Why Your A-fib Diagnosis May Not Be as Bad as You Think It Is

With breathtaking speed, atrial fibrillation has gone from “Huh?” to parlance.

“A-fib”, a common cardiac cause of palpitations, is now in the front ranks of evils lurking to smite our well-being. There is no mystery to this transformation. In 2013, the Food and Drug Administration licensed three new drugs to prevent a stroke, the fearful complication of A-fib: apixaban (Eliquis), rivaroxaban (Xarelto) and dibatigatran (Pradaxa).

This unleashed the full might of pharmaceutical marketing: the scientific data for efficacy that convinced the FDA is tortured till it convinced “thought leaders” whose opinions convinced influential journalists. Sales pitches populate print, broadcast and social media. A-fib is now more than a worrisome disease; it is a product line.

Nonetheless, A-fib can be scary for those afflicted. There are lots of choices to make and a lot of confusing, conflictual and counter-intuitive advice to deal with. Troubled by this situation, Mr. X recently sought me out to have a dialogue about his situation.

Mr. X is a 70-year-old business executive who has enjoyed robust good health and is on no prescription drugs. He exercises vigorously and is a consumer of various over the counter treatments purveyed as salutary. Like many “health-wise” Americans, he also takes 80mg of aspirin a day unaware that the benefit is minimal at best and is counterbalanced by a similar magnitude of risk.

A month earlier he had the sudden onset of palpitations, a fluttering in his chest that made him exceedingly anxious and somewhat breathless. He waited an hour before asking his wife to drive him to the local emergency room. By the time he was first seen, another hour passed. The diagnosis of A-fib followed. Another hour passed to find the consulting cardiologists debating whether to convert the A-fib to a normal rhythm by using drugs or an electrical shock.

Before they could decide, Mr X’s heart decided to behave again; he was back in a normal rhythm. It was a frightening experience for Mr. and Mrs. X. He left the ED shaken and shaky.

He also left with a follow-up appointment with a cardiologist who specialized in rhythm disorders and a prescription for a drug that slowed the conduction of electrical impulses initiating in one heart chamber, the right atrium, and traversing the heart. The normal “pacemaker” is a specialized cluster of muscle cells in the right atrium that discharges at regular intervals, initiating a current that causes the heart to contract in the synchronized fashion termed Normal Sinus Rhythm.

In A-fib, for reasons that are poorly understood, multiple pacemakers form in the right atrium leading to chaotic discharging and circular currents in the right atrium. How many of these impulses manage to exit the atrium to traverse the heart depends on the capacity of the conducting tissues; most just stay confined to the atrium causing it to quiver ineffectively.

In retrospect, Mr. X recalls multiple episodes of palpitations in recent months, though few were as prolonged and disturbing as the episode that drove him to the ED. He noted several more before he arrived at the follow-up appointment. If he wasn’t anxious before, that interview did the trick.

He was relieved that he basically had a normal heart with one serious problem; he had “PAF”, paroxysmal atrial fibrillation. This intermittent A-fib was probably more dangerous than persistent, “chronic” A-fib.

The danger in PAF was not that he felt awful during attacks; those symptoms should respond to drugs that control the heart rate. The urgent issue is that the chaotically beating chamber is prone to blood clots, pieces of which can break off as “emboli” and travel to the brain causing an embolic stroke. The cardiologist wanted to start a drug designed to keep Mr. X in normal sinus rhythm and to start one of the new blood thinners to decrease the likelihood of clots forming and thereby decrease the likelihood of an embolic stroke.

If that didn’t do the trick, the cardiologist mentioned the possibility of other drugs or even of “ablation”. This is where a catheter is introduced in the heart to identify bundles of muscle cells that were misfiring and burn them thereby creating tiny therapeutic heart attacks – a procedure that has risks, works most of the time, and is plagued with recurrences.

The plan that made sense but not enough sense for Mr. X to agree without first researching it’s the rationale, the benefit/risk ratios, and the alternatives. The cardiologist seemed to think the decisions were obvious. Mr. X knew they were not. The episodes of palpitations were still anxiety provoking but more in the sense of their portent than the associated discomfort. Mr. X needed to place the cardiologist’s advice into to a more personal context, one in which he could exercise his own values as to risk aversion.


How likely is an embolic stroke in the setting of A-fib?

There is no simple answer to this question. First of all, there has been a very impressive decrease in the incidence of fatal strokes in recent decades, and probably a decrease in the incidence of non-fatal strokes, too. That makes “old” data less and less relevant. Secondly, the epidemiology of A-fib is difficult to define because most A-fib, PAF or chronic A-fib, is asymptomatic.

Furthermore, most palpitations occur while we are in Normal Sinus Rhythm. No doubt most estimates of the risk of stroke in the setting of A-fib are overestimates; most people with A-fib never become patients with A-fib.

