Are you taking the blood thinner warfarin to manage your risk of clots and A-Fib stroke? Have you been told to avoid foods with vitamin K to prevent excess clotting? Want to know the facts about warfarin and vitamin K? Take our 5 question quiz to separate the facts from the myths.
A 5 Question Quiz about Warfarin and Vitamin K
1. True or False: Warfarin and vitamin K actually work against each other in your body.
True. Vitamin K helps your blood clot. Warfarin makes your blood clot more slowly. Your INR level is monitored to keep them in balance.
2. True or False: When taking warfarin, you should limit foods with high levels of vitamin K like dark, leafy greens.
False. You don’t need to avoid foods with vitamin K. The key is to consistently maintain your daily level of vitamin K.
Don’t confuse vitamin K with the K on the periodic table for potassium. One’s a vitamin, the other is a mineral.
3. True or False: Vitamin K information is not included on most packaged food nutritional labels.
True. So it’s often hard to determine the amount of vitamin K in your food.
by Steve S. Ryan, PHD, October 2015, Updated January 26, 2016
According to recent studies, you are better off having a Watchman device installed than spending a lifetime on warfarin.
In two randomized clinical trials comparing Left Atrial Appendage Closure (LACC-Watchman Device) to warfarin, 1,261 patients from the PROTECT AF and PREVAIL trials were studied. The follow-up period was around 3.3 years. Patients receiving the Watchman compared to patients on warfarin had significantly fewer:
• Hemorrhagic strokes
• Cardiovascular/unexplained death
• Non-procedural bleeding
• All-cause stroke or systemic embolism was similar between both strategies.
There were more ischemic strokes in the Watchman device group, but this was balanced by a greater number of hemorrhagic strokes in the Warfarin group.
However, the patients in the control group of the PREVIAL trial were considered “unusual” in that, given their risk profile, they had a much lower ischemic stroke rate than ever observed in any clinical trial. See Getting FDA Approval for the Watchman Device.
What Patients Need to Know: Watchman Actually Better Than Warfarin
The Watchman device provides similar protection against having an A-Fib (ischemic) stroke as being on warfarin.
But the Watchman device isn’t simply an “alternative” to warfarin, but rather an improvement or advance or progression. One would intuitively expect that people receiving the Watchman device would also have less hemorrhagic strokes and bleeding compared to those on warfarin, which these studies do demonstrate.
Welcome Alternative to a Lifetime on Warfarin
Warfarin and other anticoagulants work by causing bleeding and are inherently dangerous. The Watchman device is not only a welcome alternative to a lifetime on warfarin, but is actually better than warfarin.
Long-term use of anticoagulants such as warfarin have been known to not only cause hemorrhagic strokes but also microbleeds in the brain which lead to dementia.
Among other bad side effects, long-term use of anticoagulants such as warfarin have been known to not only cause hemorrhagic strokes but also microbleeds in the brain which lead to dementia. See Patient on Anticoagulation Therapy for 10 Years Develops Microbleeds and Dementia.
A 2015 study found evidence of microbleeds in 99% of subjects aged 65 or older, and that increasing the imaging strength increased the number of detectable microbleeds. Microbleeds have been suggested to be predictive of hemorrhagic stroke.
According to current research, you are better off having a Watchman device installed than spending a lifetime on warfarin. (Of course, this assumes that the doctor performing the procedure is beyond his/her learning curve. That is, when operating doctors are first performing the procedure, there is a higher risk for procedural complications.)
What About the New Anticoagulants (NOACs)?
Does this research apply to the new anticoagulants like Pradaxa, Xarelto, Eliquis and Savaysa/Lixiana? Technically no. This research only applies to warfarin. But intuitively one would expect the same general principles to apply. All anticoagulants cause bleeding. That’s how they work.
Caveat—Long-Term Effects of Watchman?
What are the long-term effects of leaving a mechanical device like the Watchman inside the heart? We know that, after a few months, heart tissue grows over the Watchman device so that the LAA is permanently closed off from the rest of the heart.
It seems unlikely that complications would develop after a long period of time as has happened with warfarin. But we can’t say that for sure until enough time has passed. The first clinical trial installation of the Watchman device in the US was in 2009 and in Europe in 2004. So far no long-term complications have developed.
