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.
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.
The accelerated approval program is designed to provide patients with earlier access to new drugs.
Pradaxa (dabigatran), a novel oral anticoagulant (NOAC), reduces the risk of clots and stroke in patients with Atrial Fibrillation. The new NOACs are alternatives to warfarin (Coumadin).
Patients on Pradaxa Were Bleeding to Death in the ER
Patients on Pradaxa have been bleeding to death in the ER while doctors were powerless to stop their bleeding and could only watch them die. See Stop Prescribing or Taking Pradaxa.
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). In one ongoing trial, the anticoagulant effect of Pradaxa was fully reversed in 89% of patients within four hours. This effect lasted at least 24 hours.
Praxbind works by binding to Pradaxa to neutralize its effect (measured as unbound Pradaxa plasma concentration). The most common side effects of Praxbind were headache, low potassium, confusion, constipation, fever and pneumonia.
Boehringer Ingelheim (a privately-held German company), which manufactures both Pradaxa and Praxbind, will be required to submit additional clinical information after approval to confirm the clinical benefit of Praxbind.
After Praxbind, Get Back on Anticoagulants ASAP!
Boehringer Ingelheim recommends that patients resume their anticoagulant therapy as soon as medically appropriate. In the clinical trials of Praxbind, five patients suffered strokes after reversal. They were not receiving anticoagulant therapy at the time of their stroke.
Other NOACs Will Soon Have a Reversal Agent
Pradaxa was the first NOAC to win FDA approval, but now there are three other new anti–blood clotting drugs available to doctors and patients.
Despite its newly approved reversal agent, Pradaxa’s advantage over the other NOACs will probably be short lived.
• Xarelto® (rivaroxaban) by Bayer Pharma/Janssen Pharmaceuticals
• Eliquis® (apixaban) by Pfizer/Bristol-Meyers Squibb (tested the best with the best safety record)
• Lixiana®/Savaysa® (edoxaban) by Daiichi-Sankyo (newest NOAC to be approved by the FDA)
Despite its newly approved reversal agent, Pradaxa’s advantage over the other NOACs will probably be short lived.
To build awareness, this is World Thrombosis Day.
A thrombosis is a blood clot that forms within a blood vessel and can be carried by either a vein or an artery. If that clot breaks free, it can lodge in an artery, travel to the brain and result in a stroke.
At A-Fib.com we write often about stroke risk due to Atrial Fibrillation (and the role of blood thinners to address that risk). A blood clot that forms as a result of A-Fib is an example of ‘arterial thromboembolism’.
A-Fib-related stroke can be particularly dangerous. Patients are twice as likely to be bedridden and more likely to die compared to patients with non-A-Fib-related stroke.
Anyone in the hospital is at major risk factor for developing a blood clot. Patients with decreased mobility or who experience blood vessel trauma due to surgery are more likely to develop blood clots.
If your loved one is being admitted to the hospital, proactively discuss their risk of stroke (i.e. venous thromboembolism or VTE ) with the hospital’s medical staff. Ask them for a VTE risk assessment to determine if they have any risk factors and whether they are at an increased chance of developing blood clots while in the hospital – or in the days or weeks after a hospital visit. Visit the World Thrombosis Day site.
Patients with A-Fib can use the CHADS2 & CHA2DS-VASc Stroke-Risk Grading Systems to access their stroke risk.
I recently wrote about how aspirin is no longer recommended as first-line therapy to prevent A-Fib stroke. (See my AF Symposium report, AHA/ACC/HRS Treatment Guideline Changes.).
But it’s not just A-Fib patients who shouldn’t be on aspirin therapy for stroke prevention.
Data indicates more than 1 in 10 patients take aspirin when they shouldn’t.
Warn your family and friends who are taking daily aspirin for stroke risk: Maybe they shouldn’t be.
50 Million in the US Take Aspirin for Prevention of Cardiovascular Disease
The problem with routinely taking aspirin is an increased risk of bleeding complications. More than one-third of all adults in the U.S. are now taking aspirin for primary and secondary prevention of cardiovascular disease (CVD).
“Primary” means preventing a first event like a heart attack. “Secondary” means preventing a reoccurrence of an event, like a second stroke.
When is Aspirin Therapy Appropriate?
As a “primary” prevention, only patients with a moderate to high 10-year risk of cardiovascular disease and stroke should be on aspirin therapy (estimated using the ACC/AHA risk-prediction calculator or similar calculator).
Aspirin is recommended for “secondary” prevention.
Try the ACC/AHA Risk-Prediction Calculator for yourself but beware:
Critics claim it overestimates CVD risk by 75-150% and could land you on lifelong statin therapy.
When is Aspirin Therapy Not Appropriate?
Aspirin is not appropriate for people who are at low risk—defined by their 10-year risk score. 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 these deaths occur in those who take low-dose (81-mg) aspirin.” The FDA in 2014 released a statement that warned against widespread use (of aspirin) in people of average risk.
Like Other Blood Thinners, Aspirin is a Pharmaceutical Drug
It’s all too easy to take an aspirin―we don’t need a prescription to get it. But taking an aspirin isn’t like taking a vitamin. Aspirin is a pharmaceutical drug.
Instead of routinely taking aspirin, you should discuss aspirin therapy with our doctor just as you’d do for any ‘by prescription’ blood thinner. (Take along a copy of this post.)
Note: Suddenly stopping daily aspirin therapy could have a rebound effect that may trigger a blood clot. If you have been taking daily aspirin therapy and want to stop, it’s important to talk to your doctor before making any changes.
Dr. John Day of the Intermountain Heart Institute, discussed how A-Fib doubles the risk of having a silent stroke. Many studies have shown that A-Fib is independently associated with dementia. “AF is associated with a higher risk for cognitive impairment and dementia, with or without a history of clinical stroke.”
In one study of 11,723 patients, those with arrhythmia were 4½ times more at risk of developing dementia.
Dr. Day described four possible mechanisms that may lead to A-Fib dementia:
1. Macro/Micro Thromboembolism (strokes)
2. Cerebral Bleeds
3. Weakened Cerebral Blood Flow
4. Systemic Inflammation
For more details about A-Fib and dementia, read my complete summary of Dr. John Day’s 2015 AF Symposium report.
AF Symposium 2015
Preventing TIA/Stroke During an Ablation
One of the reasons for getting a catheter ablation is to lower the risk of an A-Fib stroke and protect the brain. So to have a TIA/stroke during or after an ablation is, as Dr. Luigi Di Biase of the Albert Einstein College of Medicine, Bronx, NY, states “I think the worst complication ever in the field.” That’s why patients are put on anticoagulants like warfarin before and after an ablation and heperin during the actual ablation.
Most complication statistics after an ablation are of paroxysmal A-Fib patients. But Dr. Di Biase pointed out that ablations for persistent and long-term persistent often involve more tissue burns and consequently more risk of TIAs/stroke. In these cases periprocedural anticoagulation is even more important.
