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beta blocker

FAQs A-Fib Drug Therapy: Will the Beta-Blocker, Atenolol, Stop My A-Fib?

 FAQs A-Fib Drug Therapy: Atenolol

Drug Therapies for Atrial Fibrillation, A-Fib, Afib

3. I take atenolol, a beta-blocker. Will it stop my A-Fib.”

Not usually. Beta-blockers like atenolol, in addition to calcium channel blockers, and digitalis compounds are all rate-control medications. They attempt to control your heart rate (ventricular beats), but leave your heart in A-Fib. “In fact, these (rate control) drugs, which are quite valuable in achieving ventricular rate control, have not been shown in placebo-controlled studies to restore sinus rhythm.”

However, we all react somewhat differently to meds. A drug that doesn’t work for one person may be very effective for another.

If you are under the impression that atenolol or other rate control drugs will stop your A-Fib, it might be wise to check with your doctor or get a second opinion.

Resource:
Alpert, Martin A. “Medical Cardioversion of Atrial Fibrillation” Chest 2000;117:1529-1531, Last accessed Dec. 29, 2012: https://journal.publications.chestnet.org/article.aspx?articleid=1078918

Return to FAQ Drug Therapies

FAQs A-Fib Treatments: Medicines and Drug Therapies

FAQs A-Fib Treatments: Medicines and Drug Therapies

Drug Therapies for Atrial Fibrillation, A-Fib, Afib

Drug Therapies for Atrial Fibrillation

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.)

1. Which medications are best to control my Atrial Fibrillation?” “I have a heart condition. What medications work best for me?

2. “Is the “Pill-In-The-Pocket” treatment a cure for A-Fib? When should it be used?”

3. “I take atenolol, a beta-blocker. Will it stop my A-Fib.”

4. I’ve been on amiodarone for over a year. It works for me and keeps me out of A-Fib. But I’m worried about the toxic side effects. What should I do?”

5. Should everyone who has A-Fib be on a blood thinner like warfarin (Coumadin)?”

6. Which is the better anticoagulant to prevent stroke—warfarin (Coumadin) or aspirin?

7. What’s the difference between warfarin and Coumadin?

8. I’m on warfarin. Can I also take aspirin, since it works differently than warfarin? Wouldn’t that give me more protection from an A-Fib (ischemic) stroke?

9. “What are my chances of getting an A-Fib stroke?

10. “I’m worried about having to take the blood thinner warfarin (brand name Coumadin). If I cut myself, do I risk bleeding to death?

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?

13. “I just had an Electrical Cardioversion. My doctor wants me to stay on Coumadin for at least one month. Why is that required? They mentioned something about a “stunned atrium.” What is that?

14. Are natural blood thinners for blood clot treatment as good as prescription blood thinners like warfarin?”

15. “How long do I have to be in A-Fib before I develop a clot and have a stroke?

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?

18. “My last cardiologist had me on Pradaxa. My new cardiologist wants me to switch to Eliquis. Is Eliquis easier to deal with if bleeding occurs?

19. “My doctor told me about the Tikosyn drug option that I want to consider in getting rid of my 5-month-old persistent A-Fib. That seems like something that should be discussed on your web site.

20. “I hate taking Coumadin. Is there a way to get off blood thinners all together? I know I’m at risk of an A-Fib stroke.”

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?

22. “Do you have information about Hormone Replacement Therapy (HRT) and if it might help or hinder my atrial fibrillation?

23. Are Anticoagulants and blood thinners the same thing? How do they thin the blood?

24. I have A-Fib, and my heart doctor wants me to take Xarelto 15 mg. I am concerned about the side effects which can involve death. What else can I do?

25. “Is the antiarrhythmic drug Multaq [dronedarone] safer than taking amiodarone? How does it compare to other antiarrhythmic drugs?”

