We’ve added a new FAQ and answer to our section, Mineral Deficiencies & Supplements:
“I’m taking Eliquis for my risk of A-Fib stroke. I’m interested in the supplement, Krill Oil, that has natural blood thinning properties. Is It OK to take Krill Oil along with Eliquis?
Krill Oil and Eliquis Work Differently
The supplement, Krill Oil, is similar to fish oil. Both contain omega-3 fatty acids. Fatty acids are thought to make blood platelets less sticky, and thus are less likely to form clots. Krill Oil is considered superior to fish oil for not accumulating toxins the same way fish do.
Eliquis is an anticoagulant, a ‘Direct Factor Xa Inhibitor’, and affects only one stage in the anticoagulation process (the stage after platelets do their part). It works to slow or stop clotting proteins (like fibrin) from binding together and forming a clot.
13. “I’m taking Eliquis for my risk of A-Fib stroke. I’m interested in the supplement, Krill Oil, that has natural blood thinning properties. Is It OK to take Krill Oil along with Eliquis?
I wish I had a more definitive answer for you. Here’s what we know.
Krill Oil and Eliquis Work Differently
The supplement, Krill Oil, is similar to fish oil. Both contain omega-3 fatty acids. Fatty acids are thought to make blood platelets less sticky, and thus are less likely to form clots. Krill Oil is considered superior to fish oil for not accumulating toxins the same way fish do.
Eliquis: No Method to Measure Anticoagulant Effect
The anticoagulant, warfarin, has ‘one’ but Eliquis doesn’t. The effectiveness of warfarin can be determined by blood tests measuring INR levels. By comparison, there’s no method to measure Eliquis’ anticoagulant effect (or any of the new NOACs).
Antiplatelets vs Anticoagulants
We know that Krill Oil and Eliquis work differently. Krill Oil affects the clumping of blood platelets. Eliquis (and all NOACs) affect the anticoagulant process.
Intuitively one would think that since Eliquis and Krill Oil affect different stages in the anticoagulant process, it might be OK to use them together. But Eliquis is so new we have little research to definitively say this.
Bottom line: We can’t measure how Krill Oil affects the anticoagulation process when taking Eliquis.
Discuss with your Doctors
Ask your doctors about taking Krill Oil along with Eliquis (but they probably won’t know the answer). Most doctors consider nutritional supplements, like Krill Oil, of dubious value and little more than ‘snake oil’. (But this is changing in today’s medical schools.)
If you and your doctor agree to start Krill Oil, begin with a low dosage, then increase it gradually.
IMPORTANT: Keep accurate, scrupulous records of how you react to taking Krill Oil with Eliquis. Be prepared to stop the Krill Oil, if necessary.
(Thanks, Ralph, for this question. Please share your experience with us.)
Last updated: Tuesday, June 14, 2016
Return to FAQ Mineral Deficiencies and Supplements
We’ve posted a new FAQ and answer about the risks of anticoagulants and three alternatives to taking them.
“I have A-Fib, and my heart doctor wants me to take Xarelto 15 mg. I am concerned about the side effects which can involve death. What else can I do?”
You are right to be concerned about the side effects of Xarelto, one of the new Novel Oral Anticoagulants (NOACs). Uncontrolled bleeding is the primary risk (patients have bled to death in the ER.)
Be advised: No anticoagulant will absolutely guarantee you will never have a stroke.
All anticoagulants are inherently dangerous. You bruise easily, cuts take a long time to stop bleeding, you can’t participate in any contact sports; there is an increased risk of developing a hemorrhagic stroke and gastrointestinal bleeding. (Most EPs are well aware of the risks of life-long anticoagulation.)
Anticoagulants cause or increase bleeding. That’s how they work. To decrease your risk of blood clots and stroke, they hinder the clotting ability of your blood. But, they also increase your risk of bleeding. But in spite of the possible negative effects of anticoagulants, if you have A-Fib and a real risk of stroke, anticoagulants do work.
What Else Can You Do? Remove the Reason for an Anticoagulant—Three Options
The best way to deal with the increased risk of stroke and side effects of anticoagulants is to no longer need them. Here are three options…<…continue… to read my full answer…>
We’ve posted a new FAQ and answer under Drug Therapies and Medicines in our section:
Are Anticoagulants and blood thinners the same thing? How do they thin the blood? Blood clots are usually good, such as when you get a scrape or cut.
Blood clots are usually good, such as when you get a scrape or cut.
Since A-Fib increases your risk of clots and stroke, blood thinners are prescribed to prevent or break up blood clots in your heart and blood vessels and thereby reduce your chance of an A-Fib-related stroke.
Although referred to as “blood thinners”, they don’t actually affect the “thickness” of your blood.
There are two main types: anticoagulants and antiplatelet agents. They work differently to accomplish the same end effect.
Anticoagulants work chemically to lengthen the time it takes to form a blood clot.
Common anticoagulants include warfarin (Coumadin), Heparin and the NOACs such as apixaban (Eliquis).
Antiplatelets prevent blood cells (platelets) from clumping together to form a clot.
Common antiplatelet medications include aspirin, ticlopidine (Ticlid) and clopidogrel (Plavix) .
Final answer: Yes, an anticoagulant is a blood thinner, but not all blood thinners are anticoagulants.
Note: To read about ‘clot buster’ drugs or treatments that could save you from a debilitating stroke, see my article: Your Nearest ‘Certified Stroke Center’ Could Save Your Life.
Warfarin has one, but the NOACs don’t. What am I talking about?
Warfarin (Coumadin) has a way to monitor and measure its effectiveness for a specific patient. But there’s no similar way to measure the effectiveness of the new Novel Anticoagulant drugs (NOACs).
Warfarin and Your INR
With warfarin, blood testing for your INR (International Normalized Ratio) will tell your doctor what dosage of warfarin is needed to maintain your ideal INR range between 2.0 and 3.0. (Below 2.0, there’s more of a risk of an ischemic [clotting] stroke; above 4.0, there’s more of a risk of a hemorrhagic [bleeding] stroke.)
NOACs: No Blood Testing but at What Price?
From the clinical trials we know NOACs work as well as warfarin. In addition, the NOACs don’t require periodic blood testing. But the FDA, under pressure for new anticoagulants, approved the NOACs without there being any established or universally recognized method of determining their clot preventing effectiveness.
Without any method of determining their clot preventing effectiveness, how can you determine if your NOAC is working for you? … Continue reading this report…->
In a recent study, 99% of subjects aged 65 or older had evidence of microbleeds; and closer examination of the cranial MRI images revealed an increased number of detectable microbleeds (i.e., the closer they looked, the more microbleeds they found).
Microbleeds in the brain are thought to be a precursor of hemorrhagic stroke.
Cerebral microbleeds (MBs) are small chronic brain hemorrhages of the small vessels of the brain.
If Microbleeds Cause Hemorrhagic Stroke, Should I be on a Blood Thinner?
The fact that almost everyone 65 or older has microbleeds is astonishing and worrisome, particularly if you have A-Fib and have to take anticoagulants. Anticoagulants cause bleeding. That’s how they work.
In plain language, this study indicates that cerebral microbleeds lead to or cause hemorrhagic stroke. It’s not surprising then that some doctors are reluctant to prescribe heavy-duty anticoagulants to older A-Fib patients.
Being older and already having microbleeds only makes taking anticoagulants all the more worrisome.