Uninterrupted Xarelto & Eliquis in Ablations as Effective and Safe as Warfarin, But Not Pradaxa
Dr. Di Biase discussed the COMPARE trial which showed the superiority of a strategy of uninterrupted warfarin anticoagulation both before and after an ablation in reducing TIAs/stroke and “silent” lesions. (“Silent” cerebral ischemia are lesions that show up on an MRI but don’t seem to have any effect and often go away on their own. But doctors still worry about and don’t know the long-term effects of these silent brain tissue disruptions.) He pointed out that doctors should still use heperin during the actual ablation, as most centers do.
But what about the NOACs (Novel Oral Anticoagulants)? Are they as effective as warfarin? “We have preliminary data showing that uninterrupted strategies with rivaroxaban (Xarelto) and apixaban (Eliquis) dramatically reduce the amount of silent thromboembolic lesions as well, and are as safe as warfarin in terms of TIA and stroke.” He wasn’t able to produce these results with Pradaxa.
Still No Reversal Agents for Xarelto & Eliquis, But Change is Coming
With the use of both warfarin and heperin, there is an increased risk of bleeding. Dr. Di Biase described how at his center they use fresh frozen plasma for bleeding management of warfarin and heperin bleeds. But there are still no direct reversal agents for the NOACs. Dr. DiBiase seemed confident that a new reversal agent for apixaban and rivaroxaban looks very promising “to completely reverse the effects of these two drugs in less than four minutes.”
I usually don’t discuss drugs until they’ve actually been approved by the FDA. But a reversal agent for Xarelto and Eliquis does seem to be on FDA fast track for approval and would certainly be a most welcome development for A-Fib patients. It might even work better than the current reversal agents for warfarin.
(Added August, 15, 2015): 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 for all 90 patients. No serious side effects were reported. FDA approval is pending.
We shouldn’t blame the FDA for approving the NOACs without any reversal process or remedy to stop bleeding. There has been an incredible need for new, different anticoagulants for nearly 40 years. It may have been worse if the FDA had kept the NOACs off of the market.
Marzo, Kevin. Blood thinner Antidote. Bottom Line Health, Volume 29, Number 9, September 2015, p. 1.
Mundell, E.J.. Drug May Be Antidote to Bleeding Tied to Blood Thinner Pradaxa. Medline Plus. Monday, June 22, 2015. http://www.nlm.nih.gov/medlineplus/news/fullstory_153206.html
Last updated: Saturday, August 15, 2015
By Steve S. Ryan, PhD, February 2015
If you’ve had your Left Atrial Appendage (LAA) closed off using the Lariat device from SentreHeart, Inc., you must schedule follow-up tests at 3 months and one year intervals to check for total LAA closure with no gaps or leakage. Talk to your doctor about a TEE (Trans-esophageal Echocardiogram) or preferably a 3-D TEE. In a small number of reported cases the Lariat failed to fully seal off the LAA allowing tissue remnants to loosen, enter the blood stream and cause clot and stroke. (See Shannon Dickson’s first-hand story below.)
The Lariat Device
When closing off the Left Atrial Appendage (LAA), surgeons may use the Lariat II device, a noose-like device which is slipped around this small pocket of heart tissue. The ‘lasso’ is then tightened, and eventually the tissue dies and shrivels up like a grape. In effect, the Lariat II chokes off the LAA and eliminates it as a source of A-Fib signals. (For more on the Lariat see my article: Tech & Innovations: Lariat II.)
The Problem: The ‘Gunny-Sack’ Effect
In what is described as “the gunny-sack effect”, the LAA heart tissue between the lariat lasso atrophies and becomes thinner. As with a gunnysack, the multiple tight folds begin to loosen and unravel slightly leaving a hole. If the hole is large enough, blood may flow into and out of the dead LAA possibly carrying with it dead (necrotic) tissue remnants into the blood stream. These dead tissue remnants can cause clots and strokes. Normal blood thinners don’t work on them. Any hole over 2mm can create such leaks. It’s estimated that holes greater than 2mm occur in 6% of Lariat cases, but not all cause clots and strokes. The number of clot/strokes (embolic events) reported so far is very small compared with around 2,500 total Lariat cases worldwide to-date.
Easily Fixed if Discovered
Once this hole or leak is discovered, it’s relatively easy for your surgeon to fix by closing it off with an Amplatzer Atrial Septal Occluder, an Amplatzer Duct Occluder II, or a Gore Helix Septal Occluder.
Lariat II – Should Include Short-Term Anticoagulation
And even when the LAA is completely closed off, there is still a small chance (around 2%) of clots forming inside the heart at the LAA closed off location primarily during the first 4-8 weeks. This is probably related to tissue inflammation and blood platelet “clumping” at the site. It’s therefore important for you and your doctor to consider short term anticoagulation for 6-8 weeks to reduce the risk of clot forming at the closure site. (For those patient who can not take oral anticoagulation or antiplatelet agents, there will be a small temporary risk of stroke at the LAA site while the area heals.)
Shannon W. Dickson: Tells of Clots and a Stroke After Lariat II Installed
If you’d like to read a well-written first-person account of someone who experienced clots and a stroke after having a Lariat occluder installed, Shannon W. Dickson published his experience in The AFIB Report, Number 133, August/September 2014.
(Shannon Dickson says he got the Lariat II because his A-Fib was producing loads of spots in his LAA. Even after an LAA isolation ablation a year earlier (effectively disconnecting electrically from the LAA), Shannon chose the added reassurance a successful Lariat ligation can bring. Permanently removing the LAA from the ‘AFIB/Flutter equation’ insures his LAA could never again reconnect and be a source of more arrhythmia.)
Shannon is the new managing editor of The AFIB Report; a one-year subscription to The AFIB Report is $29.00.
Don’t let this risk of a leak and stroke scare you away from having a Lariat device installed if you need it. If a hole or leak does form, and it’s discovered, it’s very easily fixed. Just make sure your doctors check for leaks!
Last updated: Friday, October 14, 2016
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.
(Happily I was wrong on this prediction. 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.)
Watchman May Win 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.email@example.com. 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: Friday, November 18, 2016
23. “During an ablation, how much danger is there of developing a clot? What are the odds? How can these clots be prevented?” [Someone emailed me that she suffered both a stroke and a blood clot in her lung during her ablation. She is recovering. Why did this happen?]
Depending on how long one has been in A-Fib, clots may have developed in the heart, then be dislodged during the ablation.
Most centers do a TEE (Transesophageal Echocardiogram) before the ablation to check if there are any clots in your heart. If they find any, they administer anticoagulants to dissolve the clots before the ablation. If your center or doctor doesn’t plan to do a TEE before your ablation, you should probably go somewhere else.