Last updated: Wednesday, May 25, 2016

Back to FAQs by Patients with Atrial Fibrillation

Atrial Remodeling and the Transition From Paroxysmal to Persistent AF by Dr Jose Jalife-2014 Boston AF Symposium

Jose Jalife, MD

Jose Jalife, MD

2014 Boston AF Symposium

Experiments in Atrial Remodeling in Sheep and the Transition From Paroxysmal to Persistent A-Fib

By Steve S. Ryan, PhD

Dr. Jose Jalife of the Center for Arrhythmia Research of the University of Michigan described his experiments inducing A-Fib in sheep by pacing their hearts. He is trying to discover the mechanisms underlying the transition from paroxysmal to persistent A-Fib.

Background: Some patients remain paroxysmal (usually with anti-arrhythmic therapy), while a large proportion progress to persistent A-Fib. (In a study of 5,000+ A-Fib patients, 54% of those on rate control meds went into permanent A-Fib in one year.)1
Previous presentation summary: This talk was a continuation of Dr. Jalife’s 2013 Boston A-Fib Symposium presentation on his experimental studies with sheep. (See A-Fib Produces Fibrosis—Experimental and Real-World Data.) He implanted pacemakers in the hearts of sheep; then induced A-Fib by pacing for 6-30 seconds, then stopped, then paced again, etc. He continued this sequence until the sheep were in persistent A-Fib. He left them in A-Fib for about a year. Dr. Jalife also had a control group of sheep who were monitored but not paced into A-Fib.

Pacing Sheep into A-Fib

Once pacing started in the sheep, it took around 5.5 days to produce the first A-Fib episode. It took around 7-9 weeks of pacing for the sheep to move from Paroxysmal to Persistent A-Fib. At that point the sheep stayed in Persistent A-Fib without any further need of pacing. Dr. Jalife’s sheep developed two major types of atrial remodeling:

  • Structural Remodeling (Fibrosis)
  • Electrical Remodeling (ion channel expression changes)
(In humans, remodeling usually also results in atrial dilation. Dr. Jalife’s sheep once in A-Fib also developed significant Atrial Dilation compared to a control group of sheep.)

Unlike humans, the sheep didn’t develop heart failure, left ventricle dilation and dysfunction, or tachycardia-induced cardiomyopathy despite being in A-Fib for more than a year. This is possibly because sheep have a very good AV Node (unlike most humans) which filters the A-Fib pulses from affecting the ventricles and keeps the ventricular rate low.

Genetic Differences in Sheep

But there were differences in the sheep. Some sheep transitioned into persistent A-Fib fast (<40 days) while others needed more pacing to transition into persistent A-Fib (>40 days). Sheep from the same herd would have the same diet, environment, etc. But genetically they must have been different in their ability to hold out from transitioning into persistent A-Fib.)

Structural Remodeling

All ventricular parameters remained normal in the paced sheep, except for atrial dilation and the markers of fibrosis which increased progressively as the sheep went from paroxysmal to persistent A-Fib. Fibrosis appeared in the right atrium, left atrium and the posterior left atrium. This fibrosis was the result of collagen deposition in the atria which is a permanent remodeling effect of A-Fib.

Dr. Jalife showed slides of a normal pig’s heart compared to a pig in persistent A-Fib. Well over ½ the atria seemed fibrotic.

Mechanisms of Electrical Remodeling

As expected, sustained A-Fib shortened the atrial action potential duration and refractory period. Also, rotor frequencies were increased. For example, in one sheep the dominant frequency of the first episode of paroxysmal A-Fib was 7.3 Hz, but increased progressively to 10.3 Hz during the transition to persistent AF. When AF in that sheep became persistent, the dominant frequent had stabilized at 11.3 Hz and remained constant for up to a year.

Dr. Jose Jalife 2014 Boston AFib Symposium

Graphic used with permission

In perhaps the most important findings of Dr. Jalife’s experiments, the rate of increase in dominant frequency correlated strongly with the time at which AF stabilized. In other words, although the progression from paroxysmal to persistent A-Fib varied from one animal to another, the rate of dominant frequency increase could be used to forecast the time at which AF became persistent.

 In other words, although the progression from paroxysmal to persistent A-Fib varied from one animal to another, the rate of dominant frequency increase could be used to forecast the time at which AF became persistent.

