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…->
22. “In case I have an A-Fib-related stroke, what does my family need to know to help me? (I’m already on a blood thinner.) What can I do to improve my odds of surviving it?
Stroke is the most dreaded effect of having A-Fib. And an A-Fib-related stroke is usually worse because the clots tends to be larger. They often result in death or permanent disability.
Here are some basic facts and steps you and your family can take to prepare for and what to do if stroke strikes any member of your family.
Prepare Your Plan: The 4 Steps
For your own and your family’s peace of mind, you need to create a ‘Stroke Action Plan’.
Step 1: Learn the Signs of a Stroke
Make it a family affair. Discuss the most common signs of stroke: sudden weakness of the face, arm or leg, most often on one side of the body. Stroke may be associated with a headache, or may be completely painless. Each person may have different stroke warning signs.
Step 2―Ask Your Doctor
Discuss with your doctor what actions to take in case of stroke. For example, some doctors recommend aspirin to help avoid a second ischemic stroke (A-Fib). If so, ask what dosage.
Step 3―Locate Your Nearest ‘Certified Stroke Center’
Why a Certified Stroke Center? If a stroke victim gets to a Certified Stroke Center within four hours, there is a good chance specialists can dissolve the clot without any lasting damage.
Only a fraction of the 5,800 acute-care hospitals in the U.S are certified as providing state-of-the-art stroke care.
A certified or ‘Advanced Comprehensive Stroke Center’ is typically the largest and best-equipped hospital in a given geographical area that can treat any kind of stroke or stroke complication.
A Certified Stroke Center will have drugs such as Tissue Plasminogen Activator (tPA) to dissolve the clot. Can use Clopidogrel or acetylsalicylic acid (ASA) to stop platelets from clumping together to form clots. Or use anticoagulants to keep existing blood clots from getting larger.
So do your homework. To find the nearest certified or ‘Advanced Comprehensive Stroke Center’ check these listings:
Step 4―Post Your ‘Stroke Action Plan’
Write up the three components of your plan (i.e., the signs of stroke, aspirin dosage and location of the nearest Certified Stroke Center).
What about your workplace? Locate the nearest Certified Stroke Center to your job, too, and post a copy.
Also, print handouts with the name and address of the nearest Certified Stroke Center (Advanced Comprehensive Stroke Center) for EMS responders. Keep a bottle of aspirin nearby.
Store your ‘Stroke Action Plan’ in a special binder or post so that family can easily find the information.
If a Stroke Strikes: Work the Plan
1. Immediately call your emergency medical services (EMS)―even if the person having the stroke doesn’t want you to. (e.g., 911 in US and Canada, 0000 in Australia, 999 in the UK.)
Note: DO NOT try to diagnose the problem by yourself, and DO NOT wait to see if the symptoms go away on their own.
2. While waiting for EMS, administer aspirin in the proper dosage (if advised by your doctor before hand) to help avoid a second stroke.
Note: The emergency operator might connect you to a hospital that gives you instructions based on symptoms.
3. When EMS arrives, tell them to take the patient to your nearest Certified Stroke Center (give them a handout with the name and address).
Note: If necessary, be firm, insist they go to your choice of Certified Stroke Center. (Realize that some paramedics and ambulance services have side deals with hospitals to take patients to their hospitals, even if it’s not the right hospital for stroke victims.)
The Wrap Up
A ‘Stroke Action Plan’ with specific steps is reassuring during a medical emergency and helps everyone stay calm. Your family will be confident they’re supporting you in taking the right action at the right time.
The only guarantee of not having an A-Fib stroke is to no longer have A-Fib.
Know that quickly going to a certified or ‘Advanced Comprehensive Stroke Center’ may save you from the debilitating effects of an A-Fib stroke, or even death.
For additional reading, see Ablation Reduces Stroke Risk to that of a Normal Person.