However, most clots during an ablation come from RF charring. The heat from an RF catheter chars the heart tissue. Some of the char breaks off and becomes a clot. This problem has been minimized over the years by the use of irrigated tip catheters and the administering of heavy-duty anticoagulants like heparin during the ablation. The skill and expertise of the doctor also play an important role. But even in the best of hands, accidents can still happen.
Your chances of developing a clot during an ablation vary according to the institution and doctor. (You should ask about this the medical center or EP’s rate of clots forming when considering an ablation.) For example, the Bordeaux Group in 2010 reported an embolic event (stroke) rate of 0.2%.
With the newer technique of CryoBalloon (freezing) ablation, there is no charring and theoretically no risk of developing a clot from charring.
Last updated: Wednesday, February 4, 2015
Return to FAQ Catheter Ablation and Maze Surgeries
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
Frequently Asked Questions by Newly Diagnosed Patients
Newly diagnosed Atrial Fibrillation patients have many questions about living with A-Fib. These are answers to the most frequently asked questions by patients and their families. (Click on the question to jump to the answer)
Last updated: Monday, July 13, 2015
A-Fib-Free After Catheter Ablation, Patient on Anticoagulation Therapy for 10 years Develops Cerebral Microbleeds and Associated Early Dementia.
By Steve S. Ryan, Updated March 2016
Dr. John Day, in an editorial in The Journal of Innovations in Cardiac Rhythm Management, described his patient, Bob, who had been on anticoagulation therapy for 10 years, even though he had had a successful catheter ablation and was A-Fib free. Of concern, these new guidelines call for many more people to be on anticoagulant therapy, particularly women.
Of concern, these new guidelines call for many more people to be on anticoagulant therapy, particularly women.
Bob was suffering from early dementia. A cranial MRI revealed many cerebral microbleeds, probably caused by taking anticoagulants for years. Both antiplatelet and anticoagulant therapy significantly increase the risk of cerebral microbleeds which are associated with dementia. These microbleeds are usually permanent and irreversible.
Dr. Day asked, “Could it be that this was an iatrogenic (caused by a doctor’s activity or therapy) case of dementia? Was his 10 years of anticoagulant use for atrial fibrillation the cause of his dementia?”
The New CHA2DS2-VASc Guidelines for Anticoagulation Therapy
Dr. Day discusses the new CHA2DS2-VASc guidelines for anticoagulation therapy. He points out that none of the major studies supporting the CHA2DS2-VASc guidelines have reported the accompanying cerebral microbleed risk. He also calls our attention to the reports from many centers that long-term stroke risk following catheter ablation is very low. Ablation may reduce the total arrhythmia burden or convert recurrences to more organized rhythms, such as an atrial tachycardia, with a lower stroke risk.
This effect of A-Fib ablation isn’t recognized in the latest guidelines.
So, the question is, ‘Why the risks of life-long anticoagulation therapy if the patient has had a successful ablation procedure?’
(See more research contradicting the 2014 Guides: A study using the Taiwan Research Database of 186,570 A-Fib patients, they discounted female gender and only looked at females with a CHA2DS2-VASc score of 2 (one additional risk factor besides being female).1,2,3
Warning: The Risks of Life-long Anticoagulation Therapy
Dr. Day concludes, “Somehow I think we have lost sight of the total picture with the new A-Fib management guidelines. In my mind, I am not convinced that the long-term stroke risk of a CHA2DS2-VASc score of 1 or 2 (depending on which risk factors are present) justifies all of the risks of life-long anticoagulation therapy, particularly if the patient has had a successful ablation procedure.”4 Dr. John Mandrola echoes Dr. Day, “And if there is no A-Fib, there is no benefit from anticoagulation.”5
“But CHA2D2-VASc are just guidelines, aren’t they? Doctors don’t have to follow them, do they?”
Unfortunately once guidelines like these become official, they in effect become the law of the land. If a doctor doesn’t follow them and a patient has a stroke, the doctor is almost guaranteed a losing malpractice law suit. The first thing a trial lawyer will point out to an arbitrator or jury is that the doctor didn’t follow current guidelines.
This puts doctors in a very difficult position. Even though Dr. Day knows all too well and agonizes over the fact that his anticoagulant therapy probably caused his patient Bob’s dementia, he can’t change the guidelines.
See also my articles: Women in A-Fib Not at Greater Risk of Stroke! and Israeli Study-Being Female Not a Risk Factor for Stroke.)
Return to Index of Articles: Research and Innovations
Last updated: Tuesday, March 29, 2016
- Chao TF, et al. Should atrial fibrillation patients with 1 additional risk factor of the CHA2DS2-VASc score (beyond sex) receive oral anticoagulation? J Am Coll Cardiol. 2015 Feb 24;65(7):635-42. doi: 10.1016/j.jacc.2014.11.046. PubMed PMID: 25677422. http://www.ncbi.nlm.nih.gov/pubmed/25677422↵
- Amson, Yoav et al. Are There Gender-Related Differences In Management, And Outcome Of Patients With Atrial Fibrillation? A Prospective National Study. Arrhythmias and Clinical EP. Acc.15. JACC. March 17, 2015, Volume 65, Issue 10S. doi: 10.1016/S0735-1097(15)60469-7 http://content.onlinejacc.org/article.aspx?articleid=2198096&resultClick=3↵
- Friberg et al. Benefit of anticoagulation unlikely in patients with atrial fibrillation and a CHA2DS2-VASc score of 1. J AM Coll Cardiol. 2015; 65(3):a-232. URL: http://www.sciencedirect.com/science/article/pii/S0735109714070119. doi:10.1016/j.jacc.2014.10.052↵
- Day, John. Letter from the Editor in Chief. The Journal of Innovations in Cardiac Rhythm Management, 5 (2014), A6-A7. Last accessed May 15, 2014, URL: http://www.innovationsincrm.com/cardiac-rhythm-management/2014/may/586-letter-from-the-editor-in-chief↵
- Mandrola, John. Atrial Flutter–15 facts you may want to know. In AF Ablation, Atrial fibrillation. August 5, 2013. http://www.drjohnm.org/2013/08/atrial-flutter-15-facts-you-may-want-to-know↵
High Fibrosis at Greater Risk of Stroke and Precludes Catheter Ablation: Lessons Learned from the DECAAF Trial
By Steve S. Ryan, PhD
Presenter: Dr. Nassir Marrouche of the Comprehensive Arrhythmia Research and Management Center (CARMA) at the University of Utah Health Sciences gave a presentation entitled “The Ablation Lesion or the Atrial Disease? Lessons Learn from DECAAF.”
Background: In his BAFS 2011 presentation, (see BAFS 2011: MRI [Magnetic Resonant Imaging) Applied to A-Fib), Dr. Marrouche described the data enhancement (also called “delayed-enhancement”) MRI process which uses a metallic Gadolinium contrast dye to see in 3D and identify collagen fibrotic areas in the heart. Dr. Marrouche uses MRI to separate A-Fib patients by their degree of fibrosis into four “stages:” In addition to other factors, the amount of fibrosis in the left atrium is key to ablation treatment success.
