Atrial fibrillation Dabigatran/Rivaroxaban/Apixaban Healthy Living Knowledge

Getting the dabigatran (Pradaxa) story right… Correcting four common mistakes.

This purpose of this post is to clarify misstatements made in a recent New York Times article about the anticoagulant drug dabigatran (Pradaxa). The piece had three major inaccuracies, plus one thought-error from a cardiology leader. I write these words because the most valuable tool in the treatment of AF is knowledge. Getting it right is critical. (For readers that persist, I offer a bonus at the end.)

The thrust of the Times’ story concerned editorials in the British Medical Journal that questioned the safety of dabigatran. The first non-warfarin anticoagulant has had plenty of controversy, the most recent of which involves the findings of this RE-LY sub-study. Researchers analyzed blood samples from 9,183 patients in the original RE-LY study and found plasma dabigatran levels can vary up to five-fold. Common sense holds that five-fold variations in plasma levels of any drug might be significant. In this case, high levels of dabigatran correlated with bleeding, and low levels might have predisposed to ineffective stroke prevention though no correlation was found between stroke events and blood levels, likely due to the small number of strokes in the study. (I have had two low-risk AF patients suffer major strokes while taking dabigatran. Other colleagues have reported similar anecdotes.)

The FDA knew about these variations in dabigatran levels but felt the outcomes (strokes, bleeds and deaths) from the original 18-000-patient RELY study, which favored dabigatran without monitoring, was enough to approve the drug. The Times’ piece also mentioned the fact that Boehringer Ingelheim paid $650 million to settle thousands of claims brought by patients alleging harm from the drug.

Before addressing the article’s mistakes, it is laudable that mainstream media emphasizes the notion of weighing risks. All medical decisions are a gamble–an exercise in probability. We must get past the idea that any drug, surgery or procedure is free of tradeoffs. You cannot prevent strokes in patients with atrial fibrillation without exposing them to bleeding risks.

Now to four mistakes made in the article. They serve as good teaching points.

Warfarin flail:

“Patients [on warfarin] are supposed to avoid leafy greens and cruciferous vegetables like Brussels sprouts because they contain vitamin K, which facilitates blood clot formation.”

I am so utterly tired of correcting this mistake. It is completely wrong. Patients on warfarin can indeed eat green vegetables; they should just eat them consistently. I have vegetarians who do beautifully on warfarin. The problem comes when people vary the weekly dose of vegetables. Warfarin works by inhibiting vitamin K-dependent clotting factors. If one eats the same amount (dose) of vitamin K, the caregiver can easily adjust warfarin dose. In fact, some have even suggested adding a small dose of vitamin K to patients who have difficulty controlling INRs. This is not a nitpicky criticism; patients on warfarin have disease, and they should not be avoiding healthy plant-based foods. Plus, it’s such a rookie mistake.

Relative risks do not belong in explanatory health journalism:

“You could have had a much safer drug,” said Dr. Deborah Cohen, the investigations editor at The BMJ, who wrote two articles last month critical of Pradaxa’s record. By carefully monitoring drug levels in patients, “you could reduce major bleeds by 30 to 40 percent, compared to well-controlled warfarin,” she said.

This misleading quote should not have been allowed to stand alone. The rate of major bleeding in patients on the 150-mg-dose of dabigatran in the RE-LY trial was 3.11%; it was 3.36% in the warfarin group. If you made dabigatran perfectly safe (0 bleeds), the best it could have been was 3.36% better than warfarin, not 30-40%. Dr. Cohen was talking about relative risk reduction, which is not important to the patient considering taking a drug. Patients facing the gamble of treatment should care about absolute risks. What’s more, the sub-study that showed dabigatran levels vary and correlate with bleeding cannot determine how many bleeds would have been prevented with dabigatran monitoring. It’s possible monitoring could have made outcomes worse.

All anticoagulant drugs get riskier in complicated patients:

“Some who take Pradaxa may be at greater risk of bleeding — particularly older patients, anyone with kidney problems, those with a history of ulcers or gastrointestinal bleeding, and patients who take other drugs that increase bleeding (like aspirin).”

The problem with this statement is that all the new anticoagulants pose greater risks in patients with kidney problems, ulcers, and those taking antiplatelet drugs, such as aspirin. This is not a dabigatran specific issue. Rivaroxaban, apixaban and edoxaban have the same issues with renal clearance, to varying extents. Warfarin, too, is riskier in patients with a history of GI bleeding. It doesn’t mean we don’t recommend anticoagulant drugs in these patients–it just changes the odds of the gamble. Consider that AF patients with risk factors for bleeding are almost always at higher risk of stroke as well.