So, the relevant question is what is the risk for stroke in patients newly diagnosed with A-fib? However, the incidence of stroke in the setting of A-fib increases with age and with complicating cardiac and other diseases. Hence, the more relevant question for Mr. X is what is the risk for a 70 year old man who is otherwise well?

There is a study addressing this question in some 80,000 patients over age 65 who presented to hospital with new onset A-fib. If we follow 100 men with A-fib who are 70 years old and otherwise well for a year, one will suffer a stroke that is recorded in medical records. This is not trivial, nor is it as alarming as Mr. X was lead to believe.

How much does blood thinning reduce this risk?

There are three ways to interfere with blood clotting that are relevant. One is low dose aspirin, which Mr. X is already taking. The second is the time-honored standard blood thinner, warfarin (Coumadin), which requires laboratory monitoring and carries a risk of bleeding complications. The third are the new drugs which are more convenient since they do not require monitoring but have their own baggage.

In terms of efficacy, there is no data that the new drugs have anything to offer over warfarin. So the first issue for Mr. X is whether taking low dose aspirin each morning is good enough?

Most of the recent drug trials do not address this question; they are comparing the new anticoagulants with warfarin. However, there was a considerable earlier literature comparing aspirin with warfarin for A-fib. Some of the individual trials are better designed and particularly compelling [1]. But the literature is sufficiently robust that there have been many systematic attempts to cull a consensus from the accumulated research [2]. There is no doubt that low dose aspirin therapy is effective but not as effective as warfarin. There is also no doubt that low dose aspirin therapy leads to fewer adverse effects.

It follows that the higher the risk for an embolic stroke, the more the benefit is apparent and outweighs the harms. Mr. X has a low risk for embolic stroke; about 1% in a year without aspirin. Taking warfarin can reduce that risk by about 10%, to about 0.9% in a year (i.e. 1 in 110 might suffer an embolic stroke).

What are the hazards of reducing the risk of an embolic stroke with blood thinners?

Low dose aspirin causes easy bruising but major bleeding complications are rare. They are rare with warfarin if there is no overdosing, hence the monitoring, and with the newer oral anticoagulants – although bleeding is particularly difficult to treat as a complication of the newer agents.

But that’s the least of the risks to consider. The reason for aspirin or warfarin anticoagulation is to prevent clots and thereby embolic strokes. Both work, warfarin better than aspirin, but neither agent works perfectly. However, when aspirin fails the stroke is likely to be an uncomplicated embolic stroke; a blood clot blocks a vessel in the brain causing damage to the brain downstream by depriving that area of the brain of oxygen-carrying blood.

Most recover partially or fully from embolic strokes. But when the blood is thinned by warfarin, there is a risk of bleeding into the damaged brain converting a simple embolic stroke into a catastrophe with little likelihood of recovery. That’s what happened to Ariel Sharon.


Now Mr. X is an informed patient. He is in a position to make his decision. What would you do?

Nortin M. Hadler, MD MACP MACR FACOEM, is a professor of medicine at the University of North Carolina, is the author of Rethinking Aging(2011) and The Citizen Patient (2013). This post originally appeared in the Scientific American Blog Network.

17 replies »

  1. There is a marvellous online calculator here:
    That gives you the absolute risk of stroke without or with asirin and a bunch of anticoagulants.
    When you can count, it is impressive tha cardiologists are so assertive about the need for anticoagulants in many cases where the risk of bad complications equals or approaches the benefit.
    ANd I always have a doubt about absolute risk reductions of less than 2% a year, to say the least. Can this be reliably measured ?

  2. But again, wouldn’t this be exactly the kind of (complex) issue best decided between the helpful cardiologist and the patient?

    I find it surprising (and a bit scary) to hear that “excessive physical activity” can cause afib later in life. I must see several things a week warning of too little activity — I never can recall seeing ANYTHING warning of too much vs. long term cardiac risk — aside from watching one’s maximum pulse rate during heavy exercise.

    Must patients become doctors to do the right thing? How can ANYONE have enough information to do the right thing in every specialty? (Yes, that is a rhetorical question).

  3. To me, that’s a puzzling question.

    Since you are a cardiologist, instead of asking that question, why aren’t you providing a ball-park estimate based on your experience, or perhaps a study of how well such consultations generally work.

    In my (educated layman) experience, educated people can have meaningful input into their medical decisions, if relevant information, such as in this article, are presented in English, with meaningful statistics (round numbers are fine), and with the appropriate trade-offs mentioned. Numbers are fine if expressed in ranges, and uncertainty is actually good for educated patients to understand.

    Thoughtful, educated patients (and their families) know themselves far better psychologically, and in some ways physically, than their doctor, and IMO, should always have a voice in such decisions.

    Now, clearly there is the problem of uneducated, panicky, illogical, etc. patients — and it may be hard for a doctor (especially a specialist seeing a new patient) to tell a good candidate to help in the decision from a bad one.

    Perhaps some sort of an objective test to learn about a patients’ relevant attitudes and ability to make meaningful judgements would be a good thing(?)