Preventing Stroke in the Elderly—Even If They Don’t Have A-Fib!
One of the great potentials of the Watchman device is that it may someday be used to prevent stroke in the elderly even if they don’t have A-Fib. Imagine a world where you no longer live in fear of a stroke as you get older, where 90%-95% of stroke risk can be eliminated by a simple 20 minute procedure. The Watchman device (and other Left Atrium Occlusion Devices such as the Lariat and the surgical AtriClip) may change the way elderly medicine is practiced.
How many people turning 70 or 75 would welcome a device that would almost guarantee freedom from the most severe type of ischemic stroke (a cardioembolic stroke)? The Watchman device has the potential to greatly reduce or eliminate the threat of strokes in the elderly!
Stop Taking Warfarin―Produces Arterial Calcification
The blood thinner, warfarin (Coumadin) is a “vitamin K-antagonist” which works by blocking vitamin K (i.e., K-2, menaquinone), thereby affecting several steps in the anticoagulation pathway and decreasing clotting proteins in the blood.
But vitamin K is also essential for heart and bone health. Vitamin K determines whether we maintain strong bone density and soft pliable tissues. Without enough K-2, osteocalcin, a protein that binds calcium to bone, doesn’t function. This vascular calcification produces plaque and reduces aortic and artery elasticity.
“When calcium doesn’t stay in bones, it can end up clogging your arteries, causing a heart attack or stroke.”
Warfarin Blocks Vitamin K: Deposits Calcium in Arteries
By blocking vitamin K (K-2), warfarin deposits calcium in our arteries and progressively turns them into stone. In the absence of vitamin K, bony structures form in soft tissues. When you hear the term “hardening of the arteries,” this means that previously flexible blood vessels are turning into rigid (calcified) bony structures.
In a study of 451 women using mammograms to measure arterial calcification, after just one month of warfarin use, arterial calcification increased by 50% compared to untreated women. After five years, arterial calcification increased almost 3-fold.
Why You Should You Stop Taking Warfarin
If you are taking warfarin (Coumadin), you should talk to your doctor about switching to Eliquis (apixaban) which tested the best of the NOACs and is the safest. (See my article, Warfarin and New Anticoagulants.)
The new oral anticoagulants (NOACs) do not block vitamin K. But the NOACs do have drawbacks. In the case of severe bleeding, there is currently no antidote or reversal agent like there is for warfarin (a reversal agent for the direct factor Xa inhibitors Xarelto and Eliquis is close to FDA approval).
Added 2015: The FDA approved a reversal agent Praxbind for the NOAC Pradaxa Oct. 16, 2015. In clinical trials, 5gs of Praxbind (idarucizumab) administered by IV reversed the anticoagulant effect of Pradaxa within minutes (which is significantly faster than the current antidotes for warfarin).
Whether or not to be on an anticoagulant and which one to take is the most difficult decision you and your doctor have to make (and your initial decision may change over time as your body changes.)
If you aren’t happy with your doctor’s response, get a second opinion. You need to feel confident and at peace with this decision.
Atrial Fibrillation patients often search for unbiased information and guidance about medicines and drug therapy treatments. These are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer.)
11. “I am on Coumadin (warfarin) to thin my blood and prevent A-Fib blood clots. Do I now need to avoid foods with Vitamin K which would interfere with the blood thinning effects of Coumadin?” UPDATED
12. “The A-Fib.com web site claims that an A-Fib stroke is often worse than other causes of stroke. Why is that? If a clot causes a stroke, what difference does it make if it comes from A-Fib or other causes? Isn’t the damage the same?“
16. “I have to be on aspirin for stroke prevention. Which is better—the low-dose baby aspirin (81 mg) or a high dose (325 mg)? Should I take the immediate-release (uncoated) or the enteric-coated aspirin?”