Yes. People with AF can and should control their diet:

“The person who is 50, who has a busy professional life with a lot of travel, can’t necessarily control their diet, and actually likes to eat things like broccoli and kale — they feel liberated,” said Dr. Patrick O’Gara, the director of clinical cardiology at Brigham and Women’s Hospital in Boston.

This thought-error is on the current president of the American College of Cardiology. With respect, here is what I mean: The busy 50-year-old professional person probably has AF precisely because he hasn’t controlled his diet or travel schedule. The inference (I take) from Dr. O’Gara’s statement is that the new anticoagulants are good for professionals because they are more convenient and require less of a commitment than warfarin. This, my friends, is the core problem in the way many doctors approach the care of patients with AF. Too much convenience is why patients, especially professionals, get AF. And, let’s be honest, if a person has a heart rhythm disorder as serious as AF, he or she should damn well control their diet and travel schedule. AF patients should make a commitment to their health. The enabling of patients with pills, and other “easy” solutions to lifestyle-related diseases is one of the reasons we have so much AF, and hypertension and diabetes and degenerative joint disease. AF is a disease, yes, but it is also a window onto the overall health of the person.

The next paragraph is a bonus for readers who have persisted.

 Genetics play a significant role in dabigatran levels:

Finally, if you want to worry about dabigatran, I would be most worried about this sobering study. Researchers did genome-wide association analyses on 2944 patients from the RE-LY database and found nearly one in three patients carried a minor allele that associated with lower exposure to the active dabigatran metabolite. The Achilles heel of dabigatran looks to be its diversity of metabolism from pro-drug to active drug. Did you know that dabigatran is given as pro-drug and requires enzymatic conversion to active drug? The bioavailability of dabigatran turns on genetic determinants, and in the best case is only 6% bioavailable.

A former Indiana mentor used to holler at us: “no data was better than bad data.”


39 replies on “Getting the dabigatran (Pradaxa) story right… Correcting four common mistakes.”

Good to read some common sense emerging in this debate. The media coverage of the issue has been equally as bad down here. The NYT missed my favourite though – the one where they compare the number of adverse drug reactions to NOACs reported to ‘the regulator’ compared to the number reported for Warfarin ( see ).

Keep up the blog!

” If you made dabigatran perfectly safe (0 bleeds), the best it could have been was 3.36% better than warfarin, not 30-40%.”

No, that would be 100% better.

“Better”, by definition, means a relatively measurement.

However, I don’t disagree that absolute risk is needed to see the full picture.


I’m continually reminded why I love your blog. The point counter point format here was highly effective in conveying complex information as well.

To respond to the second comment, the problem with relative risk is one of how people interpret the data. The concept of “denominator neglect” is a well known cognitive bias where if we hear 30 or 40% reduction, we automatically assume 30 or 40/100. Even if the language is “correct” – we have enough science to know that the interpretation won’t be for the majority of people. Without a doubt, your clarification using absolute risks will lead to a more accurate understanding by the reader.

All excellent points; I’d also point out the rather unique problem of product stability (similar to nitroglycerine formulations from the past) which precludes one from using this medication in weekly “pill boxes” unless the blister pack is used. This also necessitates keeping the medication in the original, tightly closed container and even then, stability is good for only a few months. See
Also agree with life-style comment that “Dr. John” continues to emphasize… which is why I’m about to follow my egg-beaters breakfast with a brisk 45 min. hike – -taking action in part due to this blog posting 🙂 Thanks for the kick in the rear!

I enjoy your website and think a lot of what you are doing. However, I have some issues with your post. I think most of my issues have to do with your oversimplification concerning diet on Coumadin and blaming the patient for having afib. Also, not coming up with a clear position on Pradaxa. I’ve read all your posts on the drug and I don’t see any consistency over the years. I’m not a doctor, but as a patient, I’m an expert on what we patients need to make informed decisions. We need more answers not more questions. We need more consistency, not disagreement among professionals/waffling/hard to interpret statements. And lastly, wore understanding, not more blame.