Risks of Taking Anticoagulants (Blood Thinners)
Taking most any prescription medication has trade-offs. Older A-Fib patients find themselves between a rock and a hard place.
In the case of anticoagulants, on one hand you get protection from having an A-Fib stroke (which often leads to death or severe disability), but on the other hand you have an increased risk of bleeding.
For those over 65 who already have microbleeds, … Continue reading this report…->
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.
Background readings: The CHADS2 & CHA2DS-VASc Stroke-Risk Grading Systems, and my 2015 AF Symposium reports: Dr. Hugh Calkins’ remarks on the AHA/ACC/HRS A-Fib Treatment Guidelines, and Dr. Peter Kowey’ talk, All Anticoagulants Cause Bleeding;
Current European guidelines for assessing A-Fib stroke risk state that a patient with a CHA2DS2-VASc score of 1 (on a scale of 0 to 10, no risk to high risk) should be taking novel oral anticoagulants (NOACs). But a recent Swedish study contradicts this.
A Swedish National Patient Registry study looked at 140,420 patients with A-Fib who had “stroke events”. For women with a score of 1, annual stroke rates varied between 0.1% and 0.2% (depending on which “event” definition was used). For men, the stroke rate varied between 0.5% and 0.7%.
The researchers stated, “These low annual event rates call into question the need for or use of oral anticoagulant therapy in these low-risk patients.”
Similar insights were found in a study of the National Health Insurance Research Database in Taiwan among 186,570 A-Fib patients not on antiplatelet or anticoagulant therapy. Researchers concluded that “not all risk factors in CHA2DS2-VASc score carry an equal risk.”
What this Means for A-Fib Patients
Taking an anticoagulant isn’t like taking vitamins. No one should be on anticoagulants unless they have an actual risk of stroke.
While the U.S. guidelines are an improvement over the European guidelines, based on the Swedish and Taiwan studies, neither the U.S. nor European guidelines recognize that someone with a score of 1 probably shouldn’t be on anticoagulants at all.
All anticoagulants cause bleeding (that’s how they work.) So they are inherently dangerous. Why run the risk if you don’t need to?
Taking an anticoagulant isn’t like taking a daily vitamin. No one should be on anticoagulants as a precaution, there should be an actual risk of stroke.
The Decision: To Take an Anticoagulant or Not?
When you have atrial fibrillation, whether or not to be on an anticoagulant to reduce your risk of stroke (and which one to take) is perhaps the most difficult decision for you and your doctor. That decision should be based on actual risk factors and not on a “precautionary” approach.
Remember, this decision means taking medication as long as you still have A-Fib. For some patients that’s a lifetime.
AF Symposium 2015
All Anticoagulants Cause Bleeding
Updated August 2015
Dr. Peter Kowey of Lankenau Hospital in Wynnewood, PA discussed the special needs of patients with both A-Fib and Coronary Artery Disease (CAD). Sometimes, for example, these patients have to take both anticoagulant therapy for A-Fib and antiplatelets for stents. Some patients wind up taking a combination of three different drugs like warfarin, clopidogrel and aspirin.
Dr. Kowey pointed out how taking combinations of anticoagulants and antiplatelets multiplies the risk of bleeding. He cited the WOEST study which, though small, indicated that there was no real need for aspirin in addition to warfarin and clopidogrel.
All Anticoagulants Cause Bleeding
His most important point Dr. Kowey made for A-Fib patients is that all anticoagulants cause bleeding. That’s how they work. What an EP and an A-Fib patient strive for together is to find the right dose that gives the best protection versus minimizing the chances of bleeding. It’s tricky, because there are so many differences among patients. And it changes over time as we do.
NOACs May Be Dose Dependent
Dr. Kowey also discussed how the new anticoagulants (NOACs) were FDA approved on the assumption that one-size-fits-all, that one dosage works for all patients. But we know that warfarin is dose dependent. One would expect intuitively that the NOACs would work in a similar manner.
Dr. Kowey discussed the recent FDA hearings on the new anticoagulant edoxaban (Savaysa), namely that patients who had very good renal function seemed to get less of an anticoagulant effect. Patients taking the previously FDA approved NOACs may have been underdosed, because most of these drugs are renally eliminated. Unlike the INR measure in warfarin, the NOACs don’t have any standard, recognized way of measuring the anticoagulant effect as a guide to dosing. The one-size-fits-all NOAC dosage may work for most people, but others may be over- or under-anticoagulated.
Though not part of Dr. Kowey’s presentation, recent reports on Pradaxa (dabigatran) indicate that Boehringer-Inglehoff may have known that Pradaxa was dose dependent but didn’t tell the FDA. (See Claim “Misguided” That Pradaxa Needs No Blood-Level Monitoring.)
Taking anticoagulants is a trade-off. For most people, lowering the risk of an A-Fib stroke is a most welcome benefit compared to an added tendency to bleed.
All Anticoagulants Cause Bleeding and Are Dangerous
Anticoagulants are not like taking vitamins. No one wants to take an anticoagulant. Dr. Kowey’s statement that “all anticoagulants cause bleeding” and are inherently dangerous should determine how we look at all anticoagulants. This is in stark contrast with how NOACs are presented in today’s TV advertisements. (Just take an anticoagulant and live happily ever after!)
We obviously don’t have any data on the long-term effects of taking NOACS for years. Some people on long-term warfarin have been known to develop micro bleeds and dementia. Will this happen with the NOACs? We simply don’t know. But intuitively one would expect the same thing to happen, though probably not to the extent of warfarin.
NOACs Dose Dependent?
Dr. Kowey’s presentation also highlighted another important point for A-Fib patients—NOACs are probably dose dependent to some extent. One size does not fit all. If you are taking a NOAC, you may be under- or over-dosed.
How serious a problem is this? We simply don’t know. With Pradaxa many people have died in the ER from bleeding that doctors couldn’t stop. Was this because of over-dosing? It’s hard to tell. (See Stop Prescribing or Taking Pradaxa.)
One wonders how the FDA could have approved new anticoagulants with no standard, proven method of determining the anticoagulants’ effectiveness? (The NOACs were also approved with no reversal agent or antidote in case of bleeding!) But to be fair to the FDA, there was a great need for new anticoagulants to alleviate the problems with warfarin. And from the clinical trials, few could have anticipated the real world NOAC problems.
Update August 15, 2015: Reversal Agent for Pradaxa (dabigatran)
An experimental drug, idarucizumad, has show positive results as a reversal agent for Pradaxa (dabigatran). In a new study of 90 patients who had uncontrolled bleeding with Pradaxa, idarucizumad stopped this bleeding within minutes. No serious side effects were reported. FDA approval is pending.
We have previously reported on the reversal agent Andexanet Alfa which is on FDA fast track approval as an antidote to the Factor Xa inhibitors Xarelto and Eliquis. FDA approval is pending.
Update October 26, 2015: FDA Approves Reversal Agent Praxbind® for the Anticoagulant Pradaxa
Last updated: Wednesday, January 27, 2016
When I think about the field of atrial fibrillation in 2013, several thoughts come to mind. There were technical advancements, some new drug therapies, and additions to our understanding of Atrial Fibrillation (and a few accomplishments for our A-Fib.com website).
Heart Imaging And Mapping Systems
Perhaps the most important technical innovations in 2013 for A-Fib patients were the introduction of two new heart imaging and mapping systems. A third system, the Bioelectronic Catheter, represents a whole new technology with tremendous potential for A-Fib patients.