17. “I don’t want to be on blood thinners for the rest of my life. I’ve had a successful catheter ablation and am no longer in A-Fib. But my doctor says I need to be on a blood thinner. I’ve been told that, even after a successful catheter ablation, I could still have “silent” A-Fib—A-Fib episodes that I’m not aware of. Is there anything I can do to get off of blood thinners?“
21. “I”ve read about a new anticoagulant, edoxaban, as an alternative to warfarin (Coumadin) for reducing risk of stroke. For A-Fib patients, how does it compare to warfarin? Should I consider edoxaban instead of the other NOACs?”
Last updated: Wednesday, May 25, 2016
13. “After my cardioversion, my doctor kept me on Coumadin for a month. Why is that required? They mentioned something about a “stunned atrium. What is that?”
A “stunned atrium” is medically defined as a “state of temporary mechanical atrial dysfunction with preserved bioelectrical function.” In non-medical terms your heart doesn’t contract properly even though it is getting the right electrical and chemical signals to contract.
This can happen after an electrical cardioversion and is why the left atrium and, in particular, the Left Atrial Appendage tend to develop clots after an electrical cardioversion. The left atrium, and especially the Left Atrial Appendage, is “stunned” after the electrical shock and may not contract and pump out properly.
Clots can develop and be released when the LAA starts to contract again. That’s why you need to be on a blood thinner like Coumadin (generic name: warfarin) for a month after your electrical cardioversion.
Thanks to David Mobley for this question.
Dabek, J. et al. Cardioversion and atrial stunning. Pol Merkur Lekarski. 2007 Mar;22(129):224-8. PMID: 17682682 (PubMed – indexed for MEDLINE)
Grimm RA et al. Impact of electrical cardioversion for atrial fibrillation on left atrial appendage function and spontaneous echo contrast: characterization by simultaneous transesophageal echocardiography. J Am Coll Cardiol. 1993 Nov 1;22(5):1359-66. PMID 8227792
Return to FAQ Drug Therapies
10. “I’m worried about the risk of bleeding. I have to take the blood thinner warfarin ( Coumadin). If I cut myself, do I risk bleeding to death?”
In general, no.
On a normal dosage of warfarin (Coumadin) you will bleed longer if you cut yourself (minor wound). But your blood will still clot.
You will also bruise more easily. You should stay away from contact sports like hockey, football, rugby, etc. or activities where you could easily injure yourself like mountain climbing, competitive biking, etc. (Professional athletes should not be on warfarin). But you can do normal daily activities on warfarin.
However, you may want to get a Medical ID Alert wallet card, bracelet or dog tag. Then, in case of an emergency, paramedics and doctors will know you’re taking a blood thinner.
If you do have a more serious injury, you are definitely more at risk to bleed to death than if you weren’t on warfarin.
If you’re taken to an Emergency Room for treatment, most ER personnel are experienced in using proven antidotes to reverse the blood thinning effects of warfarin. But depending on the seriousness of your injury, there’s no guarantee the reversal agents for warfarin will work in time.
(The newer anticoagulants like Pradaxa, Xarelto, Elquis unfortunately have no proven antidote. Pradaxa in particular seems to be associated with many deaths in the ER where doctors currently have no way to stop people from bleeding to death. See my article, Stop Prescribing or Taking Pradaxa)
Return to FAQ Drug Therapies
8. “I’m on warfarin. Can I also take aspirin, since it works differently than warfarin? Wouldn’t that give me more protection from an A-Fib (ischemic) stroke?”
No, combining is dangerous.
Preliminary research indicates that combining anticoagulants (warfarin) and antiplatelets (aspirin) in the same patient is associated with a substantially higher risk of fatal or non-fatal internal bleeding.
There’s no indication that combining warfarin with an antiplatelet (aspirin, clopidogrel, or both) reduces the risk of ischemic stroke.
Added 8/10/15. Aspirin is no longer recommended as first-line therapy:
Aspirin has been downgraded from class 1 in the 2006 guidelines to class 2B in the 2014 guidelines.