1) “Patients on warfarin can indeed eat green vegetables; they should just eat them consistently… the problem comes when people vary the weekly dose of vegetables.”
That’s the problem. It is easy to say you should keep your vegetable intake consistent, but what does that mean? The average person (usually much older than 50 according to statistics on afib) on warfarin/Coumadin doesn’t know if there are differences in vitamin K say for spinach, broccoli, lettuce, or peas. Dark leafy greens have 5X the amount of vitamin K as broccoli, by the way. And they don’t know how to measure equivalent amounts between the green vegetables (it gets much more complicated as there are many other non-green food sources that are actually richer in vitamin K) . That’s a lot of burden to place on a patient (Self-titrating ,with diet, a drug that has a narrow therapeutic range and whose purpose is something as important as preventing stroke).
Even your post is inaccurate. The top ten vitamin K food sources in order are: Herbs (many, but not all), dark leafy greens (not light leafy greens), scallions, broccoli, chili powder/curry/paprika/cayenne (high in concentrated vitamin K and none are vegetables or green), asparagus, cabbage, pickled cucumber, and prunes (They’re purple. Hmmmm, I wonder about other fruit). I also read that you should avoid cranberries and grapefruit and their juices altogether. Then there’s COQ10, turmeric, green tea, natural supplements, chestnut, and licorice. How do you weigh basil with a high (5X) concentration against cabbage that is loaded with fiber and water? Anything that has soy added (you have to check) like peanut butter can affect INR. Did you know most multivitamins have vitamin k in them?

Many websites say you still need to limit your intake on a daily basis. That’s another thing. They say you should be consistent on a daily basis as INR can vary if you are getting a larger portion on a particular day, say, every Sunday. Seems like it would be easier/better to take a Vitamin K supplement and monitor your INR at home.

Takeaway: It’s not just green vegetables that have high amounts of vitamin K. It is much more complicated. Titrating warfarin/Coumadin with diet may be easier said than done. Only daily home monitoring is a reliable way to know for sure how your diet is impacting INR.

2) “The busy 50-year-old professional person probably has AF precisely because he hasn’t controlled his diet or travel schedule.”

Whoa! Really? Do you really believe that? Is there data to back that up? I’ve noticed that you increasingly “blame the patient” for their afib in your posts. Afib is uncommon for people 50 and under and afib, while a common arrhythmia, is only present in 2-3% of the population for all ages. Two thirds of the US population is overweight from bad diet and under activity and one third is obese. Most in their working years are busy trying to make ends meet. So how did you single out the ones with afib as being responsible for their afib? Maybe the 50 year old professional has a genetic disposition, thyroid issues, or some other factor. Larry Byrd was diagnosed in 1992, when he was 36. Oh yeah, I forgot, he was an extreme exerciser and tall. I know this example is anecdotal, but that brings me to my next criticism of your post…

3) “(I have had two low-risk AF patients suffer major strokes while taking dabigatran. Other colleagues have reported similar anecdotes.)”

What is your purpose in putting out this anecdotal information without putting it in context? Your statement will light up the afib support blogs by tonight thinking that you are saying Coumadin is better than Pradaxa in practice and thousands will hang on your every word. So… are you saying that never happened with warfarin/Coumadin in your practice? Do you know if the patients were adherent? Did you test them for the minor allele that could have prevented a major stroke? Are you doing that in the future? Do you still prescribe dabigatran/Pradaxa at all? In practice, are the number of strokes and brain bleeds fewer on Pradaxa than Coumadin as the trials suggest?

I’ve noticed that you increasingly “blame the patient” for their afib in your posts.

Thanks Pete. This is the attitude I encounter. My EP and staff are highly regarded, but customers(patients) are a nuisance. No time for us. We must get our information on the internet. When you have too many customers(monopoly), there is no customer service. Health care is just another racket.

herbs aren’t mentioned much becase the volume required to change your INR is so high and herbs are usually used sparingly. Also, Most multivitamins do not contain Vit K. I do agree that this MD seems to blame the patient for his a fib. I get it because of a congenital heart disease and have had it off and on since age 40. I take Xarelto and love the convenience.

Centrum Silver has Vitamin K. I guess many that would have afib use Centrum Silver or something similar.

Pete…Others…Thanks. Here you go:

1) The simple answer on diet is to keep it steady. Eat the same proportions of food that contain Vit K. Patients do not need an app for this. They just need to be mindful of the veggies (and other Vit K) foods over a weekly period. The thing is: in the real world, most people put on warfarin, don’t even get this fundamental knowledge. Then the NYT comes up with that false statement. Diet and warfarin is not rocket science.