• “Utah Stage 1” low scarring or fibrosis
• “Utah Stage 2” 5%-20% fibrosis
• “Utah Stage 3 20%-35% fibrosis
• “Utah Stage 4: greater than 35% fibrosis
Detecting Fibrosis with the DE-MRI
To begin, Dr. Marrouche showed slides of how the delayed-enhancement MRI (DE-MRI) is used to detect fibrosis.1 Using “Masson trichome” staining he showed slides of how normal myocytes (heart muscle) appear normal and red, while areas of collagen (fibrosis) appear blue and almost blot out the red myocytes in someone with extensive A-Fib.
DECAFF Study Findings
The Delayed Enhancement-MRI Determinant of Successful Catheter Ablation of Atrial Fibrillation trial (DECAAF) was conducted at 15 different centers worldwide between 2010 and 2011. The degree of fibrosis in patients with atrial fibrillation was followed before and after their catheter ablation.2
The DECAFF study showed that patients with more fibrosis (Utah Stage III and IV) had less successful ablation outcomes. They also had a greater risk of stroke. MRI was also used to detect ablation scarring and gaps in ablation lesions. (The various centers used different types of catheter ablation such as PVI with RF or with Cryo.) In a somewhat controversial statement, Dr. Marrouche had previously stated, “encircling the (pulmonary) veins with lesions as seen on the MRI was not important in terms of treatment success.”3
These findings support Dr. Marrouche’s previous presentation at the Boston A-Fib Symposium (see BAFS 2011: MRI [Magnetic Resonant Imaging] Applied to A-Fib).
The only predictor of atrial fibrosis was hypertension (p=0.004).
The predictors of recurrence after ablation were:
- Left atrial fibrosis (p<0.0001) Each 1% increase in fibrosis was associated with a 6% increased risk of recurrence.
- Mitral valve disease (p<0.0001)
- Left Ventricular Ejection Fraction (p<0.05)
Dr. Marrouche discussed what he called residual fibrosis “fibrotic tissue not covered with ablation lesions.” Residual fibrosis is measured by subtracting ablated scar area from pre-ablation DE-MRI. The more residual fibrosis, the more there is an increased risk of recurrence.
DECAFF Conclusions: Utah Stage III & IV Fibrosis Levels Not Recommended For Catheter Ablation
Dr. Marrouche concluded from the DECAFF study that “Atrial fibrosis detected using DE-MRI is a strong and independent predictor of procedural outcome in patients undergoing ablation of atrial fibrillation.” For all patients in Utah Stage IV and for many in Utah Stage III, they are not recommended for catheter ablation but should be put on life-long medication instead. Because of the extent of their fibrosis, they have less successful ablation outcomes.
Patients with High Levels of Fibrosis More at Risk of Stroke
One of the most important findings for patients from Dr. Marrouche’s studies is that patients with high levels of fibrosis are more at risk of stroke. Utah Stage IV patients were four times more likely to have a stroke than patients with a low level of atrial fibrosis. In his previous work, Dr. Marrouche found that even patients in simple early-onset paroxysmal A-Fib can have high levels of fibrosis. (Many other factors besides A-Fib can produce fibrosis in the heart.) Anyone in A-Fib should probably have an MRI to measure their level of fibrosis. Instead of the less empirical CHADS2 score, an MRI would quantify whether or not a person needs to be on anticoagulants. MRIs to measure fibrosis should become a routine diagnostic tool.
Hypertension Produces Fibrosis
In Dr. Marrouche’s studies, hypertension was the only guaranteed predictor of developing fibrosis. We already knew that hypertension was a cause or trigger of A-Fib. Thanks to Dr. Marrouche, we also now know that hypertension causes or triggers fibrosis. If you have real hypertension, do what you can to lower it (diet, exercise, medications, etc.) Though sometimes this is very hard to do.
More research needs to be done on the link(s) between hypertension, fibrosis and A-Fib. If we induce hypertension, for example in animal studies, does it produce both fibrosis and A-Fib at the same time? Or does the A-Fib develop first, then produce fibrosis?
High Fibrosis Precludes Catheter Ablation
Sad news for patients? According to Dr. Marrouche’s studies, high levels of fibrosis preclude having a catheter ablation, that catheter ablation has a poor success rate in cases of high fibrosis (Utah Stages III and IV). Dr. Marrouche recommends that these high fibrosis patients reconcile themselves to living the rest of their lives on meds, that they can’t be cured of their A-Fib by catheter ablation. (It must be devastating for a patient to hear this.)
But many centers and doctors specialize in ablating patients with persistent and long-standing persistent A-Fib. For example, in a live case ablation at the 2014 Boston A-Fib Symposium at Orlando, Dr. Mélèze Hocini from the Bordeaux Group using ECGI successfully ablated a patient with persistent A-Fib and a fibrosis score of 22% (Utah Stage III) who also had a huge dilated left atrium. Fibrotic heart tissue doesn’t preclude or prevent making catheter burns in the heart. Rather, high levels of fibrosis are usually associated with more difficult-to-ablate cases where there are more A-Fib signals sources than just in the pulmonary veins. But some doctors and centers do these kinds of ablations all the time with high success rates.
If someone tells you that you have too much fibrosis to have a successful catheter ablation, get a second opinion. But you probably shouldn’t go to your local EP. Instead you need to go to more experienced doctors and centers like the Bordeaux group who specialize in tracking down, mapping and isolating A-Fib signal sources coming from other spots in the heart than the pulmonary veins. (See my list of EPs specializing in Persistent and Long-standing Persistent A-Fib.)
“encircling the (pulmonary) veins with lesions as seen on the MRI was not important in terms of treatment success.”
Practically all the centers in the study started by isolating the PVs. But success (freedom from recurrence) in the DECAAF study was dependent on the previous amount of fibrosis. However, the PVs usually do need to be isolated for treatment success.
“Residual Fibrosis”, from the perspective of A-Fib patients, isn’t all that different from ablation burns. Catheter ablation doesn’t change fibrotic heart tissue to normal tissue. In both cases the heart tissue is scarred, dead, immobile, with little or no blood flow and transport function. That’s why most EPs try to keep catheter ablation burns to a minimum.