The ECGI System
The ECGI system, combined with a CT scan, produces a complete 3-D image of your heart along with identifying all the A-Fib-producing spots. Think of it as an ECG with 256 special high resolution electrodes rather than 12. It greatly reduces your ablation time and your radiation exposure.
A day before your ablation, you simply don a special vest with 256 electrodes covering your upper torso, and lay down. The 3-D image created is a road map of your heart with all the focal and rotor areas (A-Fib-producing spots) identified. During your ablation your EP simply ablates the “guilty” areas. Read more of my article…
The FIRM System
The FIRM system uses a different approach to mapping the heart and the A-Fib producing spots. It uses a basket catheter inside the heart to map large areas in a single pass and reveal the location of foci and rotors. Read more of my article…
Why are these two technologies important? ECGI allows your imaging & mapping to be performed the day prior to your ablation, rather than during your ablation. This shortens the length of your ablation procedure. In addition it reduces your radiation exposure and produces remarkably accurate 3D images of your heart and identifies where A-Fib signals are coming from. The FIRM system, though performed during an ablation rather than before it, may be a significant improvement over the Lasso catheter mapping system now in current use. Both systems may mark a new level of imaging/mapping for A-Fib.
Stretchable Electronics Meets the Balloon Catheter
The merging of living systems with electronic systems is called “bioelectronics”. Key is a flexible, pliable circuit made from organic materials—the carbon-based building blocks of life. Bioelectronics have entered the EP lab with a prototype of a ‘bioelectronic catheter’, the marriage of a pliable integrated circuit with a catheter balloon.
In a mapping application, the deflated bioelectronic balloon catheter is slipped into the heart, then pumped up. The inflated integrated circuit conforms to the heart’s grooves and makes contact with hard-to-reach tissue. It can map a hundred electrical signals simultaneously, across a wider area and in far greater detail than had been previously possible. And it’s being developed to function in reverse. For ablation applications, instead of detecting current, it can apply precise electrical burns. This is a potentially breakthrough technology that may well change the way catheter mapping and ablation are performed. (Thanks to David Holzman for calling our attention to this ground-breaking research article.)
This is a remarkable time in the history of A-Fib treatment. Three very different technologies are poised to radically improve the way A-Fib is detected, mapped and ablated. We’ll look back at 2013 as a watershed year for A-Fib patients.
Three New Anticoagulants
In 2013 we saw three new anticoagulants, a welcome development for A-Fib patients. Note: the new anticoagulants are very expensive compared to the proven anticoagulant warfarin.
How do they compare to warfarin?
Warfarin seems to have a slightly higher chance of producing intracranial bleeding.
In general stay away from Pradaxa. There are horrible ER reports of patients bleeding to death from even minor cuts, because there is no antidote or reversal agent. Read more about my Pradaxa warning…
Eliquis, in general, tested better than Xarelto in the clinical trials, but it’s so new we don’t have a lot of real-world data on it yet. And, as with Pradaxa, neither have antidotes or reversal agents.
In addition, there was what some consider a major problem with the clinical trials comparing the new anticoagulants to warfarin. ‘Compliance’ rates by warfarin users were poor (many either weren’t taking their warfarin or weren’t in the proper INR range). Did this skew the results?
And finally, unlike warfarin where effectiveness can be measured with INR levels, we don’t have any way to measure how effectively the new blood thinners actually anticoagulate blood. Read more of my article “Warfarin vs. Pradaxa and the Other New Anticoagulants“.
Keep in mind: ‘New’ doesn’t necessarily mean ‘better’ or ‘more effective’ for You.
High Blood Pressure with Your A-Fib? Is Renal Denervation a solution?
As many as 30% of people with A-Fib also have high blood pressure which can’t be lowered by meds, exercise, diet, etc. There was hope that Renal Denervation would help.
With Renal Denervation, an ablation catheter is threaded into the left and right arteries leading to the kidneys, then RF energy is applied to the nerves in the vascular walls of the arteries, hopefully reducing ‘Sympathetic Tone’, lowering high blood pressure and reducing A-Fib. For many people Renal Denervation seemed the only realistic hope of lowering their high blood pressure. However, the Medtronic Simplicity-3 trial indicated that renal denervation doesn’t work. Read more of this article… For 2014 news on this topic, read more…
A Study of Obesity and A-Fib: A-Fib Potentially Reversible
Obesity is a well known cause or trigger of A-Fib, probably because it puts extra pressure and stress on the Pulmonary Vein openings where most A-Fib starts.
In 2013 A research study report focused on obese patients with A-Fib. Those who lost a significant amount of weight also had 2.5 times less A-Fib episodes and reduced their left atrial area and intra-ventricular septal thickness.
Good news! Losing weight can potentially reverse some of the remodeling effects of A-Fib. Related article: Obesity in Young Women Doubles Chances of Developing A-Fib.
Obstructive Sleep Apnea and A-Fib
Obstructive Sleep Apnea (OSA) is another well recognized cause or trigger of A-Fib. Anyone with A-Fib should be tested for sleep apnea.
Earlier studies have shown approximately two-thirds (62%) of patients with paroxysmal or persistent A-Fib suffer from sleep apnea. In 2013, research reports showed that the worse one’s sleep apnea is, the worse A-Fib can become. In addition, sleep apnea often predicts A-Fib recurrence after catheter ablation.
Before an ablation, Dr. Sidney Peykar of the Cardiac Arrhythmia Institute in Florida, requires all his A-Fib patients be tested for sleep apnea. If they have sleep apnea, they must use CPAP therapy after their ablation procedure.
A-Fib.com: Our New Website’s First Year
The original A-Fib.com web site was created using the phased out software MS FrontPage. Thanks to a “no strings attached” grant from Medtronic, A-Fib.com was reinvented with a more up-to-date but familiar look, and features more functionality (built on an infra-structure using Joomla and WordPress). We can now grow the site and add features and functions as needed.
It involved a tremendous amount of work. A special thanks to Sharion Cox for building the new site and for technical support. My wife, Patti Ryan, designed the look and all graphics. (I can’t thank Patti enough; I’m so lucky!)
Update the Directory of Doctors & Facilities
Back when I started A-Fib.com in 2002, there were less than a dozen sites performing ablations for A-Fib. Today our Directory of Doctors and Facilities lists well over 1,000 centers in the US, plus many sites worldwide.
Increasingly, doctors were writing me asking why they weren’t included, or why their info was incorrect since they had moved, etc. To update our records and our service to A-Fib patients, starting in July 2013, we prepared and mailed letters to over 1,000 doctors/facilities. We asked each to update/verify their listing (and include a contact person for our use).
The response to our bulk mailing was great. The data input started in October and continued for several months (as time allowed). Recently, we cut over to the ‘new’ Directory menu and pages.
What’s Ahead for A-Fib.com in 2014
2014 Boston AFib Symposium Reports: Check out my new reports from the 2014 Boston A-Fib Symposium (BAFS) held January 9-11, 2014 in Orlando FL.
The first two reports are posted. Look for more reports soon. I usually end up with 12-15 reports in total.
Our a-Fib.com Directory of Doctors & Facilities: Work on updating our listings is still underway. We need to contact those who did not respond to our request for verification or updating of their listing. (Shall we write again or maybe make phone calls?)