2) You are not alone in the thesis that my words come off as blaming the patient. Sorry about that. To be clear, there exists a small minority of AF patients that have strong valvular or genetic or congenital causes of AF. These represent a small minority of AF patients in the US. I would submit that they, too, could be helped by aggressive lifestyle intervention.

Mostly, I have 2 (sometimes overlapping) populations of AF patients: One are my A-students–the frowny-face crowd. These are the “busy” professionals who are perpetually “on the gas,” mentally, physically, and metaphorically. The athletes, CEOs, engineers, doctors, and the like. They don’t rest; they don’t seem to enjoy things. You look at them and you see inflammation. One commenter here noted that they are out there making ends meet. My observation is that they are often out there making enough for big houses and cars. Sometimes they look healthy on the outside, but are not so on the inside. A middle aged woman with AF once told me a few years ago she had no stress in her life. She wanted for nothing, and led a blissful life, other than her AF. It struck me as an almost reportable case. Later, over the years, the more I got to know her, the more I realized that she was not as laid-back as she seemed. (BTW: I read a survey recently that noted Harvard students report extremely low happiness measures. Imagine being at Harvard and being unhappy? See what I mean.)

The second population of AF patients I see is the more common group. Earlier this month, I saw three AF patients in a row whose combined weight was more than a thousand pounds. Two of the three drank more than 3 bourbons nightly. One of them smoked. Lifestyle-related AF is extremely common. Many, many patients come back to me in follow-up and report feeling better when they heed my advice on sleep, diet and exercise. AF in America likely parallels are insatiable appetite for all things big and convenient.

Finally, Pete, I am not a therapeutic nihilist when it comes to controlling AF. But I see AF-rhythm-control meds and ablations as strategies to help patients get jump-started on the road to health. Sometimes AF happens after an infection or trauma. And it is often the case that patients need our help getting out of AF for a period of time. I do not, however, see AF drugs or ablation, as cures in and of themselves. Cure of AF, if it comes at all, comes only from teamwork between patient and doctor.

3) My reason to mention anecdotes of patients who have had strokes on dabigatran is that it is true. And these events influence how we/I judge the world. Yes, I have seen patients who have had strokes on therapeutic warfarin, but it is rare–and these patients have been high-risk older patients. And you are right, my views of dabigatran have been all over the map. This is normal. Our knowledge and experience with new strategies evolve over time. I am sure of so little in this job.

My husband, who is young and healthy enough that any of these drugs would have a smaller statistical net benefit than he considers worth it, and I tried to explain to every -ologist he ever saw that there is no such thing as a diet that is affordable, palatable, healthful, AND invariant. They universally failed to get it (and with an average salary of over $400K, that’s perhaps understandable). You can stuff yourself with the same imported fresh greens and fruits year-round, but you must have plenty of money to keep it up for long (then hope you never get sick and can’t eat your greens for a week or two, or travel to a place where the food is all rice and chicken parts). At the moment, most “middle-income” Americans could still afford to eat frozen broccoli and canned spinach year-round, but, blech, how boring – which will drive many back to a more enjoyable, but less healthful, meat and starch diet.

The only way to have a cheap plant-food diet that is more interesting and positively health-promoting than PB&Js, spaghetti or mujadarrah day after day is to buy (and if possible grow and eat) whatever fruits and vegetables are in season. Seasonal eating on warfarin is dangerous. But seasonal eating may offer many people the best chance they’ve got of genuinely improving their health, rather than just hoping to drag out their years of infirmity a little longer. Putting a man whose most urgent need is for weight loss on warfarin seems like writing him off. Those specialists who take it as dogma that patients can never get better are intolerant of any acknowledgement that there is a tradeoff involved.

These are thought-provoking comments. I’m an advocate of “seasonal” eating. Seeking out local, responsibly farmed produce does tend to be more expensive and difficult. I can see how that would complicate the management of an AF patient on warfarin. As mentioned elsewhere in this thread, there is evidence that daily consumption of Vit K in the form of a pill reduces the variability of overall Vit K consumption from dietary fluctuations. More daily warfarin is needed in this management strategy but it would allow a lot more flexibility in consumption of Vit K containing foods. Another strategy would be to commit to eating a salad daily, even if it meant getting it from a bag.

