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Atrial Fibrillation and Stroke

January 2, 2014

My mother is a smart woman.  All her life she has valued intellectual pursuits above all else.  She is an accomplished pianist and teacher.  She can do my father’s taxes and diagram sentences.  She is getting older.  Her greatest fear is to have a condition that leaves her mentally incapacitated.  She has Atrial Fibrillation.

Jane Brody of the New York Times recently wrote a very nice summary of atrial fibrillation (AF for short).  In it she discusses the risk of stroke in patients who have AF.  Some estimate that one in every 5 or 6 strokes is a result of AF.  This is because the atrium of the heart, where blood goes before it flows into the ventricles and is pumped out to the body, is not pumping normally in AF.  It is sort of jiggling ineffectively.  This causes a ripple effect like you see in rivers, where flowing water in the middle of the stream is contrasted with slowly moving or standing water on the edges.  In the case of blood, stasis causes the blood to clot, or form lumps.  If the lumps stay in the atrium it’s ok, but every so often one of those clots can break off and journey into the ventricle, and thus out into the body.  The clot flows along until it runs into a vein or artery that is too small and the clot gets caught and blocks the flow in that vessel.  If that vessel is in the brain, a stroke, or decrease in blood flow to a part of the brain, results.

This is why people with AF often take a blood thinner, or anti-clotting agent.  So that pooling blood does not clot.  The problem with that of course is that the drugs that we use cause ALL blood to not clot, not just the blood in the atrium.  So if you are on a blood thinner and you fall and hit your head, a relatively small problem can get very big very fast if the vessels in your head get broken and blood doesn’t clot.  Hmm.  So if you don’t take the blood thinner you could get a stroke, but if you do you could get bleeding in your brain.  Either way it sucks.

So you try to mediate the effect of the drug by measuring how much is there and getting the amount just right.  The drug most often used is called Warfarin, or Coumadin.  This drug is a pain in the tuckus.  Everybody metabolizes it slightly differently, so you don’t know how much to take at first, so you’re in the doctor’s office every week or so getting lab tests to determine how well it’s working.  Plus, Warfarin has interactions with a lot of other drugs AND has interactions with some foods as well, muddying the waters even further.  In short, having a diagnosis of AF chains you to the health care system pretty tightly.  If the risk of having a stroke is the worst thing you can think of.  Like for my mother.

There are, of course, newer drugs that purport to do the same thing that Warfarin does, and better.  They have ridiculous names like Dabigatran, Rivaroxaban, Edoxaban, and Apixaban, and since nobody can pronounce those we doctors just call them “Novel Oral Anticoagulants” and because that’s too long to write we shorten it to NOAC.  We doctors are not so creative with names.  Are these drugs better?  The same?  Worse?  They’re certainly more expensive.  So I go to my cardiologist blogger friend John Mandrola.  He writes at Dr.JohnM and, among other places.  Here is what he says:

“An AF patient who has accepted the net benefits of anticoagulation (an important decision in and of itself) wants to know something simple: what is the risk of an event [stroke or bleed] on a novel anticoagulant vs warfarin? That’s how they judge value. It’s also how payers judge value.”

My mother has accepted the net benefits of anticoagulation.  She hates sitting in the lab every week.  There are these drugs that cost 50 times as much but reduce the hassle factor by multiples.  Is it worth it to go for the new thing?  How does she choose? She wants to know this very simple thing:  Is my risk of a stroke or a bleed in my brain on NOACs higher, lower, or the same as with warfarin?  You gotta read this analysis by Dr. Mandrola (at or medscape.  Of course with medscape you have to have an account.  But it’s free).  The article is called Novel Oral Anticoagulants vs. Warfarin: The Truth is Relative.  It’s fantastic, even if I don’t understand the math.

Here’s what the drug makers say:

Dr Saurav Chatterjee (Brown University, Providence RI) and colleagues studied the risk of ICH in AF patients treated with either novel anticoagulants or warfarin. They used the phase 3 randomized clinical trials that compared the three FDA-approved novel anticoagulants and warfarin (edoxaban is still investigational). Publishing in JAMA Neurologythey also reported that novel anticoagulant therapy reduced the relative risk of ICH by 50%.”

Wow.  That sounds awesome and worth it!  To a person without Dr. Mandrola’s prodigious mathematical abilities that sounds like the new drugs decrease the relative risk of bleeding (ICH) by 50%.  That’s what the literature from the drug makers is going to say.  But this is misleading.  It turns out that for any individual patient the chance of not having either a stroke or an ICH (the absolute risk) is about 99% for both NOACs and Warfarin.  The drugs are effectively the same.  Now, the hassle factor might be significant enough to convert those who have really awesome health insurance or can afford to pay out of pocket.  The hassle factor argument is a fair one.  The effectiveness argument is not.

All this is to point out, as Dr. Mandrola does, that all the research in the world doesn’t help the patient sitting in the office if the doctor can’t or won’t explain the data in a way that makes sense for the individual.  This requires understanding the way the studies are constructed and evaluated or, like me, running them by someone who does.  This applies to patients as well.  If my mother had heard of these NOACs and looked them up on the web, it’s very likely she would have gotten industry statistics.  Any time you (the patient) go on-line to check out the latest drugs, please be aware that the data presented are NOT interpreted for YOU.  Beware of data.  Get facts whenever possible.



From → Healthcare

  1. thetinfoilhatsociety permalink

    Wasn’t it Churchill who said “Lies, damned lies, and statistics!” regarding data…? 🙂

  2. Phillip Gale permalink

    The information that kept us with warfarin was how fast the effects of the drug could be reversed in case a a bleeding situation. Our understanding is that the NOAC drugs do not reverse easily or quickly. That is too big a risk for us so we put up with the hassle of regular blood test.

  3. Jeff permalink

    One tie-breaker that hasn’t been considered here is the prospect of having your vasculature calcify due to the long term effects of warfarin.

    Warfarin is effective because it is vitamin K antagonistic. But K is much more than a coagulation factor. K1 and particularly K2 see to it that calcium is handled properly in our bodies — namely, that it winds up in our bones and not our arteries.

    Little enough effort has gone into research on this, but even less to let the public know of it. I’d like to see some sophisticated math on stroke vs coronary artery calcification while on warfarin, and then while on the alternatives.

    PS. Come on, “warfarin” is not a ridiculous name??

    • Thanks for reading Jeff! I had actually forgotten that vascular calcification was an issue with Warfarin. Thanks for pointing it out. And yes, Warfarin is a terrible name, but at least it has the appropriate ratio of consonants to vowels. 😉

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