If you find any errors on this page, email us. Y Last updated: Wednesday, April 27, 2016
by Steve S. Ryan, PHD, October 2015, Updated January 26, 2016
According to recent studies, you are better off having a Watchman device installed than spending a lifetime on warfarin.
In two randomized clinical trials comparing Left Atrial Appendage Closure (LACC-Watchman Device) to warfarin, 1,261 patients from the PROTECT AF and PREVAIL trials were studied. The follow-up period was around 3.3 years. Patients receiving the Watchman compared to patients on warfarin had significantly fewer:
• Hemorrhagic strokes
• Cardiovascular/unexplained death
• Non-procedural bleeding
• All-cause stroke or systemic embolism was similar between both strategies.
There were more ischemic strokes in the Watchman device group, but this was balanced by a greater number of hemorrhagic strokes in the Warfarin group.
However, the patients in the control group of the PREVIAL trial were considered “unusual” in that, given their risk profile, they had a much lower ischemic stroke rate than ever observed in any clinical trial. See Getting FDA Approval for the Watchman Device.
What Patients Need to Know: Watchman Actually Better Than Warfarin
The Watchman device provides similar protection against having an A-Fib (ischemic) stroke as being on warfarin.
But the Watchman device isn’t simply an “alternative” to warfarin, but rather an improvement or advance or progression. One would intuitively expect that people receiving the Watchman device would also have less hemorrhagic strokes and bleeding compared to those on warfarin, which these studies do demonstrate.
Welcome Alternative to a Lifetime on Warfarin
Warfarin and other anticoagulants work by causing bleeding and are inherently dangerous. The Watchman device is not only a welcome alternative to a lifetime on warfarin, but is actually better than warfarin.
Long-term use of anticoagulants such as warfarin have been known to not only cause hemorrhagic strokes but also microbleeds in the brain which lead to dementia.
Among other bad side effects, long-term use of anticoagulants such as warfarin have been known to not only cause hemorrhagic strokes but also microbleeds in the brain which lead to dementia. See Patient on Anticoagulation Therapy for 10 Years Develops Microbleeds and Dementia.
A 2015 study found evidence of microbleeds in 99% of subjects aged 65 or older, and that increasing the imaging strength increased the number of detectable microbleeds. Microbleeds have been suggested to be predictive of hemorrhagic stroke.
According to current research, you are better off having a Watchman device installed than spending a lifetime on warfarin. (Of course, this assumes that the doctor performing the procedure is beyond his/her learning curve. That is, when operating doctors are first performing the procedure, there is a higher risk for procedural complications.)
What About the New Anticoagulants (NOACs)?
Does this research apply to the new anticoagulants like Pradaxa, Xarelto, Eliquis and Savaysa/Lixiana? Technically no. This research only applies to warfarin. But intuitively one would expect the same general principles to apply. All anticoagulants cause bleeding. That’s how they work.
Caveat—Long-Term Effects of Watchman?
What are the long-term effects of leaving a mechanical device like the Watchman inside the heart? We know that, after a few months, heart tissue grows over the Watchman device so that the LAA is permanently closed off from the rest of the heart.
It seems unlikely that complications would develop after a long period of time as has happened with warfarin. But we can’t say that for sure until enough time has passed. The first clinical trial installation of the Watchman device in the US was in 2009 and in Europe in 2004. So far no long-term complications have developed.
Preventing Stroke in the Elderly—Even If They Don’t Have A-Fib!
One of the great potentials of the Watchman device is that it may someday be used to prevent stroke in the elderly even if they don’t have A-Fib. Imagine a world where you no longer live in fear of a stroke as you get older, where 90%-95% of stroke risk can be eliminated by a simple 20 minute procedure. The Watchman device (and other Left Atrium Occlusion Devices such as the Lariat and the surgical AtriClip) may change the way elderly medicine is practiced.
How many people turning 70 or 75 would welcome a device that would almost guarantee freedom from the most severe type of ischemic stroke (a cardioembolic stroke)? The Watchman device has the potential to greatly reduce or eliminate the threat of strokes in the elderly!
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
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