That is a pretty sad statement:

” The busy 50-year-old professional person probably has AF precisely because he hasn’t controlled his diet or travel schedule.”


I am 50. Had afib at 45. I eat 80% organic. Have a relaxed lifestyle. Never had any other health problems other than migraines every few years. Still, no other health problem than this dam afib.

I guess afib it is my fault.

The full story on Pradaxa and the NOACs continue to emerge. As an early user of Pradaxa and a former speaker for Xarelto, the second NOAC to be improved, I feel like I have a very good understanding of the risks and benefits and how to use these agents safely as alternatives to warfarin. I no longer speak for Xarelto and I am amazed at the PR blitz from free steak dinner talks to “CME” by industry sponsored doctors to our major cardiology journals dominated by advertisements for these drugs.
The majority of my patients with a fib, both new and old, continue on warfarin after I have a detailed discussion with them about risks and benefits and primarily after they realize what they will be paying for the drugs even after their insurance kicks in.
I think it is a disgrace that all 3 of the manufacturers are charging the same exorbitant price.
Comments on two points in John’s piece in particular
1. I do not advise warfarin patients to avoid vitamin K in their foods. If they eat a consistent amount of green leafy vegetables over a week long period, we do fine in adjusting warfarin to keep a consistent INR. Those who avoid the green leafy vegetables end up with the most erratic values.
2. There are large variations in the AUC of the NOACs depending primarily on renal function and interacting drugs. Amiodarone, a drug utilized commonly for a fib in conjunction with NOACs, raises both Pradaxa and Xarelto levels significantly. The elderly patients we start on these drugs frequently have kidney function which is on the border between mildly impaired and moderately impaired and will shift kidney function depending on concomitant conditions. GI bleeds were 50% more common with both Pradaxa and Xarelto likely related to some of these variations in levels and effectiveness.
Thus, although warfarin is a difficult drug and requires frequent monitoring , at least we know where the patient stands at any given time.

Anthony. Thank you for reiterating my point on warfarin. And on your second point, I believe pharmacology knowledge is a weak spot for many physicians. For it were not, can you imagine any doctor allowing elderly patients to be on the pages and pages of medicines that are so typical? We forget that drugs interact with each other and have disparate effects in the body–not just on the targets we are aiming at. I’ve always been conservative with prescribing, but this midlife journey I am on into pharmacology makes me even more so.

Don’t forget about the same interactions with Pradaxa and Multaq. That combination had me bruising, bleeding, tearlng my skin to shreds and feeling awful. At the time, the interaction was not yet published.

It wasn’t until I came off the Multaq and switched to xarelto that things calmed down. I was getting tired of going to the GP every few weeks to get another skin tear taken care of.

Thank goodness i didnt have a major event from that combo,.

I don’t have to take anything anymore, a total lifestyle transformation seems to have taken care of my afib (none since a cardioversion over a year and a half ago), so I can back up John’s statements regarding lifestyle, at least for some. I was determined to not have to take those damn meds the rest of my life.

In defense of Multaq, I feel it was what helped my cardioversions work and stick, following unsuccessful ones, but that’s another story.

I should have also mentioned that there also is some genetic component in my case as well.

Would you mind going into the lifestyle changes you made that have worked? What dietary changes did you make and what kind of diet do you now follow. Is it a strict diet (e.g. No more sugar ever?).

Did you make changes to reduce stress and slow down? Did you change jobs to a less stressful job or give up endurance exercise? Do you get more sleep? I would really like to know what you did to eliminate your Afib.

I’m surprised by the ‘blame the patient’ backlash. I see the message in the opposite light. It’s great news.

There’s a good chance that I can do something significant to improve my situation. With no drugs, no needles, 0 co-pay, and without one of those awkward gowns 🙂

That’s a fantastic message!

In my case, PVC’s in the evening are a sign that I need to step off the gas. A few nights of better sleep (and poor sleep usually comes along with the stress and extra work of pushing a deadline) makes them disappear every time.

I think the “blame the patient” message stings the most for those people who have AF not attributable to any of the usually-cited cofactors or causes. As Dr. Mandrola states, “To be clear, there exists a small minority of AF patients that have strong valvular or genetic or congenital causes of AF. ” Personally, I feel it is more than a small minority who have AF for unclear reasons where lifestyle changes will not make a difference. I wish the research and knowledge-base were better.