In a Danish registry study, aspirin didn’t show any benefit for stroke prevention.1 And in the European ESC guidelines, aspirin is not recommended as first-line therapy for patients with a CHA2DS2-VASc score of 1.2
Return to FAQ Drug Therapies
- Olesen, JB et al. Risks of thromboembolism and bleeding with thromboporphylaxis in patients with atrial fibrillation: a net clinical benefit analysis using a ‘real world’ nationwide cohort study. Thromb Haemost 2011;106:739-749↵
- Camm, AJ et al. 2012 focused update of the ESC Guidelines for the management of atrial fibrillation: an update of the 2010 ESC Guidelines for the management of atrial fibrillation. Developed with the special contribution of the European Heart Rhythm Association. EUR Heart J 2012;33:2719-47↵
7. “What’s the difference between warfarin and Coumadin?”
“Warfarin” is the name of the generic medication, whereas “Coumadin” is the brand name. In general, generic medications are very similar to the brand name medications.
There is anecdotal testimony that Coumadin may be more effective than warfarin. It’s up to you and your doctor to determine which is better for you.
Return to FAQ Drug Therapies
6. “Which is the better anticoagulant to prevent stroke in atrial fibrillation patients—aspirin or warfarin (Coumadin)?”
See August 2015 update below.
People with less risk factors for stroke are sometimes put on aspirin. People more at risk for stroke such as those over 65 years old with frequent A-Fib episodes are often on warfarin (Coumadin) (baring other risk factors such as peptic ulcer, etc.).
Aspirin and warfarin work differently.
Aspirin is an antiplatelet drug that decreases the stickiness of circulating platelets (small blood cells that start the normal clotting process), so that they adhere to each other less and are less likely to form blood clots.
Whereas warfarin (brand name Coumadin) is an anticoagulant that works by slowing the production of blood clotting proteins made in the liver.
Current research indicates that aspirin is not as effective in preventing blood clots (and therefore, strokes) as Coumadin.
Younger people with a low risk of an A-Fib stroke “appear to derive little benefit from warfarin. And, indeed, warfarin may do more harm (intracranial hemorrhage) than good (prevention of ischemic A-Fib stroke).”
Bottom line: Weighing the various risk/benefit ratios is a decision for you and your doctor and may change as you grow older.
August 2015 Update: Aspirin is No Longer Recommended as First-Line Therapy for A-Fib
Aspirin is no longer recommended as first-line therapy for Atrial Fibrillation patients according to the 2014 AHA/ACC/HRS Treatment Guidelines for Atrial Fibrillation. Though not a new finding, it should be noted that aspirin has been downgraded to a class 2B drug.
A similar directive is included in the 2012 European ESC guidelines for the Management of Atrial Fibrillation: aspirin is not recommended as first-line therapy for patients with a CHA2DS2-VASc score of 1.
Aspirin is not appropriate for people who are at low risk of cardiovascular disease and stroke. For these people, the risks of gastrointestinal bleeding and hemorrhagic strokes outweigh any potential benefit. “Among the more than 16,000 deaths each year linked to bleeding…,about one-third of those deaths occur in those who take low-dose (81-mg) aspirin.” The FDA in 2014 warned against widespread use of aspirin in people of average risk.
Aspirin also causes stomach ulcers in 13% of those using it. And these ulcers usually develop without any warning symptoms. Many of these ulcers will cause a serious stomach bleed at some point. Also, taking low-dose aspirin on a regular basis more than doubles your risk of developing wet macular degeneration. On the positive side, people regularly taking low-dose aspirin have a significantly lower chance of getting cancer. But according to Dr. Randall S. Stafford of Stanford, “no one should take daily, low-dose aspirin solely for the purpose of preventing cancer.”
When is aspirin appropriate? Aspirin is recommended for “secondary” prevention of cardiovascular disease such as to prevent reoccurrence of a stroke or heart attack. Aspirin significantly reduces the risk for a second heart attack or stroke.
Return to FAQ Drug Therapies
Last updated: Thursday, September 24, 2015
5. “Should everyone who has A-Fib be on a blood thinner like warfarin (Coumadin)?”
Not necessarily. The biggest danger of A-Fib is the increased risk of stroke, because your heart isn’t pumping out properly.
A blood thinner is used to help protect you from stroke. Your doctor will evaluate your risk of an A-Fib related stroke. If you are young, athletic and in overall good health, your doctor may rate your risk of stroke as low and not put you on a blood thinner.
