOD post John! As you state – the overall risk of developing stroke in the literature appears to be comparable for persistent AFib as with PAF (paroxysmal or intermittent AFib) for a variety of reasons. And the reality is that Holter studies show >90% of AFib episodes are “silent” (= the patient is UNAWARE) – so it is difficult to truly determine the risk any given patient has (probably has to do with lifestyle features you emphasize; size and function of the left atrium and ventricle; frequency and duration of AFib episodes when they occur). In general – beyond “60 or so” (which at my age now is “young”) – the risk of stroke in a patient with AFib goes way up. Therefore – while fully emphasizing lifestyle measures as you do along with informed-consent decision-making – I have felt the balance overall seems to favor at least an attempt at anticoagulation unless/until side effects/difficulties made one reassess that strategy. What I myself would do if I now developed intermittent AFib at age 64 would probably depend on global assessment of frequency & duration of episodes integrated with assessment of cardiac chamber size and function …. but EACH patient needs to make their own informed decision. GREAT topic for discussion!

P.S. THANK YOU for confirming my impression that new anticoagulant drugs are 99.3% similar in efficacy and safety but more than 100 times the cost!

Does “Amount” equal frequency? A patient that has 1 afib episode per year has the same risk for stroke as a patient with 10 afib episodes per month (given the duration per episode is equal)??

GREAT question Joe – and I don’t know that there is any real way to answer this given the clinical reality that ~ 90% of all AFib episodes in patients who go in and out of this rhythm are asymptomatic …. Simplistically – I always thought about it in this way: IF someone has frequent short, self-limited episodes of AFib (ie, less than 12-24 hours or so …. ) – then they would seem less likely to develop the sustained stasis likely to lead to clot development. Such patients would therefore seem at less risk of thromboembolism.

On the other hand – IF a patient has longer-lasting episodes (greater than 48-72 hours) – then they would seem at greater likelihood of developing clot – and therefore at potentially greater risk of throwing a clot the next time they went back into sinus rhythm.

The above suppositions are based on the theory that: i) It is going back-and-forth to sinus rhythm after clot formation that conveys the period of greatest risk of throwing a clot; and ii) That it generally requires a certain amount of sustained “stasis” (ie, AFib) to develop clot. This “amount” has been theorized to be between 48-72 hours – but data for that amount is poor – again, with the clinical reality that there is no practical way given the frequency of asymptomatic episodes to know if “frequency” equals “amount” in terms of risk predisposition ….

Otherwise – my impression has been that cardiac factors (ie, left atrial and ventricular size and ventricular function) and presence or absence of other underlying heart disease (“lone” AFib or not) as well a
s age of patient (stroke risk increasing greatly after 55-60 years old) all conveyed an important contributing role to the equation regarding “risk” of thromboembolism in addition to “frequency” and “duration” factors ….

Thanks for the reply! Hopefully the use of ILRs and other devices will help to clarify this.

Dr. John says that he would use warfarin and home monitoring if AF returned – how often do you prescribe home testing for your patients? The issue about less ICH with warfarin from the studies with the new agents may not be the case – ICH with warfarin was about 50% to 100% higher than in earlier AF studies and there were a significant number of Asian study sites where the rate of hemorrhagic stroke was increased by 2.4 fold compared to other sites even though the INRs were lower. Aspirin (used in about 25 to 35% of patients) almost doubles the risk of ICH with warfarin and systolic blood pressure elevations of 9 to 12 mm Hg can increase ICH by 2 to 3 fold (all studies with the new agents allowed BPs of up to 180/100 mm Hg….. wonder how they got that by the IRBs?). Lastly, a large systematic review and a large data base analysis indicate that as little as 15% increase in INR time in range (ex: 60 to 75%) is associated with a > 50% reduction in major events. Agree with Dr. John… frequent self testing and keeping INR in range is likely the best option for stroke prevention.

Guess I am in the “fluke” category! 32 years old and just had an ablation for persistent a-fib. On xarelto and flecainide for 3 months, with no noticeable side effects so far. I enjoy the blog!

Hi Matt

I’m 33 and was diagnosed with paroxysmal afib last year. No other health issues and no family history of afib. However, I was under a great deal of stress when I had my first episode.

So what is classified as a paroxysmal AF “episode” to be concerned about, in terms of duration? A few seconds of tachycardia, a few skips in a row, or events lasting hours or days?

Just curious regarding terminology.

Great post! Thanks for sharing your thoughts on this forum.
If I read this correctly you would go on Warfarin and monitor yourself if PAF is present? I have about one episode per week and naturally stroke is heavy on my mind. Anti- coagulation full time for 3 to 4 episodes per month seems a bit like over medicating?
Thank you!

Another thing. I too try to get on a mountain bike as much as possible. To be on anti-coagulants with the threat of a crash and a possible bleed seems like a bigger risk than a stroke by not using anti-coagulant drugs. Your thoughts?

Steve – have you ever gotten that question answered? What is the risk/benefit of anti-coagulants for infrequent episodes; and do you have to give up the mountain bike? I’ve asked the cardiologist I used to see and could not get a straight answer with numbers and percentages when he spoke.

Dr. Mandrola, I look forward to meeting you on Friday the 15th. This blog is the reason why I have decided to consult with you. I live 7 hours away. I am young and have persistant AFib. I am tired of it. I am tired of the medicines. I am tired of the doctors telling me to up my medicine and to perform a third ablation. I need someone to tell me something different and what might work better. I look forward to what you have to say.

Bayesian analysis of available published data on high-dose aspirin suggested that it was more effective than low-dose aspirin and only modestly inferior to warfarin. This has not been followed up in recent years. However, in AVERROES, the minority given moderate or (in 7%) high doses of aspirin, by doctor’s discretion, had conspicuously lower stroke/embolism rates than those on low-dose aspirin (2.4% vs. 4.3%). Fortunately for the sponsor, those taking apixaban and 2-4 placebo baby aspirins also had lower event rates than those taking apixaban and 1 placebo baby aspirin (1.1% vs. 1.9%). Apixaban also luckily caused over 30% less bleeding in people taking more than one placebo aspirin. Some of this is doubtless attributable to doctors’ willingness to dish out more possible aspirin pills to those who seem healthy enough to endure it, who will also have lower stroke rates, but we can’t assume as a matter of dogma that all of it is. If no further trials are done using high-dose aspirin, how is the public to evaluate the genuine potential utility of aspirin?

Interesting articles, yes.

Do we know, from this, that AF is the ultimate culprit – cause and effect established?

First: Current treatment standards would have you anticoagulated in any presentation of AF in order to prevent associated maxi infarcts – stroke and death, or might-as-well-be. So much for mini.

Then: It’s well known that diabetes is a major risk factor for AF. AND, even moderate elevations of blood sugar are associated with dementia.

Mightn’t glucose be behind it all?

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