At the risk of attracting ire, I’ll point out that most of us (myself included) are very bad at objectively evaluating our own situation. We look around the office and say “I’m not working too hard” when all of us are burning the candle at both ends. We look around the restaurant and say “see, my diet isn’t so bad” when all of us have 1300 calories on our plates. We look around the gym and say “see, I’m not that out of shape” when we’re really seeing a typical cross section of our obese society.

Modern life has eliminated most of the limiting mechanisms that slowed us down as our bodies evolved. We work and play well into the night, we have constant access to abundant food, we typically move via machine instead of under our own power, and we enjoy a longevity of life that is unprecedented. All of this seems ‘normal’ to us, but it’s all very abnormal over the arc of human history.

Simply put, our bodies aren’t designed to handle all of this. Our version of ‘normal’ is quite unusual.

I know that small minority of AF patients exists. I strongly suspect that more than a small minority think they are in the small minority.

One other comment: I have doubts that Dr. Mandrola’s AF patient population is truly representative of the total AF population out there in the real world. I suspect he gets a higher percentage of the Type A overachievers/fat-cats than in the general population because those patients are precisely the ones most likely to be referred to, or to self-seek, a doctor such as Dr. Mandrola (prominent public profile and reputation).

and: “Earlier this month, I saw three AF patients in a row whose combined weight was more than a thousand pounds. Two of the three drank more than 3 bourbons nightly. One of them smoked.” Well, gotta love Kentucky, LOL. 🙂

This blog, I bet, is read by and commented on far more by otherwise truly healthy and engaged AF sufferers than by the lifestyle abusers. They’re too busy.

Those of us with a sincere interest in eating truly well know the value of VARIETY in diet. Some from this group resort to stultifying sameness in their personal menus for the sake of K stability AND get INRs all over the map nonetheless.

Dabigatran has tartaric acid added so that the needed 6.5% of the stuff in the teeny pellets in the giant capsule can actually be absorbed.
This product is ridiculous. The two “_bans” are more reasonable.
Six days on dabigatran can cause six months of diarrhea.

No one here has commented on the various researches that generally conclude that long-term (How long is that?) use of warfarin can result in osteoporosis and calcified arteries.
Is that a good trade-off??

I will assume the role of the AF patient in control and accept all blame for my condition. I did over drink, under exercise, overeat and ignore my health prior to this condition. It begs the question once again if lifestyle change does nothing to cure the condition, than do drugs stand a better chance? I am most disappointed to accept that fact I may have little control over my health and this condition. Eliminating triggers may not cure anyone of AF, however at some point we should arrive at the realization that anything beneficial is counted as good overall health whether or not AF is markedly reduced. I have the hope that eventually all that I am adding in the way of a good diet/supplements and reducing bad lifestyle/diet decisions, will defeat AF, but if not, I am the better for it.

You clearly must be paid by the makers of Pradaxa to be writing this nonsense! I am a newly retired cardiologist and I have been on Coumadin for 14 years, with a 6 month stint on Pradaxa that nearly killed me… I won’t get into the details but simply enough there is no antidote for these new NOACs and no way to monitor how it is interacting with ones body chemist. If someone simply has an decreased glomerular filtration rate (GFR) the drug can build up to a very dangerous and irreversible level with no way to detect this.

I managed thousands of patient’s anticoagulation therapy and found that the best out patient treatment was Coumadin with weekly patient self testing. I do this myself and it is as easy as a blood glucose test and takes no time to do, even when traveling. There are plenty of companies out there that do this and it costs patients and healthcare a whole lot less than the NOACs. If my patients were ever out of range I knew right away and easily adjusted their dosage to get them back in range. My patients enrolled with the weekly home testing program stayed in their safe therapeutic range about 85% of the time.

This is my big issue here with the RELY study, it is not reliable. Patients on Coumadin in the RELY study were in range less than 60% of the time! They do not specify how often patients were having their INR tested but I would put money on it that was at most once a month in a lab. If Pradaxa was compared to patients on Coumadin being safely monitored through weekly self testing the numbers would be hugely in favor of Coumadin being the safer choice. The STABLE study was published a number of months ago that actually takes a closer look at this and pokes all sorts of holes in the NOACs biased and flawed studies.

When we start thinking of our patients first maybe we will see some sort of change in the healthcare industry to “protect” instead of “profit”.

Dr Fletcher,
As a long-term warfarin user, I wonder if you might share the status of your arteries and of your skeletal health at this point in time. This scattering of articles tell a scarey tale.
Is it true?
Did you take measures to avoid these problems?