Amazon Best Sellers list: Our book sales continue to grow. Did you know that our book ‘Beat Your A-Fib’ has been on Amazon’s Best Sellers list continually in two categories (Disorders & Diseases Reference and Heart Disease) since its debut in March 2012? Visit Amazon.com and read over 40 customer reviews.
Help A-Fib.com Become Self-sustaining: We plan to step up our efforts to make A-Fib.com a self-sustaining site. (Since 2002, Steve and Patti Ryan have personally funded A-Fib.com with an occassional reader’s donation.)
In our efforts toward sustainabiliy, several years ago we added a PayPal ‘Donate’ button (you don’t need a PayPal account to donate) and invited donations toward our onlline maintenance costs.
Our newest effort is our ‘A-Fib can be Cured! shop with T-shirts and more at Spreadshirt.com. With each shirt purchase $2 goes to support A-Fib.com. (We will roll out new designs every quarter or so).
Posted February 2014
Help A-Fib.com become self-sustaining! Help keep A-Fib.com independent and ad-free.
Will 2014 be the year you help support A-Fib.com?
Last updated: Wednesday, February 11, 2015
Report by Steve S. Ryan, PhD
This is my only report from the November 2014 meeting of the American Heart Association. Unlike the annual (Boston) AF Symposium, the AHA had only a few sessions on Atrial Fibrillation.
About Dr. Peter Kowey: An internationally respected expert in heart rhythm disorders. His research has led to the development of dozens of new drugs and devices for treating a wide range of cardiac diseases. Note: In his disclosure statement, he lists being a consultant for most of the major pharmaceutical companies.
Dr. Kowey’s first point is a sobering statement about today’s antiarrhythmic drugs (AADs).
Fact #1 “An antiarrhythmic drug is a poison administered in a therapeutic concentration.”
(Like most meds, antiarrhythmic drugs, (AAD), are a trade-off. We trade the unnaturalness and possible toxicity of AADs in the hope that they will alleviate our A-Fib symptoms and keep our A-Fib from getting worse. But AADs are unnatural substances not normally found in our body. Our body has a tendency to react to them like they were toxins.)
Fact #2 Amiodarone is by far the most effective of the antiarrhythmics but is also the most toxic.
The “protean toxicity” of amiodarone is grossly underappreciated by practicing doctors. The average GP or cardiologist often doesn’t understand how severely amiodarone can affect people and often don’t monitor patients closely enough.
Amiodarone has never been reviewed or approved by the FDA for the treatment of A-Fib (this is called “off label” use).
Though doctors use the 200 mg dose, the best dosage is unknown. The degree and rate amiodarone is absorbed into the circulation (bioavailability) can range widely from 15% to 85%.
An antiarrhythmic drug is a poison administered in a therapeutic concentration.
Fact #3 We choose antiarrhythmic drugs based on their relative chances of harm, not comparative efficacy.
Doctors usually start out by prescribing the least dangerous antiarrhythmic first or the least likely to have bad side effects in a particular patient, rather than the drug most likely to suppress A-Fib.
Fact #4 Antiarrhythmic drug therapy is highly empiric, but exposure-related.
For example, in practice doctors don’t use plasma monitoring to determine how much of an antiarrhythmic is actually in a patient’s blood.
In clinical practice most doctors don’t continually adjustment dosage based on patient response.
Fact #5 Antiarrhythmics drugs require surveillance of varying intensity.
• Amiodarone requires intense surveillance—lungs, thyroid, eyes, liver, skin, heart. (For more see my article, Amiodarone: Most Effective and Most Toxic.)
• Flecainide/Propafenone: check for ischemic effects (swelling)
• Sotalol/Dofetilide: check for renal function
• Sotalol: monitor kidneys as 100% is renally eliminated
Fact #6 Antiarrhythmic drugs with multi-channel effects may be more effective than those that target single channels or receptors.
Dr. Kowey discussed Vanoxerine which is a dopamine transporter antagonist developed for Parkinson’s and depression but is being studied for A-Fib conversion.
In one study, ‘Pill-In-The-Pocket’ didn’t reduce A-Fib symptoms but did significantly reduce emergency room visits and hospitalizations.
Fact #7 Antiarrhythmic drug therapy of A-Fib is imperfect.
The goal is palliation (treatment without dealing with the underlying cause) and not total eradication of symptoms.
Fact #8 Antiarrhythmic drug therapy can be creative.
Instead of taking an antiarrhythmic drug on a continuous basis, one can instead use a strategy like Pill-In-The-Pocket. The A-Fib patient only takes an antiarrhythmic drug at the time of an A-Fib attack (or as a booster—taking more of an AAD at the time of an A-Fib episode).
In one study, Pill-In-The-Pocket didn’t reduce A-Fib symptoms but did significantly reduce emergency room visits and hospitalizations.
Fact #9 Antiarrhythmic drugs may supplement the efficacy of other interventions like catheter ablation.
After a catheter ablation during the 3 month blanking period, patients are often given an antiarrhythmic drug to help their heart ‘learn’ to beat normally again, to prevent their heart from slipping back into A-Fib.
About the 3 month blanking period, Dr. Kowey says “the rationale for which is unknown.” (But it generally takes that long for the scarring from an ablation to heal and for the heart to return to normalcy.)
There haven’t been any clinical trials to guide the choice of drug and dose during the 3 month blanking period.
The concept of “enhanced efficacy” has not been grounded or tested.
Fact #10 Taking antiarrhythmic drugs does not obviate the need for stroke prevention.
There is an inadequate data to form a firm conclusion regarding withdrawal of anticoagulation after a successful ablation. (For more see the FAQs question #15: “I’ve had a successful Pulmonary Vein Ablation to cure my A-Fib. Do I still need to be on blood thinners like Coumadin or aspirin?”
Some studies indicate that anticoagulants can be stopped 3-6 months after a successful Pulmonary Vein Ablation. As Dr. John Mandrola says, “and if there is no A-Fib, there is no benefit from anticoagulation.”)
Abundant data prove the prevalence of silent A-Fib.
Dr. Kowey stated that there is an unwarranted assumption regarding the relationship between A-Fib appendage function and clot. (But some studies indicate that 90%-95% of A-Fib clots come from the Left Atrial Appendage (LAA), that closing off the LAA does reduce A-Fib stroke risk.)
After a successful Pulmonary Vein Ablation…and if there is no A-Fib, there is no benefit from anticoagulation. -Dr. John Mandrola
Fact #11 The holy grail is prevention.
But there is no proof that any treatment is conclusively effective in this regard. Dr. Kowey discussed the new drug in development ‘LCZ696’ by Novartis AG which shows promise in preventing A-Fib.
Dr. Kowey’s Conclusions
• If doctors made better and more intelligent use of antiarrhythmic drugs, patients would fare better and we would do fewer ablations.
• Intelligent use requires an in-depth knowledge of pharmacology and familiarity with all aspects of clinical use, especially dosing.
• Antiarrhythmic therapy is not perfect, but it can improve quality of life and functionality for a significant percentage of A-Fib patients.
Dr. Kowey’s statement that “an antiarrhythmic drug is a poison administered in a therapeutic concentration” should set off alarm bells for patients. In the US, we’ve been conditioned to think “ if we’re sick, just take a pill”. But today’s antiarrhythmic drugs have poor success rates (often under 50%), often have unacceptable side effects, and when they do work they tend to lose their effectiveness over time. In general, antiarrhythmic drugs are toxic substances which aren’t meant to be in our bodies―so our bodies tend to reject them.