Stuart, C. MRI may help identify best candidates for ablation. Cardiovascular Business. Feb 05, 2014. Last accessed March 16, 2014, URL: http://tinyurl.com/DECAAFTrial
Return to Index of Articles: AF Symposium: Steve’s Summary Reports
Last updated: Saturday, February 13, 2016
- VIDEO: 3D Model of Left Atrium Demonstrating Left Atrial Fibrosis in a Patient with Atrial Fibrillation. Last accessed March 16, 2014. URL: http://tinyurl.com/DECAAF3DModel↵
- Marrouche NF, et al. Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. JAMA. 2014 Feb 5;311(5):498-506. doi: 10.1001/jama.2014.3. PubMed PMID: 24496537.↵
- O’Riordan, Michael. DECAFF Published: MRI Aids in AF Ablation Success. Heartwire, February 5, 2014. http:”//www.medscape.com/viewarticle/820230↵
A-Fib and Stroke: Women Under-Diagnosed & Under-Treated:
A Woman’s Perspective
By Lynn Haye
Stroke prevention is the primary focus for all people with A-Fib; men and women, young and old – regardless of the type of A-Fib. Patients with A-Fib have a 5-fold increased risk of stroke. This risk factor increases steeply with age (1.5% at ages 50-59 to 23.5% at ages 80-89)1 In addition, since A-Fib is often asymptomatic and may go clinically undetected, the stroke risk attributed to A-Fib may be substantially underestimated.
The National Stroke Association estimates that at least 1 in 6 strokes are actually caused by A-Fib and that A-Fib strokes are more debilitating with higher rates of mortality. However, three out of four A-Fib strokes can be prevented in patients who have been diagnosed with A-Fib and are receiving appropriate treatment.2
Her A-Fib Stroke Risk
Recent publications have highlighted the gender differences in stroke risk.3,4 Women have a higher lifetime risk of stroke from all causes, and this is probably related to both life expectancy and treatment variables. The question of female sex as a separate risk factor for stroke in A-Fib is a bit more complicated.
There are two stroke risk tools currently used by physicians to predict risk in A-Fib patients; CHADS2 in the US and the newer CHA2DS2-VASc in Europe.5 The newer tool adds an independent risk factor for female sex and lowers the age range to 65 for risk. (To read more about CHADS2 and CHA2DS2-VASc see our article: The CHADS2 Stroke-Risk Grading System.) This development puts younger women with A-Fib into consideration for anticoagulation medication. Because of the increased risk for bleeding on these medications, there is concern about putting more and younger patients on them. Anticoagulants are not like taking vitamins. No one should be on anticoagulants unless there is a real risk of stroke.
A recent Danish study 6 found that while female sex increased stroke risk by 20% in A-Fib patients older than 75, it did not do so in female A-Fib patients age 65-74. This suggests no increased risk for younger women, while older women remain at risk due to age. The current UK protocol in the GARFIELD study 7may answer this difference as they are evaluating the significance of female sex as an independent risk factor for A-Fib stroke in younger patients, age 65-74.
As with other cardiovascular disorders, women with arrhythmias in the US have been under-treated and under-referred. This less aggressive and/or less effective treatment for A-Fib may put women at higher risk for stroke overall. Studies have shown that women with A-Fib have been less likely to receive anticoagulation and ablation procedures compared to men, although their treatment benefits are comparable.4
Let’s take the example of Elaine, a college-educated professional who marries at age 25 to Bob, a 32-year-old accountant. They both lead busy but fulfilling lives and have two wonderful children. Elaine is naturally protected from a stroke during her child-bearing years by her menstrual cycle. The blood she loses every month thins her blood and makes her less susceptible to forming clots and having a stroke. But once Elaine enters menopause and no longer has her menstrual cycle, all too soon her risk of stroke becomes the same as her husband, Bob.
Bob unfortunately passes away at age 76 leaving Elaine a widow at age 69. (Women in the US live an average of five years longer than men.) As Elaine ages she becomes more limited in her physical activities. Her blood becomes thicker and less viscous. Clots can more easily form in her heart, especially in the Left Atrial Appendage (where 90-95% of A-Fib clots form). She may develop A-Fib which is more likely to happen as people get older. At age 81 Elaine has an A-Fib stroke.
Unfortunately this scenario is an all too common for women.
Preventing Her A-Fib Stroke
Is there anything women can do to reduce their risk of stroke? Some things come to mind:
Recognize Important Signs
If you haven’t been formally diagnosed with A-Fib, be sure to take seriously signs such as palpitations, shortness of breath, fatigue, dizziness, chest pain and fainting. These signs may be significant, not just moods or the result of an ‘off’ day. Check your pulse for any irregularity – it’s the rhythm not the rate that should concern you here. Remember, A-Fib stroke may be avoided with early diagnosis and treatment.
See an Electrophysiologist (EP)
If you are newly diagnosed, have you followed up with a cardiologist or, better still, an electrophysiologist (EP)? EPs see arrhythmias all the time and are usually more current on treatment options. Sometimes it feels just ‘too’ serious or inappropriate to contact a ‘heart’ specialist, but it’s really more comforting when you are in the care of someone who regularly treats A-Fib.
If you need help locating an electrophysiologist in your area, check the provider list on this web site.
Be Aware—We Women Communicate Differently
Most women agree that we tend to communicate differently! Contrary to some popular opinion, we often hesitate to complain or report symptoms – even when we know we should. Some women still see heart problems as ‘masculine’ and can feel awkward presenting cardiac symptoms, particularly to a male physician. Just watch the comedic video by Elizabeth Banks at the American Heart Association website for a very insightful rendition of how we can minimize symptoms (AHA, Go Red for Women, “Just a Little Heart Attack”). It’s painfully funny….
Prepare for Your Electrophysiologist (EP) Appointment
Your physician may have limited time, so be prepared before going in for your appointment. It helps to take a list of questions or concerns to help you stay focused and make the best use of your time. This also demonstrates the level of seriousness and concern that you bring to the session.
Importance of Blood Thinners for Women
Anticoagulation therapy is so basic to stroke prevention in A-Fib that any woman diagnosed with non-valvular A-Fib should make sure to discuss this with her physician at her first appointment. But ‘Blood thinners’ carry the risk of bleeding, so your physician may check your risk on the HAS-BLED score.8 before prescribing blood thinners for you.
The newer, novel anticoagulants such as Pradaxa and Xarelto can make adherence easier for women. This is because the lack of dietary restrictions suits the diet of the typically ‘dieting’ woman. However, the new, novel anticoagulants do not yet have reversal agents and should be used with caution. The other option, warfarin, requires frequent blood monitoring, and women are often very reluctant to add more required tasks to their already busy schedules. There is a procedure for those who cannot tolerate anticoagulation medication. This procedure involves closing off the left atrial appendage and involves a more detailed and complex risk-benefit analysis.
Know the Symptoms of Stroke!
• Sudden numbness or weakness of face, arm, leg—especially on one side of the body.
• Sudden confusion, trouble speaking or understanding
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking, dizziness, loss of balance or coordination
• Sudden severe headache with no known cause
And the Other Symptoms Unique to women!
• Sudden face and limb pain
• Sudden hiccups
• Sudden nausea
• Sudden general weakness
• Sudden chest pain
• Sudden shortness of breath
• Sudden palpitations
Call your emergency service (dial 911 in the US or 999 in the UK) if you have any of these symptoms, and make sure that your family and friends know that time is critical with stroke. Everyone should know the simple test to act F.A.S.T.