Dr. Jalife and his team also identified the mechanisms of electrical remodeling in sheep, which ion channels in the heart are responsible for transitioning sheep from paroxysmal to persistent A-Fib. Sodium and calcium heart electrical currents were lowered, while potassium and IK1 currents were increased. These electrical changes were associated with gene expression changes “in the alpha subunits of the L-type calcium (CACNA1C) and sodium (SCNSA) channel protein.”

  1. “Sustained AF reduces L-type calcium (Caᵥ1.2) and sodium (Naᵥ1.5) protein expression”
  2. “Sustained AF reduces the rapid sodium inward (INa) and L-type calcium (ICaL) currents”
  3. “Sustained AF reduces the transient outward current (Ito)”
  4. “Sustained AF increases the inward rectifying potassium current (IK1)  and protein expression of the Kir2.3 channel”

Conclusions

The sheep model explains the structural and electrical remodeling that occurs in humans.

As in humans, there is a variable progression in time from paroxysmal to persistent A-Fib.

The rate of dominant frequency increase during such a progression predicts the time at which AF stabilizes and becomes persistent, reflecting changes in Action Potential Duration and densities of ICaL, IK1, INa and Ito.

Predicting the transition from paroxysmal to persistent A-Fib is feasible, at least in some patients, by measuring the increase in dominant frequency over time.

Editor’s Comments:
No one seeing Dr. Jalife’s presentation could doubt that A-Fib produces fibrosis. (Though even among sheep in the same environment, diet, etc. and with a similar gene pool, there were differences in how fast the individual sheep progressed to persistent A-Fib.) As patients with A-Fib, we have to base our medical decisions on the conclusion that A-Fib produces fibrosis; that if we stay in A-Fib over a significant period of time, we will progressively develop fibrosis which is currently irreversible and can lead to a host of other heart problems.

A common strategy today…is to leave you in A-Fib but control your heart rate by the use of beta-blockers, etc. But leaving you in A-Fib produces fibrosis which is irreversible and very damaging to the heart.

A common strategy today for treating A-Fib is to leave you in A-Fib but control your heart rate by the use of beta-blockers, calcium-channel blockers, etc. But leaving you in A-Fib produces fibrosis which is irreversible and very damaging to the heart. If your doctor wants to leave you in A-Fib, Dr. Jalife’s experiments would recommend that you get a second opinion, and ASAP.
One of the major advantages of a successful catheter ablation (and surgery) is it probably reverses the electrical remodeling effect of A-Fib. This makes intuitive sense. A heart beating in normal sinus rhythm (NSR) doesn’t usually produce those weird ion channel currents. But more research needs to be done before we can conclude this. However, a successful catheter ablation does not reverse fibrosis (structural remodeling), though it may reduce atrial dilation.
By identifying the actual mechanisms of electrical remodeling, Dr. Jalife’s ground-breaking experiments may lead to new therapies and drugs to combat not only the transition from paroxysmal to persistent A-Fib, but how to prevent patients from developing A-Fib in the first place. And using dominant frequency to predict when a patient is transitioning to persistent A-Fib, can be an invaluable tool for doctors (and reassuring for patients).
One of the scariest parts of Dr. Jalife’s presentation was how fast he could pace those sheep into persistent A-Fib. Obviously sheep aren’t people. But we know that for most people, there is a relatively short window of time when they progress from paroxysmal to persistent A-Fib (about a year). When you have A-Fib, you can’t count on genetics, diet, life style, environment, etc. to protect you from progressing to persistent A-Fib. Right now we just don’t know why some people stay paroxysmal for years, while most become persistent after a relatively short time. Worst case scenario, you have about a year. Act accordingly.

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Last updated: Wednesday, September 2, 2015 

References    (↵ returns to text)
  1. Peykar, S. Atrial Fibrillation. Cardiac Arrhythmia Institute/Sarasota Memorial Hospital website. Last accessed Jan 5 2013. URL:http://caifl.com/arrhythmia-information/atrial-fibrillation/

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