Antiarrhythmic drugs are certainly better than living a life in A-Fib. They are useful for many patients. But as Dr. Kowey states, they are “palliative” (without dealing with the underlying cause) and are seldom a lasting cure for A-Fib.
Last updated: Sunday, February 15, 2015
20th Annual AF Symposium
by Steve S. Ryan, PhD
This overview should give you a sense of the topics floating through the three days in Orlando and the over sixty presentations by fifty A-Fib experts and researchers. (Most recent brief reports listed first)
(Please be advised that the Symposium organizers go to great lengths not to identify or unfairly publicize one device over another. When writing these reports I often have to do a good deal of research to correctly identify and describe particular devices that are demonstrated, as a service to readers. But this in no way implies or suggests that one device is superior to another.)
Dr. Gerhard Hindricks of the University of Leipzig in Germany gave a dynamic presentation of a catheter ablation of a 46-year-old female with paroxysmal A-Fib using the Rhythmia 3-dimensional multipolar mapping system by Boston Scientific. Along with his colleagues Drs. Andreas Bollmann and Jedrzej Kosiuk, they used the Rhythmia special basket catheter to generate a 3-D map of electrogram voltages and activation times. To me it seemed amazingly fast. The eight-splined bidirectional catheter produced 1,000 data points per minute. In what seemed like only a few passes, they produced a 3-D color reconstruction of the patient’s left atrium.
The actual ablation was routine. They terminated the A-Fib into sinus rhythm without having to use Electrocardioversion. But they found that the PV isolation was incomplete. Using the same Rhythmia 3-D mapping catheter, they were easily and quickly able to locate the gap in the Left Superior PV and ablate it.
Dr. Vivek Reddy from Mount Sinai School of Medicine in New York City gave a very well referenced and persuasive presentation on the Watchman device which closes off the Left Atrial Appendage to prevent clots and strokes. The theory behind the Watchman device 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. (For more, see my article, The Watchman Device: The Alternative to Blood Thinners).
Dr. Reddy certainly persuaded me that the FDA should approve the Watchman device. Dr. Reddy, earlier in Washington, had made the same persuasive arguments before the FDA.
Dr. Andrew Farb from the FDA took the bull by the horns and gave his perspective on the various LAA Closure (Occlusion) Devices. But as one would expect, he didn’t indicate how the FDA would rule on the Watchman device, since deliberations were still ongoing.
After his presentation, I asked him several pointed questions about this, but he was, of course, careful not to comment about current FDA deliberations. My guess? If body language, momentum, mood of the presentations, and more importantly recent research indicate anything, the Watchman device probably will not be approved by the FDA.
There was a palpable sense of sadness at the end of these presentations. The attendees realized that the game may be over for the Watchman device. I hope I am wrong, since the Watchman device would be an important tool to help A-Fib patients. Once the FDA rules and the current clinical trials of the Watchman device end, you will probably have to go to Canada or overseas to get a Watchman device installed.
Watchman May Win FDA Approval
Updated March 13, 2015: The Watchman Device by Boston Scientific finally wins FDA approval
In my earlier brief reports on the Orlando AF Symposium, based on the recent research and the FDA presentation, I said the Watchman device probably won’t be approved in the US. I’m happy to say that I am most likely wrong.
At the LAA Symposium 2015 in Marina del Rey, CA, it was suggested that the Watchman device may be approved by the middle of this year. One presenter described how the FDA chairman talked with several people who were going to Canada to have the Watchman device installed. He seemed embarrassed that the Watchman was available everywhere in the world but not in the US and said that it has to be approved.
Other doctors I talked with at the LAA Symposium were of the same opinion. Presenters described how clinical trials for other LAA closure devices were on hold so that they could get approved in comparison to the Watchman (Non-Inferiority Trials). Dr. Dhanunjaya Lakkireddy of the University of Kansas Medical Center said that we are at a “tipping point” for the (A-Fib) industry.
As everyone, including the FDA, is well aware, A-Fib innovations usually start in Europe where they are more easily approved. Then only later do they move to the US for FDA approval, since the FDA generally requires more data than European regulators.
Drs. Jun Dong and Andrew Farb from the FDA described the FDA’s ‘Easy Feasibility Study’ (EFS) program where medical device innovations could be evaluated in the US without having to go to Europe first. He encouraged researchers and attendees to take advantage of the new EFS program. This is major news and may make the development of A-Fib innovations much easier to accomplish in the US.
For further information, contact: Andrew Farb, Email: Andrew.firstname.lastname@example.org. 301-796-6317
Dr. Luigi Di Biase from the Albert Einstein College of Medicine in the Bronx, NY and Dr. Daniel Singer from Massachusetts General Hospital in Boston each described potentially great developments in reversal agents for apixaban (Eliquis) and rivaroxaban (Xarelto).
Dr. Di Biase described studies where leaving people on uninterrupted rivaroxaban and apixaban before, during and after an ablation dramatically reduced the amount of silent thromboembolic lesions and were as safe as warfarin with regards to stroke and TIAs. (This didn’t work with dabigatran [Pradaxa].) But if patients develop bleeding or effusion during the ablation, they are in trouble because there is no direct reversal agent as there is for warfarin. He has used Factor IV as an indirect reversal agent. Dr. Singer also described how Factor IV was used as a reversal agent for apixaban.
But there are new reversal agents for apixaban and rivaroxaban which promise to completely reverse the effects of these two drugs in less than four minutes. The FDA is speeding up studies on these reversal agents. But one never knows when or if the FDA will approve them.
Dr. John Day of the Intermountain Heart Institute in Murray, UT (and recently elected president of the Heart Rhythm Society) may be the first A-Fib leader to publicly question whether women should be given one point on the stroke risk CHA2DS2-VASc scale just because of their gender. Many doctors have said this in a circumspect way. Dr. Eric Prystowsky in a presentation at last year’s AHS meeting thought that most doctors would agree with Dr. Day, “as long as there wasn’t a camera focused on them.” He gave the example of a 45-year-old woman in good health and a 45-year-old man with hypertension who according to current guidelines should both be given one point on the stroke risk CHA2DS2-VASc score.
As readers of A-Fib.com, you know that’s been my opinion ever since the original European guidelines came out. Women in their child-bearing years are much less at risk of stroke because of the blood-thinning effect of losing blood each month. And even after menopause women have less risk of stroke. But eventually they do have more strokes. But not because of an innate inferiority, but because women live longer than men. Stroke is age related. An observational Danish registry study documents this.
For more, see The Denmark Study: Women in A-Fib Not at Greater Risk of Stroke Contrary to CHA2DS2-VASc Guidelines!) (Be advised that the original European guidelines were written by doctors with major conflicts of interest.) These guidelines may be a not so very subtle form of gender bias.
Living in A-Fib is more dangerous than having an ablation, according to Dr. Josef Kautzner from Prague, the Czech Republic. Studies have documented that the adverse effects of living in A-Fib, having to take A-Fib drugs and anticoagulants for life are both pragmatically and statistically worse than having an ablation. Dr. Kautzner discussed how A-Fib can cause or is associated with silent brain lesions and dementia. Any time you go into a hospital is a risk. And no one would say that a catheter ablation is a walk in the park. But an ablation is a low risk procedure, though not risk free. The risk is similar to having your tubes tied. The possible adverse effects of an ablation procedure (like bleeding at the groin) are generally temporary, unlike the lasting, permanent damage you can do to your heart, body and brain by living in A-Fib for years.