    I am simply astounded at how little actual value, in this case, Warfarin has in this case, vs. the far safer and more convenient baby asparin. As such a patient, I would not have known that without getting lucky in my reading on the situation — unless my “helpful cardiologist” pointed the data out to me. Surely many patients could at least navigate the obvious trade-offs for that decision.

  4. Dr. Hadler, why not suggest that Joe and Joel look at the more recent meta-analysis of antithrombotics for stroke prevention in AF:

    Ann Intern Med. 2007;146:857-867

    And by the way, there were available at the time of this blog publication meta-analyses of the new anticoagulants compared to warfarin with over 60,000 patients studied showing a lower risk of death on the newer agents. While the absolute risk difference < 1%, that's a lot of deaths when patient populations are considered.

  5. The British Medical Journal article by Fiona Taylor is fascinating. Nortin, you hint at a future discussion of ablation for atrial fibrillation. I would love to see that discussson. My observation is that this procedure is rising in popularity, despite cloudy outcome data.

  6. In response to the request by “Joe” on 4 August above, and the comment by Joel above, anticoagulation became acceptable therapy around the millennium because of RCTs comparing warfarin with aspirin for non-valvular AF. Hence, there is considerable data that speaks to the increment in risk reduction achieved if a patient is treated with warfarin rather than aspirin alone. It is this data that underpins my argument. The easiest access to this literature is a systematic review published in the British Medical Journal by FC Taylor et al (BMJ 2001 Feb 10;322:321-6.)

  7. I do not agree with several assertions you make. ASA alone has very little ability to reduce the risk of stroke in a fib. The idea that a stroke on ASA would be smaller is not supported by any science and has never been studied. The firmest endpoint in all such trials is the total # of strokes in each trial arm, not size. Aside from all cause mortality there’s no hint of an effort to assess “severity” in these trials ( although various scales are used.) Long before cardiologists were inundated with the new drugs there was a great appreciation for the fact that TOO MANY preventable strokes occur every year because of the reluctance of PCPs to use warfarin ( and therefore default to ASA which is largely useless in this setting ).

  8. TV ads by the pharmecutical industry is marketing the “maintenance” of A-Fib. Why not aim for a cure? (Answer: less patients/customers taking your medications.)

    For more information about Atrial Fibrillation look at A-Fib.com. We discuss all these topics with footnotes to the research citations to backup what we write. ‘Atrial Fibrillation: Resources for Patients’ was started in 2002 by a former A-Fib patient, Steve S. Ryan, PhD (cured in 1998) and is a non-profit, patient education website. We are the patient’s independent source of unbiased, well-researched information on A-Fib. (We ask no advertising paid or otherwise.) We spread the word: A-Fib can be Cured!

  9. Your take is consistent with the science, Travis. How you act on this interpretation has to be consistent with your values, including your level of risk aversion and your willingness to swim against the current “current”.
    Stay well…..

  10. Thanks for the reply. One other question I have…after reading this article a few more times, it seems to me that aspirin is the better option as far as a blood thinner goes. The risk of stroke without aspirin is only slightly greater than if you are on warfarin according to this post (1% vs 0.9%) – and if you take aspirin and it fails, you’ll likely have a stroke you can at least recover from. I keep hearing aspirin is not effective or even recommended as a blood thinner to prevent stroke in afib patients but then I read this article and it seems to be suggesting just the opposite – that aspirin *might* be a better option after all. You have less side effects and if you have a stroke, it probably won’t be as bad. What am I missing?


  11. Travis, ablation is mentioned in the essay. See the penultimate paragraph before the “A Little Truth…” heading. That paragraph concludes that ablation is, “a procedure that has risks, works most of the time, and is plagued with recurrences.”

    I probably should write another essay on ablation. However, you must demand more information from your cardiologist so that you can make an informed decision.

  12. While the success rates may not be as high for people in this age bracket, why isn’t ablation one of the options mentioned? I guess if I were this gentleman I would skip the blood thinner and take aspirin and have an ablation.


  13. The medical decision making may seem straightforward about medications, but it is less so with regard to lifestyle. There are plenty of physically active 60 and 70 year olds with afib, who probably got it from a lifetime of excessive physical activity and have no coronary artery or valve disease. It is difficult to do even a moderate degree of exercise in chronic atrial fibrillation, there is no good guidance for those with episodic afib to avoid chronicity, and many previous exercise patterns can be disrupted by anticoagulation.

    For those people they may go from being very active to stopping their activities and suddenly feeling old. For many people that is worse than all of the medical decisions.

  14. Lets say risk 1.5%/yr. Actuarially, the patient can live 10-15yrs. The longer the life, the greater the risk of bleeding, but also the greater risk of stroke. Stroke and loss of functional QOL amongst the highest fears of seniors.

    If cost not an issue, I advise newer agent, due to administration ease and non-inferiority with coumadin. If cost a problem, go with the latter.