See, also, the FAQ question “Which is the better anticoagulant to prevent stroke?”
Return to FAQ Drug Therapies
By Steve S. Ryan, PhD, updated March 2015
Do you hate having to take Coumadin or other blood thinners? Hate the side effects? Or are you allergic to them? A replacement to taking blood thinners is the Watchman, an occlusion device.
The theory behind the WATCHMAN™ LAA closure technology is that most A-Fib clots originate in the Left Atrial Appendage (LAA). The Watchman closes off the LAA where 90-95% of A-Fib strokes come from. It’s a very low risk procedure that takes as little as 20 minutes to install. Afterward, you would usually not need to be on blood thinners.
How It Works
The Watchman device comes in multiple sizes from 21mm to 33mm to accommodate the different sizes of LAAs. Once a patient’s Left Atrial Appendage is measured, a wide-sheathed catheter with a spline is used to insert the Watchman device which has a self-expanding Nitinol (a special metal) open-ended circular frame.
The atrial surface of this frame is covered with a thin, permeable 160 μm (micron) pore filter made of polyester material (Polyethylene Terephthalate known as Dacron or PET). This filter allows blood to pass through while stopping clots. Little hooks or anchors called fixation barbs at the middle of the device make sure it is attached firmly to the LAA wall.
Before the catheter is removed (which fixes the Watchman in place), contrast agents are used to make sure the Watchman is stable and entirely closes off the LAA opening. Over time heart tissue grows over the polyester (PET) material so that it completely closes off the LAA with smooth heart tissue similar to other heart surfaces.
In this Occlusion image, heart tissue has completely covered the Watchman device after only nine months.
Patients on Coumadin continue to take it for six weeks after the Watchman device is inserted. They are then examined using a TEE (Transesophageal Echocardiogram) to make sure there is complete closure of the LAA. At that time they are taken off of Coumadin and put on a different type of blood thinner called clopidogrel (Plavix) until six months after the implant procedure.
Think of the Watchman as a replacement for blood thinners; both reduce but do not totally eliminate the risk of stroke. The stroke risk is reduced to that of a person with a normal heart.
Even while you are waiting for or trying to decide on having a Pulmonary Vein Ablation, you can have the Watchman inserted and reduce your stroke risk to that of a person without A-Fib.
Just as closing off the LAA is standard practice in the Cox Maze/Mini-Maze operations, in the future, the Watchman device could become part of most catheter ablation procedures. If included with the ablation procedure, the Watchman would protect the patient from blood clots even if the catheter ablation procedure was unsuccessful. The Watchman device may become standard therapy for anyone at risk of a stroke, not just for people with A-Fib.
For a list of US doctors installing the Watchman device, go to Steve’s Lists/Doctors Installing the Watchman Device.
Update: The U.S. Food and Drug Administration (FDA) approved Boston Scientific’s WATCHMAN™ LAA closure technology for use in the U.S. on March 13, 2015. It has been available internationally since 2009. The FDA approval of the WATCHMAN device is based on the clinical program which consists of numerous studies, with more than 2,400 patients and nearly 6,000 patient-years of follow-up. The Watchman device will be available first at U.S. centers where it has been used in clinical studies.
ATRIA Findings: Anticoagulants for Stroke Prevention Versus Risk of Intracranial Hemorrhage
Anticoagulants are prescribed for Atrial Fibrillation patients to reduce the risk of clots and stroke. But anticoagulants can also increase the risk of intracranial hemorrhage. So, who benefits and who may be harmed?
The “AnTicoagulation and Risk Factors in Atrial Fibrillation” Study (ATRIA) has contributed significantly to better understanding which A-Fib patients will benefit most from anticoagulant therapy.
A-Fib and Stroke Risk
As a consequence of atrial fibrillation, the pooling of blood in the atrial chambers of the heart significantly increases the risk of formation of blood clots. If a piece of a blood clot breaks off and travels to the brain it can occlude (block) a blood vessel and prevent blood from reaching the affected area of the brain. This condition is known as an ischemic stroke and can cause severe disability including the inability to walk or talk.