The most hotly discussed topic at this year’s symposium was rotors. The opinions expressed about rotors were at times very heated, more than I had ever seen at an AF Symposium. Dr. Shih-Ann Chen of Taipei, Taiwan disagreed with Dr. Sanjiv Narayan of Stanford, CA about the basic concepts of rotors and how they should be defined. Dr. Ravi Mandapati of UCLA and Loma Linda University disagreed with Dr. Narayan which was all the more striking in that he had worked with Dr. Narayan when he was at UCLA. Dr. Pierre Jais of Bordeaux, France said that the FIRM mapping system misses 40% of the atrium area.
Drs. Haissaguerre and Jais from Bordeaux and Dr. Sebastien Knecht of Brussels, Belgium gave presentations on how they were using the CardioInsight body surface mapping vest to perform ablations of “drivers” at many different centers, while Dr. Karl-Heinz Kuck from Hamburg, Germany using a different body surface mapping system said that he couldn’t ablate rotors. Dr. Narayan says the FIRM system finds a maximum of 2-3 rotors in the atria, while other systems find as many as seven. The FIRM system says rotors are usually relatively stable and can last as long as 30 seconds while others say they rotate in one fixed spot for only one or two rotations, that they tend to migrate within a certain area.
The presenters obviously didn’t share a consensus of basic concepts of what rotors are, how they work, their importance in A-Fib, how they should be correctly identified, used, and ablated. (It seems to me the Bordeaux group has the best understanding and pragmatic use of rotors. They refer to “rotors” and focal sources as “drivers.”) But the CardioInsight system Bordeaux uses isn’t currently available or isn’t being tested in the US.
Obesity was one of the most often discussed topics. There is a growing consensus among EPs that it isn’t enough to just give obese patients a catheter ablation while not dealing with their obesity. If the obesity isn’t dealt with, their A-Fib is very likely to re-occur. A-Fib will develop in other spots that haven’t been ablated. The condition (obesity) that triggered or caused the A-Fib will trigger or cause it again, if it isn’t taken care of.
Dr. Prashanthan Sanders of Adelaide, Australia described the great results he is getting in his clinic which includes a weight loss program and counseling. He convinces his overweight patients to buy into the program, lose weight, and keep it off. The program works so well that just by losing weight patients become A-Fib free. This program is a holistic approach to health and also is developed to work for diabetes, sleep apnea, hypertension, binge drinking and smoking.
Dr. Sanders foresees a world where some patients become A-Fib free simply by changing their life style, where they don’t have to have a catheter ablation to become A-Fib free.
Many other doctors commented that A-Fib treatment at many centers today includes or should include much more than A-Fib ablation and drugs. A-Fib centers should have nutritionists, exercise therapists, sleep apnea specialists, etc. as part of their A-Fib program.
Dr. John Day of the Intermountain Heart Institute in the Challenging Cases Discussion described his experience with the dreaded Atrial Esophageal Fistula. Though very rare, this is one of the few possible complications of a catheter ablation that can kill you. An ablation, if not done with caution, can irritate and damage the esophagus which often lies right next to the heart. Over 2-3 weeks stomach acid can eat through this damaged area to produce a hole or fistula from the esophagus into the heart.
As soon as Dr. Day saw this patient, he knew it was a fistula and immediately called surgeons and a GI doctor. All the surgeons were doing operations and didn’t want to do the surgery in the EP lab. Dr. Day described how he and his colleagues ran down the hospital hallway to the operating room while giving the patient a transfusion and at the same time pumping out the blood escaping from his heart.
The GI doctor got there first and put in a stent in the esophagus to plug the hole. There was lots of discussion as to whether this was the best approach, but it worked. The patient survived but had to spend a month in the hospital.
This cautionary and very dramatic tale certainly got the attention of all the attendees. No matter how rare a fistula is, every EP and A-Fib center must have an established protocol in place to deal with it. I remember Dr. Hugh Calkins in a previous Symposium advising, “There are only two kinds of EPs—those who have not had an Atrial Esophageal Fistula and those who have!” (Dr. Calkins’ patient with fistula also survived.)
Dr. Peter Kowey of Lankenau Hospital in Winnewood, PA described a case that illustrates the kind of dilemma both doctors and patients often have to face. A 92-year-old woman with paroxysmal A-Fib who had been treated for many years with warfarin had some bruising and nuisance bleeding, but never anything major.
Dr. Kowey thought that ethically he should tell her about the different new anticoagulants which may be superior to warfarin, then see if she wanted to change. She went with apixaban (Eliquis), then six months later had a stroke even though she was taking apixaban properly and conscientiously. Happily, she made an almost full recovery. She returned to warfarin which had worked for her in the past and which she was comfortable using.
One of the reasons Dr. Kowey discussed the new anticoagulants with his 92-year-old patient was because warfarin is considered more apt to cause bleeding in older patients. The newer anticoagulants in clinical trials caused less bleeding. But we don’t have much data from the clinical trials on people over 90 years old.
Can we say that apixaban didn’t work or was ineffective? No. Anticoagulants reduce but do not totally eliminate the risk of an A-Fib stroke. Just because she had a stroke doesn’t mean apixaban didn’t work.
Dr. Jeremy Ruskin pointed out that there has never been and probably never will be a head-to-head comparison of the three new anticoagulants. But in my opinion apixaban (Eliquis) appears to have tested better and is safer than the others
For more, see my 2013 BAFS articles, The New Anticoagulants (NOACs) and Warfarin vs. Pradaxa and the Other New Anticoagulants.
In the satellite case live presentations, Drs. Rodney Horton and Amin Al-Ahmad from the Texas Cardiac Arrhythmia Institute in Austin, TX surprised us by doing an ablation without wearing the standard lead aprons to prevent fluoroscopy exposure. Even more surprising was one of the lab assistants who was pregnant. She could work on the ablation because no fluoroscopy was used. The doctors did the whole ablation using ICE (Intracardiac Echo) and 3D mapping. They showed for example how ICE can be used to thread the catheter up into the heart and into the left atrium. Dr. Horton said that not having to wear those heavy lead aprons would probably add 5-10 years to his ablation career.
(They didn’t wear surgical masks during the ablation which was surprising to me. I will write them for an explanation.)
The live satellite case from Beijing, China was technically flawless and probably a first of its kind. But it wasn’t much of a learning experience for the attendees. The Chinese EPs only used one catheter and had to frequently pull out the mapping catheter and replace it with the ablation catheter, etc. When the expert panel asked them questions, the Chinese EPs either didn’t understand or simply didn’t answer them. They seemed very uncomfortable. It seemed like a throwback to ablation techniques of 20 years ago.
Drs. Claudio Tondo, Gaetano Fassini, Massimo Moltrasio, and Antonio Dello Russo from Milan, Italy showed how they do a catheter ablation for A-Fib and install the Watchman device in the same procedure, when it’s needed. They do the ablation procedure first. Then when the patient is in sinus rhythm, they install the Watchman device. (This can’t be done in the US, because the Watchman device hasn’t received FDA approval. In later discussions including representatives of the FDA, there was an all too real possibility that the Watchman will never receive FDA approval.)