Thanks for those links! Invaluable stuff!

I will never take warfarin, or the others. I accept any and all risks, but believe that modern medicine is scary, imperfect, and grotesquely profit-driven, and very few practitioners have your long-term best interests at heart.

Dr. M is the rare and precious exception, IMO.

I will continue to take the supplement regimen that I have been on for 11 years, since having Stage 4 recurrent cancer, including Vitamin K & K2, as well as eating as many veggies and spices as I possibly can.

“Let food be thy medicine, and thy medicine be thy food.”
Hippocrates, 5th Century BC

As a patient I enjoy your blog but believe that EPs and cardiologists should educate patients about healthier life styles instead of lecturing us. That doesn’t help build a better Doctor-Patient relationship.

Also, what study or studies have been done that show only a small minority of Afib is do to “valvular or genetic or congenital causes”?


With all due respect, My experience as been that EPs and Cardios are not trained nor qualified to educate patients about nutrition, but to diagnose and prescribe drugs. Not a criticism just a fact.

OTOH, if you see a large enough population of low-risk patients with toenail fungus you will eventually see two of them have strokes. The “low-risk person who had a stroke” is frequently used to scare patients into believing that if they have arrhythmia, no risk above zero is low enough, but there are also low-risk people in sinus rhythm who have strokes, which doesn’t mean everyone should be on OACs. Healthy people with lone AF don’t have a stroke risk significantly higher than the general population of their age (which of course includes people with a variety of other risk factors), and even if one’s risk at 40 was raised to be comparable to that of a 60-year-old without AF, it might be reasonable to ask oneself whether one would take warfarin for life for the “condition” of being 60-plus. Someone who waits to take potent medication until his stroke risk is high enough that he’d consider it worth medicating if it was attributable to other risks will, among other things, run a lower risk of ending up with side effects that may develop with long-term use.

Excellent post. I take Pradaxa 110mg twice daily. My doctors believe it is safer than Coumadin in my case — I have micro-bleeding of the brain along with various heart problems. Last week I suffered a bowel obstruction, my intestine was closed down by a band that had formed around the intestine. I needed emergency surgery at 9 a.m., just less than 12 hours after taking my last dose of Pradaxa. Luckily the surgeons were exceedingly skillful and managed to remove the band without causing a great deal of tissue damage. Bleeding was minimal. As you say and as my doctors have made very clear to me: Medical decisions are a gamble — an exercise in probability. Having fine doctors helps to tip the odds in one’s favour.

Dr. John:
Thanks for taking the time to answer my post. I seem to have a knack for “stimulating” conversation.

The only categories I can put myself into are maybe the first group of people that push a little hard and have too much stress. I also have “treated ” sleep apnea that is related to the position of my jaw. I am muscular and in great shape. I have none of the bad habits you list. Cholesterol 146. HDL great. Blah blah blah. All that stuff. Coronary calcium scans good and yadda yadda…

Lately, I have been thinking about how much money I really need. I am driven and feel like I always have to be doing something to make more money. We have a large house in a top community. After retiring 11 years ago, I have been working providing professional services and hating it pretty much. I’ll be 66 in December, so I will have my retirement, social security, and a salary. My wife is also a professional. We have saved a lot of money and really don’t “need” a house this big. No-one needs to make this much money either. I’m not sure how I got on this ride. In reality, I want to just stay home and write… do things with my family. Maybe sail again. Those are the things I always enjoyed.

It was me that said we are “making ends meet”. Ha! Maybe the afib is my body saying something to me. I know you got my attention with your “frowny face” crowd comment. I will think this some more. Maybe I’ll apply for a job writing advertising for Boehringer Ingelheim (only kidding!).

One last thing, you said-

“I have had two low-risk AF patients suffer major strokes while taking dabigatran. Other colleagues have reported similar anecdotes.”

“Yes, I have seen patients who have had strokes on therapeutic warfarin, but it is rare–and these patients have been high-risk older patients.”

just want to be clear… you are saying that you and your colleagues are seeing a higher rate of strokes in patients on Pradaxa, including low risk patients, and rarely see strokes with patients on Coumadin under your care? That is very important for me to know as it contradicts the trials and what your expectations were of Pradaxa in the past. I think it is important for you to clarify your position if you have CHANGED your mind on use of Pradaxa based on real life experience. If Coumadin is better, I’ll buy one of those home INR monitoring kits.