F = FACE Ask the person to smile. Does one side of the face droop?
A= ARMS Ask the person to raise both arms. Does one arm drift down?
S= SPEECH Ask the person to repeat a simple phrase. Is their speech slurred or strange?
T= TIME If you observe any of these signs, call 911 immediately. 2
Aim to be A-Fib Free
Probably the best thing to know about A-Fib stroke prevention is to not have A-Fib! As Steve Ryan points out so well in his book, “Beat Your A-Fib”, the best preventive for A-Fib stroke is get rid of your A-Fib, to ‘Beat Your A-Fib’.
(posted October 2013)
Prevent an A-Fib stroke—first ‘treat’—then ‘beat’ your A-Fib!
LYNN HAYE, Ph.D. is a clinical psychologist and former A-Fib patient. She studies and writes about current trends in the treatment and diagnosis of atrial fibrillation and has a special interest in women’s health issues. Dr. Haye and her family live in Orange County, CA.
Return to Index of Articles: Research and Innovations
Last updated: Saturday, August 15, 2015
- American Heart Association, Heart disease and stroke statistics 2013 update. www.heart.org↵
- National Stroke Association www.stroke.org↵
- True Hills, M., ‘Gender Matters: Why Afib is More Fatal for Women’ EP Lab Digest 2013. www.eplabdigest.com/articles/Gender-Matters-Why-Afib-More-Fatal-Women↵
- Curtis, A.B., Narasimha, D., ‘Arrhythmias in Women’ Clinical Cardiology, 2012 Mar; 36(3) www.ncbi.nlm.nih.gov/pubmed/22389121↵
- Mikkelsen, A., et al, ‘Female gender increases stroke risk in AF patients aged greater than 75 years by 20%’ European Society of Cardiology. 2012 www.escardio.org↵
- An international longitudinal registry of patients with atrial fibrillation at risk of stroke (GARFIELD): the UK protocol. 2013 www.biomedcentral.com↵
- Curtis, A.B., Narasimha, D., ‘Arrhythmias in Women’ Clinical Cardiology, 2012 Mar; 36(3) www.ncbi.nlm.nih.gov/pubmed/22389121↵
- National Stroke Association www.stroke.org↵
Denmark Study—Being a woman not a risk factor for stroke
The new guidelines for stroke prevention in A-Fib (CHA2DS2-VASc) state that simply being a woman is a risk factor for stroke. But a recent comprehensive study from Denmark indicates this may not be true. (The guidelines were first adopted in Europe in 2012 and in the US in May 2014).
The Danes seem to have an effective health care system for everyone which includes, among other benefits, data on anyone with A-Fib. They looked at 44,744 women with A-Fib. Female gender did not increase the risk of stroke in patients aged less than 75 years. (According to most guidelines, being over 75 years old is a risk factor for stroke irrespective of whether one is female or male.) According to the study’s Dr. Anders Mikkelsen, “This suggests that female sex should not be included as an independent stroke/TE risk factor in guidelines or in risk stratification schemes used in treatment of patients with atrial fibrillation.”
(Added August 31, 2015: An Israeil observational study of 100,000 people came to the same conclusions as the above Denmark study. See Israeli Study—Being Female Not a Risk Factor for Stroke.
Dr. Day—Risks of Life-Long Anticoagulant Therapy
Dr. John Day, in a May 2014 editorial in The Journal of Innovations in Cardiac Rhythm Management, discusses the new CHA2DS2-VASc guidelines for anticoagulation therapy that call for many more people to be on anticoagulant therapy, particularly women. Dr. Day does not go so far as to say the new guidelines are in error (as I do), but he does ask,” What about the 35 year old woman with borderline hypertension and only one A-Fib recurrence each year? Should she now take anticoagulants for the rest of her life even if she has had a successful ablation?”
This editorial was very personal for Dr. Day. One of his patients, after a successful catheter ablation, was on anticoagulant therapy for 10 years and developed early onset dementia. A cranial MRI revealed many cerebral microbleeds. Both antiplatelet and anticoagulant therapy significantly increase the risk of cerebral microbleeds which are associated with dementia. Microbleeds are considered permanent and irreversible.
Dr. Day concludes, “Somehow I think we have lost sight of the total picture with the new A-Fib management guidelines. In my mind, I am not convinced that the long-term stroke risk of a CHA2DS2-VASc score of 1 or 2 (depending on which risk factors are present) justifies all of the risks of life-long anticoagulation therapy, particularly if the patient has had a successful ablation procedure.” For more of Dr. Day’s comments, see The New CHA2DS2-VASc Guidelines and the Risks of Life-Long Anticoagulation Therapy.
Dr. John Mandrola echoes Dr. Day, “And if there is no A-Fib, there is no benefit from anticoagulation.”
Intuitively it doesn’t make sense that simply being a woman makes you more at risk of having an A-Fib stroke. This study seems to confirm what common sense would indicate and is most welcome news for women.
Anticoagulants Not Like Taking Vitamins
Women (and men) should be aware that anticoagulants increase the risk of bleeding disorders* and should be given only to patients at a real risk of stroke. “In addition to bleeding, Pradaxa can cause stomach upset or burning, and stomach pain.” (Pradaxa Fact Sheet PX81802) (These statements don’t capture the actual human toll—burning throat, roiling intestines, diarrhea, burning anus, lasting intestinal damage, etc. that Pradaxa can produce in some people.) According to Dr. David Graham of the FDA, the anticoagulant “Coumadin provides a benefit, but it is also responsible for probably more deaths than any single drug currently marketed.”
Many people have problems when taking anticoagulants and would prefer not to have to take them. One bruises easily, cuts take a long time to stop bleeding, one can’t participate in any contact sports or any activities like mountain climbing, bike riding, etc. If in an accident, one risks 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 an hemorrhagic stroke and gastrointestinal bleeding. And anticoagulants often have other bad side effects, make one feel sick, and diminish one’s quality of life.
TV Ads for Anticoagulants
But recent advertising campaigns give the impression that you must take anticoagulants if you have A-Fib, that anticoagulants are the be-all and end-all for treating A-Fib, that if you take anticoagulants, then you will live happily ever after. (Actually anticoagulants are not a treatment for A-Fib, but for the risk of an A-Fib stroke). However, no matter how altruistic these national campaigns sound in trying to increase people’s awareness and knowledge of A-Fib, be advised that their primary purpose is to sell pharmaceuticals.
Gender Bias to Sell More Anticoagulants
If someone tells you that you must take anticoagulants because you are a woman, it may be time to get a second opinion. Don’t let a form of gender bias intimidate you into taking anticoagulants.
Realize also that adding a point to a person’s risk score translates into a huge increase in sales for pharmaceutical companies. The guidelines were written by doctors with major conflicts of interest.