Drs. Kevin Heist and Moussa Mansour from Massachusetts General in Boston showed in a live case how they used a Contact Force Sensing catheter combined with Jet Ventilation. (There are two Contact Force Sensing catheters approved by the FDA—the ThermoCool Smart Touch device by Biosense Webster (approved Feb. 24, 2014) and the TactiCath Quartz Contact Force Ablation Catheter by St. Jude Medical (approved Oct. 27, 2014). This live case used the TactiCath catheter but didn’t imply or suggest it is superior to the ThermoCool catheter. For a description of each, see my 2014 AF Symposium report The New Era of Catheter Ablation Technology: Force Sensing Catheters.
This combination of Force Sensing Catheter with Jet Ventilation for RF ablation probably represents the most advanced RF ablation strategy available today. Jet Ventilation doesn’t stop the heart from beating as in bypass surgery. But to this observer it seemed to put the heart in a type of slow motion with a lot less movement than when the heart is beating in normal sinus rhythm. You could really see a difference when they turned the Jet Ventilation off and on. Slowing down the heart like this helps the ablation doctor make lesions in hard-to-access areas and makes it easier to hold the catheter steady and apply the right contact pressure.
Drs. Michel Haissaguerre and Pierre Jais from Bordeaux/LYRIC gave presentations on the ECGI system. The day before their ablation, the patient lies down on his/her back and a technician places a vest-like device with 256 electrodes over his/her chest and stomach. These electrodes combine with rapid CT (Computed Tomography) scans to produce a very detailed 3D color map of the heart. (For a detailed description and discussion of the ECGI system, see 2013 BAFS: Non-Invasive Electrocardiographic Imaging [ECG]) The system automatically detects rotors and foci and computes them into a “Cumulative Map” or movie. These driver regions are ranked, based on statistical prevalence.
Then, Dr. Sebastien Knecht from CHU Brugmann, Brussels, Belgium, described the AFACART trial design and preliminary results using the CardioInsight ECGI system. Many centers in Europe including four in Germany are now using the CardioInsight. Requiring very little training, technicians and EPs using the CardioInsight system are getting similar great results like the Bordeaux group. Though these studies just started, it looks like the CardioInsight ECGI mapping and ablation system is poised to revolutionize the way EPs map and perform ablations.
Dr. Jose Jalife of the University of Michigan in Ann Arbor, MI, continued his exciting research on fibrosis and A-Fib. In previous Symposiums Dr. Jalife demonstrated how A-Fib produces fibrosis. When he paced sheep into A-Fib, their hearts became fibrotic within a very short time. The markers of fibrosis (collagen and scarring) increased progressively as the sheep went from paroxysmal to persistent A-Fib. (See A-Fib Produces Fibrosis—Experimental and Real-World Data.)
Fibrosis is tissue that has fiber-like characteristics which develop in place of the normal smooth walls of the heart. Fibrotic tissue is scarred, immobile, basically dead tissue with reduced or no blood flow and no transport function. It results in a loss of atrial muscle mass. Over time it makes the heart stiff, less flexible and weak, overworks the heart, reduces pumping efficiency and leads to other heart problems. Fibrosis, up to now, was considered permanent and irreversible. But Dr. Jalife gave his sheep a Gal-3 inhibitor GM-CT-01 that actually prevented and reduced fibrosis! (For his previous presentations, see 2014 BAFS: The Holy Grail: Preventing A-Fib by a GAL-3 Inhibitor.)
In his continuing studies of sheep, Dr. Jalife found that fibrosis predicts recurrence, and that fibrosis can not be reversed if it is well established, even with GAL-3 Inhibitors.
Last updated: Thursday, January 21, 2016
20. “Is there a way to get off blood thinners all together? I hate taking Coumadin. I know I’m at risk of an A-Fib stroke.”
To get off blood thinners all together you must solve the underlying reason why you’re on the drug in the first place.
You must cure your Atrial Fibrillation and address any other contributing issues that puts you at risk of clots and stroke. For example, if you have undiagnosed sleep apnea, your EP will want you tested and put on an appropriate treatment. The same is true if you have heart valve disease, high blood pressure, diabetes or are severely overweight.
You may need to change doctors, too. You want an electrophysiologist (EP) who specializes in heart rhythm problems and Atrial Fibrillation in particular. Seek an EP whom you are comfortable with, someone who will partner with you to seek your cure. For help, see “Finding the Right Doctor.”
Your EP will evaluate you and your Atrial Fibrillation and other conditions impacting your health. You may discuss a catheter ablation procedure. Or if you have other heart problems or you don’t qualify for an ablation, you may look at the Cox maze or Mini-maze, or a Hybrid Surgery/Ablation procedure.
Caution: It’s important to understand that you should not stop taking Coumadin without the guidance of your doctor or a health care professional.
Return to FAQ Drug Therapies
15. “After my successful Pulmonary Vein Ablation, do I still need to be on blood thinners like Coumadin or aspirin?”
You may still have a high CHADS2 stroke risk score or other factors that make it necessary for you to stay on blood thinners.
But if you no longer have A-Fib, you are no longer in danger of having an A-Fib stroke. So, in most cases, you don’t need to be on blood thinners.
A recent observational study involving nearly 38,000 patients found that the stroke risk of patients who had a successful catheter ablation was similar to patients with no history of A-Fib. When you are in sinus rhythm, your stroke risk is basically the same as a normal heart-healthy person.
However, there is no medication or treatment that would absolutely guarantee one would never get a stroke, even for people in normal sinus rhythm.
“Anticoagulant treatment for people with A-Fib ranks as one of the highest-risk treatments in older Americans.
∼Thomas J. Moore, MD
A study in 2010 indicates that anticoagulants, like warfarin, can be stopped 3-6 months after a successful Pulmonary Vein Ablation (Isolation).
Silent A-Fib May be Appear Post-Ablation
However, though feeling cured of your A-Fib, you may still be experiencing ‘silent A-Fib’ (A-Fib with no symptoms) which can be dangerous.
But doctors today are very good at spotting silent A-Fib and have a wide variety of monitoring devices (such as the Zio patch which you wear like a Band-Aid for two weeks). These monitoring devices would capture any silent A-Fib episodes you may have and alert your doctor that you may still need to be on anticoagulants. If you’re worried about being in silent A-Fib, ask your doctor for more extensive monitoring. Short episodes of silent A-Fib in general aren’t likely to cause a clot.
Danger of Taking Anticoagulants
No one should be on anticoagulants unless there is a real risk of stroke. Anticoagulants have their own risks and dangers.
No one should be on anticoagulants unless there is a real risk of stroke. Anticoagulants have their own risks and dangers. No one wants to be on blood thinners like warfarin (Coumadin). You bruise easily, cuts take a long time to stop bleeding, you can’t participate in any contact sports or any activities like mountain climbing, bike riding, etc.
If taking the newer anticoagulants (NOACs) and you’re in an accident, you risk bleeding to death, because there is currently no practical way to reverse the anticlotting effect.
(Added October 26, 2015: The FDA granted “accelerated approval” to Praxbind®, a reversal agent (antidote) to Pradaxa®. Praxbind is given intravenously to patients who have uncontrolled bleeding or require emergency surgery.)
Even a low dose like a baby aspirin (81 mg) can cause bleeding and intestinal problems.