Ischemic Stroke Versus Intracranial Hemorrhage
In order to reduce the risk of ischemic stroke in people with atrial fibrillation, anticoagulant (blood thinner) medications are often prescribed. The most commonly used blood thinner is warfarin (Coumadin) although aspirin may also sometimes be used. While blood thinners can prevent ischemic stroke in people with atrial fibrillation, paradoxically, they can also cause bleeding into the brain, a condition known as intracranial hemorrhage.
Unfortunately, doctors don’t have a fool-proof method of determining which patients with atrial fibrillation will benefit from blood thinners (prevention of ischemic stroke) and which patients may be harmed by blood thinners (cause an intracranial hemorrhage).
Clearly, more research is necessary to more accurately identify those patients who would benefit the most from taking blood thinners as opposed to those who are more likely to be harmed by taking blood thinners.
The “AnTicoagulation and Risk Factors in Atrial Fibrillation” Study (ATRIA)
The “AnTicoagulation and Risk Factors in Atrial Fibrillation” Study (ATRIA) published in 2009, by a collaborative group of researchers from the Massachusetts General Hospital, the University of California at San Francisco, and Kaiser Permanente of Northern California, has contributed significantly to better understanding which patients with atrial fibrillation would benefit most from receiving anticoagulants for stroke prevention.
The study population consisted of 13,559 people with atrial fibrillation with a median age of 73 years. Twenty (20) percent of the subjects had no major risk factors for ischemic stroke. The major risk factors for ischemic stroke include older age (75 years or older), previous history of stroke, diabetes, hypertension, and congestive heart failure. This stroke-risk classification system is known as the CHADS2 grading system and is used by doctors as a basis for classifying patients with atrial fibrillation into stroke risk categories (low, intermediate, or high).
The researchers followed the clinical course of these 13,559 patients for a median of 6 years. At the time of enrollment into the study, 53% of the subjects were receiving warfarin (Coumadin) as prophylaxis for stroke prevention. During the follow-up period, the researchers identified a total of 1,092 thromboembolic events (occlusion of a blood vessel by a blood clot) among the study subjects, the overwhelming majority of which (1,017 cases or 93%) were ischemic strokes. Of the patients who experienced a thromboembolic event, 37% were receiving warfarin and 63% were not receiving warfarin.
The researchers also identified 299 patients among the study cohort who experienced an intracranial hemorrhage, of which 193 patients (65%) were receiving warfarin.
ATRIA Study Key Findings
The major findings of the study can be summarized as follows:
• The greatest benefit of anticoagulation therapy for the prevention of ischemic stroke was observed among patients with a history of ischemic stroke and those in the highest stroke risk category as determined by the CHADS2 stroke-risk grading system.
• In general, the net benefit of receiving warfarin anticoagulation therapy increased with advancing age. Patients with atrial fibrillation in the oldest age group (85 years of age or older) derived more benefit from warfarin prophylaxis than patients in the 75 to 84 year age group, although the benefits of warfarin prophylaxis was apparent in this age group as well.
• This finding strongly suggests that elderly people with atrial fibrillation who are not taking warfarin are at increased risk for ischemic stroke, however, adding warfarin for prevention of ischemic stroke in elderly people does not significantly increase the risk of intracranial hemorrhage.
• Younger people with atrial fibrillation (64 years or younger) who are considered at low risk for developing an ischemic stoke as measured by the CHADS2 stroke-risk grading system, appear to derive little benefit from warfarin prophylaxis and, indeed, adding warfarin may do more harm (intracranial hemorrhage) than good (prevention of ischemic stroke).
Who Will Benefit, Who May Be Harmed
In summary, this study has contributed significantly to more clearly identifying which patients with atrial fibrillation will derive the most benefit from warfarin anticoagulation therapy and which patients may be harmed by this treatment.
If you have atrial fibrillation, talk to your doctor about the risks and benefits of taking blood thinner medications. In general, older people and those at highest risk for ischemic stroke as determined by the CHADS2 stroke-risk grading system will gain the most from anticoagulation therapy.
Blood thinners, however, may not be advantageous and may cause more harm than good in younger patients with atrial fibrillation who are considered to be at low risk for developing an ischemic stroke.
Last updated: Sunday, February 15, 2015