However, if you know the risks and bad side effects of taking anticoagulants but still want to take them, that is certainly an option to discuss with your doctor.
(Thanks to David C. Holzman for calling our attention to this important study for women.)
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Last updated: Wednesday, September 2, 2015
By Steve S. Ryan, PhD, Updated Nov 2014
In the US, doctors use what is called a CHADS2 stroke-risk grading system to help estimate the risk of stroke in patients with atrial fibrillation. A high CHADS2 score corresponds to a greater risk of stroke, while a low CHADS2 score corresponds to a lower risk of stroke. The CHADS2 score is simple and has been validated by many studies.
The patient’s stroke risk, i.e., their CHADS2 score, is estimated by adding together the points that correspond to the patient’s conditions.
“C” Congestive Heart Failure Score = 1
“H” Hypertension Score = 1
“A” Age over 75 Score = 1
“D” Diabetes Score = 1
“S2” Previous Stroke or TIA Score = 2
A CHADS2 score of 2 or over would indicate someone should be on a blood thinner such as warfarin.
The CHADS2 score has been superseded in clinical use by the CHA2DS2-VASc score that is designed to give a better stratification of low-risk patients. It utilizes the same 5 major risk factors considered by CHADS2 but assigns a score of ‘2’ for patients older than 75 years, and adds 3 new risk factors: a history of vascular disease, age 65-74 years, and female sex which increase stroke risk. But according to the original study, “there was no statistically significant difference found between the CHA2DS2-VASc and CHADS2 risk stratification schema in predicting TE events”.
A-Fib Stroke Risk Calculators
Classification of CHADS2 vs CHA2DS-VASc
In both scoring systems, a score of 0 is “low” risk of stroke, 1 is “moderate”, and any score above 1 is a “high” risk. The CHA2DS2-VASc system has three more variables and therefore will classify a greater number of patients into a high-risk group.
Editor’s comment: There is some controversy about the increased stroke risk for females. See articles on Dr. John M’s blog post and Aging Well magazine.
See also our article: Women in A-Fib Not at Greater Risk of Stroke, and The New CHA2DS2-VASc Guidelines and the Risks of Life-Long Anticoagulation Therapy.
Last updated: Thursday, September 3, 2015
The Role of the Left Atrial Appendage (LAA) & Removal Issues
By Steve S. Ryan, PhD
In the first trimester or two of our time in the womb, The Left Atrial Appendage (LAA) was originally our left atrium (LA). When the final real Left Atrium (LA) formed gradually from the conjunction and evolutionary development of the four pulmonary veins, the actual LA chamber grew and ballooned out, pushing the smaller remnant LA up to the left top of the Left Atrium where it became became known as the Left Atrial Appendage (LAA) with its own functions and behaviors.
But as we age and as heart disease/A-Fib, etc. start to set in, the LAA can turn into “the most lethal, no longer essential appendage in the human anatomy.” (Thanks to Shannon Dickson for these insights about the LAA.)
One considered advantage of the Mini-Maze operations is that the Left Atrial Appendage (LAA) is closed or cut off. Most A-Fib blood clots which cause stroke come from the Left Atrial Appendage. By closing off the LAA, most but not all risk of stroke is eliminated even if you are still in A-Fib.
Failure to Completely Close Off the LAA is Common
Also see my article, Left Atrial Appendage May be Important for Heart Repair
Also see my article, Left Atrial Appendage May be Important for Heart Repair
According to Dr. Marc Gillinov of the Cleveland Clinic, staplers “can be hard to apply to the appendage and tend to leave a little cul-de-sac and also cause bleeding and tearing, so they are not particularly safe or effective.”2
However, the AtriClip device (FDA approved June, 2010) makes it much easier for surgeons to close off the LAA during open heart surgery. The surgeon positions the rectangular-shaped device around the LAA and then closes it like a clamp. Blood no longer flows into and out of the Left Atrial Appendage.3
AtriCure has developed a version of the AtriClip which can be used in Mini-Maze surgery.
Should the LAA be routinely cut out, stapled shut or closed off in all A-Fib patients?
Some question the need or benefit of removing the Left Atrial Appendage (LAA) if someone is no longer in A-Fib.
Some question the need or benefit of removing the Left Atrial Appendage (LAA) if someone is no longer in A-Fib.
Another important consideration, even if a person is no longer in A-Fib, is that closing off the LAA may still prevent a stroke. The LAA is where most clots originate. If a surgeon is already working on the heart, why not close off the LAA and reduce the patient’s chance of having a future stroke? (If a surgeon didn’t close off the LAA, they could be sued if a patient later had a stroke, even if the patient was no longer in A-Fib.) Life (no stroke) is more important for most people than a possible reduced exercise intolerance.
In the future even people without A-Fib may have their Left Atrial Appendage closed off if it prevents or reduces the risk of a stroke. This may become a way to prevent stroke in older people, particularly women, who are more at risk of stroke as we age. There are currently a variety of devices, surgical and non-surgical, which can do this. LAA closure may become an important new way to reduce strokes, particularly in the elderly.
Functions of the Left Atrial Appendage
Some question the need or benefit of removing the Left Atrial Appendage (LAA) if someone is no longer in A-Fib. For a patient made A-Fib free, would their heart function better or more normally if they still had their LAA?
The LAA functions like a reservoir or decompression chamber or a surge tank on a hot water heater to prevent surges of blood in the left atrium when the mitral valve is closed.4Without it there is increased pressure on the pulmonary veins and left atrium which might possibly lead to heart problems later.
Cutting out or stapling shut the LAA also reduces the amount of blood pumped by the heart and may result in exercise intolerance for people with an active life style. (In dogs the LAA provides 17.2% volume of blood pumped.5) This is usually not a problem for patients with Persistent (Chronic) A-Fib, whose LAA has stopped contracting along with the fibrillating atrium. Cutting out or stapling shut the LAA won’t affect their cardiac output. But this may not be the case for patients with Paroxysmal A-Fib who still have large amounts of normal rhythm and whose LAA still functions normally.
But would a non-functioning LAA return to normal when someone with, for example, longstanding persistent (Chronic) A-Fib becomes A-Fib free?
The author isn’t aware of any surgeons (or EPs) who do pre- and post-LAA closure measurements of exercise ability, heart pumping function, etc. with and without the LAA.
(When doctors do a TEE [Transesophageal Echocardiogram] of the LAA of someone in A-Fib, the LAA doesn’t move at all and blood does not move. Doctors refer to this as “SMOKE” which is shorthand for Spontaneous Echo Contrast. The blood not moving looks like smoke inside the LAA.)
The LAA also has a high concentration of Atrial Natriuretic Factor (ANF) granules which help to reduce blood pressure.6Some preliminary research indicates that when the LAA is closed or cut off, the Right Atrial Appendage produces more ANF to compensate for the lost of the LAA.