Even a low dose like a baby aspirin (81 mg) can cause bleeding and intestinal problems.
Whether you should be on anticoagulants after a successful catheter ablation is a judgment call for you and your doctor.
August 2015 Update: Aspirin is No Longer Recommended as First-Line Therapy
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 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.
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.
When is aspirin appropriate? Aspirin is recommended for “secondary” prevention of cardiovascular disease such as to prevent a reoccurrence of a stroke or heart attack.
Return to FAQ Catheters
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
18. “My last cardiologist had me on the anticoagulant Pradaxa. My new cardiologist wants me to switch to Eliquis. Is Eliquis easier to deal with if bleeding occurs?”
There have been horrendous stories of people on Pradaxa (dabigatran) bleeding to death in the ER even from minor cuts while the ER doctors and staff can only watch as they die. Unlike for warfarin, there is no reversal agent or antidote for Pradaxa. The other NOACs, Eliquis and Xarelto, also don’t have reversal agents. But anecdotally they don’t seem to have as many bleeding deaths associated with them.
Added October 26, 2015: The FDA granted “accelerated approval” to Praxbind®, a reversal agent (antidote) to Pradaxa®. Praxbind is given intravenously to patients who have uncontrolled bleeding or require emergency surgery. In clinical trials, 5gs of Praxbind (idarucizumab) reversed the anticoagulant effect of Pradaxa within minutes (which is significantly faster than the current antidotes for warfarin).
Through an analysis of data from the ‘FDA Adverse Event Reporting System’ by AdverseEvents, Inc., Eliquis has received an “RxScore” safety score of 39.45 on a 100 point scale (1=lowest risk, 100=highest risk). In comparison, Coumadin (warfarin) had a score of 67.57. Pradaxa (dabigatran) had a score of 67.15, Xarelto (rivaroxaban) 67.08.
The FDA’s database comprises all the reports made by doctors, patients and other healthcare providers, which means it’s not a “scientific” finding with the authority of a clinical trial. AdverseEvents applies logic, math and software to the database to sift out the important data.
For Eliquis, “the rate of suspect cases was lower in every type of adverse-event report, from hospitalization to death.” For example, among Eliquis patients reporting side effects, only 21% cited hospitalization, while Pradaxa had 39%, Xarelto 43% and Coumadin (warfarin) 50%.
The results all point to the same general conclusion: Eliquis may be a safer choice among the new NOACs.
For more about the new anticoagulants, see Warfarin vs. Pradaxa and the Other New Anticoagulants.
Medical ID: If you’re on any blood thinner, it’s a good idea to carry some kind of medical ID. (See our Resources and Links for MedIDs free medical ID wallet card generator.) If you have an accident involving bleeding, EMTs don’t normally carry anticlotting meds. But they can call ahead to the ER and get the staff ready to help you.
Examining the Comparative Safety of Blood Thinners: An Analysis Utilizing AdverseEvents Explorer, February 2014, Special Report Download. http://info.adverseevents.com/special-report-blood-thinner Last accessed July 10, 2014.
Staton, Tracy. Eliquis earns best safety score in its class in analysis of FDA adverse event reports. FiercePharma, February 26, 2014. Last accessed July 10, 2014, http://www.fiercepharma.com/story/eliquis-earns-best-safety-score-its-class-analysis-fda-adverse-event-report/2014-02-26.
Return to FAQ Drug Therapies
17. “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 because 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?”
If you’re no longer in A-Fib, you’re also no longer in danger of having an A-Fib stroke. But you can have a “normal” stroke: i.e., a stroke that doesn’t originate from being in A-Fib. That’s probably what your doctor is worried about.
“Silent” A-Fib isn’t as much a problem as in the past. Today’s A-Fib catheter ablation doctors follow their patients for long periods of time after a successful catheter ablation and use an extensive array of monitoring devices to tell if a patient is in “silent” A-Fib. (See: A Primer: Ambulatory Heart Rhythm Monitors) It’s unlikely you’d experience a long period of silent A-Fib without your doctor being aware, though doctors and monitoring devices aren’t infallible.
Most doctors say you don’t need to worry about short A-Fib episodes. Conventional wisdom says it takes 24-48 hours of being in A-Fib for a clot to form. Though some doctors think it takes as little as 5 1/2 hours of being in A-Fib for a clot to develop.
Don’t be hesitant about getting a second opinion if you’re worried about having to be on an anticoagulant. Anticoagulants increase the risk of bleeding disorders. In addition to bleeding, Pradaxa can cause stomach upset or burning, and stomach pain. According to Dr. David Graham of the FDA, “Coumadin (the most commonly prescribed anticoagulant) provides a benefit, but it is also responsible for probably more deaths than any single drug currently marketed.” No one should be on blood thinners unless there’s a real risk of stroke. (See my article: Women in A-Fib Not at Greater Risk of Stroke!)
(Be advised that no anticoagulant regimen or procedure will absolutely guarantee you will never have a stroke. Even warfarin [Coumadin] only reduces the risk of stroke by 55% to 65% in A-Fib patients.)
No one wants to be on blood thinners. You bruise easily, cuts take a long time to stop bleeding, you can’t participate in any contact sports or any activities like mountain climbing, bike riding, etc. If in an accident, you risk bleeding to death, because there is currently no practical way to reverse the anticlotting effect of the newer anticoagulants. When taking anticoagulants, there is an increased risk of developing a hemorrhagic stroke and gastrointestinal bleeding. And anticoagulants often have other bad side effects, make one feel sick, and diminish one’s quality of life.
(Added October 26, 2015:
The FDA granted “accelerated approval” to Praxbind®, a reversal agent (antidote) to Pradaxa®. Praxbind is given intravenously to patients who have uncontrolled bleeding or require emergency surgery.)
Alternatives to Anticoagulants
Here are some alternatives to taking anticoagulants (discuss with your doctor before making any changes in your treatment plan):
• “Pill-In-The-Pocket”: Katharine had a successful catheter ablation several months ago. She emailed me that she now carries rivaroxiban (Xarelto) with her wherever she goes, though she’s never had to use it.
Rivaroxiban is a newer fast-acting anticoagulant which Katharine would use if she felt she was having an A-Fib episode. If Katharine were in an A-Fib episode, the rivaroxiban would work to prevent a clot from forming. No clinical trials have been done using this strategy, but it makes sense.
This “Pill-In-The-Pocket” approach means Katharine doesn’t have to risk taking heavy-duty anticoagulants for long periods of time or for the rest of her life. (Katharine hasn’t had any A-Fib episodes since her successful catheter ablation. But she’s happy to have rivaroxiban with her just in case.) See also: Treatments/Drug Therapies.
Be advised that this web site is not recommending or suggesting that you quit taking prescription blood thinners.
• “Natural” Blood Thinners: Do your own research, then discuss this option with your doctor. There are several informative articles about Natural Blood Thinners at LIVESTRONG.COM and an extensive article, “Blood Thinners and Nutritional Supplement” by Dr. Lam on his website. See also Question #14 above.
• Left Atrial Appendage (LAA) Occlusion Devices: The theory behind these devices which close off the opening of the Left Atrial Appendage is that 90%-95% of A-Fib clots come from the LAA. See Technical Innovation/The Watchman Device and Technical Innovations/The Lariat II.
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Last updated: Wednesday, May 18, 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
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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)
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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
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- 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↵