A note of encouragement, in case you decide to slow down a bit. Lots of people die with extra cash saved. No one dies with extra time.

Time is the real currency we have to spend in life, and no one knows how much we have in the bank. Don’t squander it.

Great conversations, and, as usual, great post Dr. John. In my practice (Int Med, not Cards) I have seen more patients on Pradaxa suffer strokes, relative to my far larger population on warfarin. Anectdotal, yes, but after a while in practice you tend to notice these “trends.”
Also, all of my patients can use any supplements and eat as many green leafy veggies as they want. We just check INRs a bit more frequently. I was on warfarin for 6 months (DVT), and had no issues eating veggies and salads…Yes, it does take a little attention, but it is not a difficult task.
I didn’t appreciate your “blame the patient” tone. If I were an AF patient, perhaps I would be more sensitive to this. Truth be told, many conditions (perhaps most) are catalyzed, if not caused, by poor lifestyle choices. We do need to take responsibility for these. I do blame myself for my metabolic issues. Genetics may set you up, but often we accelerate the disease trajectory by our poor choices. I don’t know enough about AF precipitants, but do know about metabolic disorders.

Pradaxa has moved down in your mind, okay. But I can’t get the old quotes of yours (see below) about “rat poison” out of my head. Did Coumadin suddenly become attractive? For us patients, it is disheartening to think rat poison is our best choice. I think it would be great if you and other doctors would use social media to share your experiences with other doctors/patients and take a position on the safety and effectiveness of all the anticoagulants. If you sent out a clear message about your experiences with these drugs it would save lives. There should be enough history to come out with some data and findings, particularly with Pradaxa, as it has been out 4 years. Data viewed objectively from your population of afibbers is not anecdotal. If the same pattern is showing up among many EPs, that is something that should be shared. Don’t EPs talk about this stuff? As you say, stroke is the worst and irreversible outcome, and preserving the brain is the most important goal.

“From the beginning, warfarin was known as the active ingredient in rat poison; this has been (and still is) a tall hurdle to overcome. Moreover, everyone seems to know someone who was ‘killed’ by warfarin.”
“How much extra out-of-pocket cost will patients tolerate to free themselves from “rat poison,” and to reap the benefits of dabigatran’s improved stroke prevention and lower risk of intracranial bleeding?”
“Though all that high-tech stuff is exhilarating, it’s fair to say that the most remarkable thing in AF medicine today is the novelty of thinning the blood with a pill that isn’t rat poison.”
“For my entire career, I have heard the downsides of warfarin. Now, we have two drugs that prevent more strokes than warfarin, don’t require blood checks, have no dietary interactions, minimal drug-drug interactions and are not used to poison rats. Do they worsen bleeding when one falls? Yes. So does warfarin.”
“Patients will have before their eyes a clearly superior drug with less bleeding risk –a substitute for rat poison.”
“Until only four months ago, the only way to prevent stroke in patients with AF was to use a rodenticide. No one likes warfarin (Coumadin). Doctors don’t like it because of its variable effects, risk of under or over-treatment, and multiple drug/dietary interactions. In the best case, in closely supervised clinical trials, warfarin-treated patients are in therapeutic range only two-thirds of the time. Patients dislike warfarin because of the hassle of frequent INR measurements, and because they are scared to take a drug which can cause excess bleeding. Who wants to take a rat poison?”
“Dr Relman makes a huge deal of the fact that the authors did not discuss one subgroup (the Euro cohort), nor did they point out that warfarin dosing was off in 1/3 of the patients. Since when is cherry-picking one subgroup allowed? And I’m not sure about in Cambridge, but here in the east end of Louisville, 65% in range with warfarin is pretty good. Is he really touting warfarin? Or worse: that developing novel new blood-thinners that compete with rat poison lies at the crux of our healthcare crisis?”

Call the CDC, AHA, AMA, state police, FBI and CIA!! A medical doctor suggesting that just maybe patients change their lifestyle and diet instead of coming at us with a vile full of Pharmed product? Say it aint so Joe!

Thanks for the corrections. I updated an article we wrote on Also, I quoted your bit about warfarin and vitamin K and posted on our A-Fib News page.
Patti Ryan
A-Fib, Inc.
Publisher of ‘Beat Your A-Fib: The Essential Guide to Finding Your Cure’ by Steve S. Ryan, PhD

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