Editor’s comment: If you are thinking of having a Cox Maze or Mini-Maze, discuss removing the LAA with the surgeon. Ask if they close off the Left Atrial Appendage and with what: sutures, stapler or the AtriClip.
Posted June 2013
Last updated: Sunday, February 15, 2015
- Damiano, Jr., RJ. “What Is the Best Way to Surgically Eliminate the Left Atrial Appendage?” Journal of the American College of Cardiology 2008, Sept. 9; Vol. 52, No. 11:930-1.↵
- AtriCure’s AtriClip system receives FDA 510(k) clearance (press release). June 14, 2010. ↵
- AtriCure’s AtriClip system receives FDA 510(k) clearance (press release). June 14, 2010.↵
- Al-Saady, N M, et al. Left atrial appendage: structure, function, and role in thromboembolism↵
- Hondo T. et al. “The Role of the left atrial appendage. A volume loading study in open-chest dogs.” Jpn Heart J 1995 Mar;36(2):225-34. http://www.ncbi.nlm.nih.gov/pubmed/7596042↵
- Atrial natriuretic peptide. Wikipedia.org. Last accessed April 13, 2014, URL: http://en.wikipedia.org/wiki/Atrial_natriuretic_peptide.↵
Cardioversion for Atrial Fibrillation
Your doctor may recommend a cardioversion to restore your heart to normal sinus rhythm (NSR). There are two types of cardioversion: chemical and electrical. Cardioversion through the use of drugs is called chemical cardioversion. Electrical cardioversion uses a low-voltage, timed electrical shock to restore normal rhythm.
Most cardioversions are planned and scheduled several weeks in advance.
On the other hand, if your A-Fib is so irregular and rapid that it is life threatening, you may be sent to the emergency room, given the intravenous anticoagulant Heparin, and an electrical cardioversion performed.
The goal of chemical cardioversion is to make your heart beat regularly (in normal sinus rhythm). It is usually done in a hospital. Some combination of medications (see Treatment/Drug Therapies) is administered intravenously, such as Cardizem, verapamil, ibutilide, or adenosine (a class V antiarrhythmic agent). Doctors monitor you closely for adverse side effects.
Chemical cardioversion is often done in combination with Electrical Cardioversion described below.
Electrical Cardioversion is a medical term for giving your heart a low-voltage electrical shock to synchronize it, that is, to make it beat regularly (in normal sinus rhythm). It is often used in combination with Chemical Cardioversion.
Note: Electrical cardioversion is not the same as Defibrillation. In defibrillation, doctors use high-voltage shocks to treat life-threatening arrhythmias or a heart that has stopped.
During Electrical Cardioversion you are anesthetized and are unconscious when you receive the shock. The shock causes the signal producing areas of your heart to discharge all at once. This stops all electrical activity in your heart momentarily, hopefully allowing your normal heart rhythm to take over. Usually only one shock is required to restore NSR.
Low Risk Treatment But High Risk of Clots Forming
Electrical Cardioversion is considered a low risk procedure. But it is a ‘shock’ to the body and requires general anesthesia. (It’s like a mini electrocution. The metal paddles or patches, for example, can potentially leave burn marks on the chest.)
Cardioversion does carry a high risk of forming clots and causing stroke.2
Why? An Electrical cardioversion “stuns” your heart along with your Left Arial Appendage (LAA). Clots may form in the LAA while your heart is stunned and not beating. The clot can break away and enter the blood stream with the potential of causing a stroke. (The LAA is where most A-Fib clots originate.)
To dissolve potential clots, your doctor will have you take an anticoagulant like warfarin (Coumadin) before the treatment and in the three to four weeks following treatment.
While on warfarin (Coumadin), your blood will be tested for how long it takes to clot (a prothrombin time test, PT). The goal is to keep your INR (International Normalized Ratio) score between 2.0 and 3.0. Your dosage will be adjusted if necessary. You may have to have your blood tested weekly until your doctor determines you are in the proper INR range.
Success Rate of Cardioversion
Electrical Cardioversion (often combined with Chemical Cardioversion) is considered a standard, routine, low risk treatment option, particularly for recent onset A-Fib patients. If your A-Fib has just started, it may be a momentary aberration; and an Electrical Cardioversion may correct it.
Cardioversion has a very high initial success rate, returning up to 95% of A-Fib patients to NSR.
While the conversion rate is high, recurrence of A-Fib is high too. As few as 23% of patients remain in normal sinus rhythm for more than one year post-procedure. For most, their A-Fib returns within the first five days.4
Are Repeated Electrical Conversions Dangerous?
People with A-Fib often ask, “How often can I be Electrical Cardioverted? Does it ever become counterproductive or dangerous?” Right now we just don’t know the answer to this question.
Former Senator and NBA basketball player Bill Bradley had three successful Electrical Cardioversions from 1996-1998 without any apparent ill effects.5 I’ve heard of an A-Fib patient who received an Electrical Cardioversion once a month for a year without any apparent problems.
VIDEO 2: Watch an actual Electrical Cardioversion recorded at the patient’s request: “Me Being Cardioverted” posted by reddy321.6But be advised: the patient in this video is partially awake (this is not the norm). This video is a bit unsettling to watch (but not dangerous or painful for the patient).
Don’t Be Frightened
Don’t let this type of video frighten you. It may look and sound traumatic, but Electrical Cardioversion is in fact non-invasive and is one of the easiest and safest short term treatments available for A-Fib.
And don’t let TV shows with emergency room scenes frighten you either. In fact, those scenes are usually depicting defibrillation, not cardioversion (defibrillators use high-voltage shocks to treat a heart that has stopped beating).
In her Personal Experiences story, Kris tells of accidentally being awake during an electrical cardioversion (see Personal Experiences story #37). According to Kris, the shock is relatively mild compared to what you often see portrayed in medical dramas on TV.
Last updated: Wednesday, April 6, 2016
- VIDEO 1: Short animation explaining electrical cardioversion when in Atrial Fibrillation. YouTube video posted by eMedTV; Last accessed Oct 12, 2014; URL: http://www.youtube.com/watch?v=-jkhQ5Tl2fs↵
- Haines, D. “Atrial Fibrillation: New Approaches in Management.” Un. of Virginia multi-media presentation, 1999, p.2. http://www.a-fib.com/HainesUnOfVirginiaAtrialFibrillation.htm↵
- Boos C , More RS, Carlsson J. Persistent atrial fibrillation: rate control or rhythm control. BMJ 2003;326:1411–2.↵
- Gorman, Christine, “A Candidate’s Racing Heart,” TIME, Sunday, Dec. 12, 1999. http://www.time.com/time/printout/0,8816,35831,99.html↵
- VIDEO 2: Me Being Cardioverted YouTube video; Last accessed February 22, 2013; URL: http://www.youtube.com/watch?v=2nsN0vdXZuY&feature=fvw.↵