Medicines or ‘Drug Therapies’ for Treatment of A-Fib

by Steve S. Ryan, updated Feb 2018

The various medications, or drugs, for treatment of Atrial Fibrillation can be overwhelming. What they are for, how they work and how they might affect you can be confusing. We’ll give you a basic understanding of the various ‘drug therapies’ you may be prescribed, so that you can become an intelligent participant in your own healing process.

  A Two-Pronged Approach

Drug therapy treatment of Atrial Fibrillation is a two-pronged approach:

•  Management of increased risk of clots and stroke

•  Drugs to control the heart rate (rate control), or to regain and maintain normal heart rhythm (antiarrhythmics).

Word of Caution

Always be cautious when taking prescription medications. “Adverse effects of medications are the fourth-leading cause of death in the US (after heart disease, cancer and stroke).”¹ In an average year, there are roughly 200,000 deaths and over 500,000 adverse events reported due to prescription drugs.²

Sir William Osler, first chief of medicine of the most prestigious medical school in the world, Johns Hopkins, and considered to be the father of modern medicine because of his methodical, scientifically based approach, made this sobering warning, “One of the first duties of the physician is to educate the masses not to take medicine.”³

Medicines, by definition, are almost all unnatural. Medications are not like taking vitamins. They need to be taken with caution. Our bodies see most medications as toxins and try to eliminate or clear them. But if one has A-Fib, medications may sometimes offer hope of stopping A-Fib or making it more bearable.

In general, don’t expect miracles from current medications. To date, the magic pill that will cure your A-Fib probably doesn’t exist.⁴ “Drugs don’t cure A-Fib but merely keep it at bay.”⁵

  Treatment for stroke Risk

Blood Thinners

Blood thinners are used to prevent blood clots and stroke (anticoagulants like warfarin, Coumadin, Jantoven; antiplatelets like Aspirin, Ecotrin, Plavix, Ticlid); or Lovenox (an anticoagulant taken by injection), and Heparin (used in hospitalized patients. (Plavix and Ticlid are antiplatelet drugs like aspirin but they are not the same or interchangeable with aspirin. If your doctor prescribes Plavix or Ticlid, you should not substitute aspirin for them.)

But blood thinners are not like taking vitamins. They have their own set of risks and side effects. However, preventing a stroke is for most people a welcome trade-off for any bad effects of anticoagulants. (Be advised that most “blood thinners” do not actually thin the blood, i.e. make blood less thick and viscous, but work to make blood less likely to form clots.)

Blood thinners reduce but do not totally eliminate the risk of stroke.

Warfarin

Warfarin is a Vitamin K-antagonist. It works by blocking vitamin K thereby affecting several stages in the coagulation process.

Warfarin (Coumadin), first aproved in 1954, was for years the only anticoagulant available to most A-Fib patients and was effective in preventing A-Fib stroke. (It was and is still used in higher doses as a rat poison.) It’s primary danger and main risk is bleeding. In a study in the United Kingdom, warfarin was one of the most common causes of adverse drug reactions and hospitalizations with symptoms such as:
• Blood in the stool and urine
• Coughing up blood
• Vomit that looked like dirt
• Joint pain and swelling
• Bruising without injuries
• Bleeding into the brain (hemorrhagic stroke)
• Blocking vitamin K in the body (we need Vitamin K for bone health, brain function, and to prevent coronary artery disease). (Some of our healthiest foods are loaded with Vitamin K.)

To be effective warfarin must be maintained at a certain level in the blood stream (INR—International Normalized Ratio between 2.0 and 3.0). Above 4.0 you run the risk of having a hemorrhagic (bleeding) stroke. Below 2.0 you are more in danger of having an ischemic (clotting) stroke, the kind that most often occurs in A-Fib.

VIDEO: Stroke Prevention in A-Fib and Anticoagulant Therapy.Through interviews and animations, explains how atrial fibrillation can cause stroke and why anticoagulation is so important; Discussion of: warfarin (generic name), the required [monthly] monitoring, interactions with food, alcohol and other drugs: newer anticoagulants do not required regular testing. (2:01)

It is often difficult to maintain this INR, especially when you first start on warfarin. You may have to take sometimes weekly PT tests in your doctor’s office till you get the warfarin dosage and INR right. There are home use kits available for testing your own INR (for example, see http://www.PTINR.com}.

In general, aspirin is less effective than warfarin⁶ and doesn’t work very well to prevent an A-Fib stroke. (For more, see FAQs questions: Which is better—warfarin or aspirin? Be advised that aspirin therapy can be dangerous for otherwise healthy people, “Regular aspirin therapy use in healthy people increased the occurrence of serious internal bleeding by 31%, but had no significant effect on fatal heart attack or any kind of stroke.” ⁷

You should also get tested for variations in the CYP2C9 and VKORC1 genes which influence how you respond to warfarin (Coumadin). If your doctor doesn’t provide this testing, you may want to think about getting a second opinion. These tests could save you heart problems related to over- and under-dosing of warfarin.

An Alternative to Blood Thinners

(If you can’t or don’t want to take blood thinners, an option is to have a device installed to  close off the Left Atrial Appendage where 90-95% of A-fib strokes come from; See my articles: Watchman: the Alternative to Blood Thinners and Steve’s Lists/Doctors Installing the Watchman Device.)

Removing or closing off the Left Atrial Appendage (LAA) may affect how well the heart pumps and is of special concern to athletes and to those with heart pumping problems. In canine studies the LAA provided 17.2% of the whole left atrial volume of blood pumped.⁸ It’s possible that removing or closing off the LAA may lead to heart pumping problems. The LAA is like a surge tank on a hot water heater. When the Mitral Valve closes, the LAA absorbs the surge of blood. When the LAA is amputated or closed off, this may cause increased pressure in the Pulmonary Veins and exercise intolerance. Few, if any, centers currently perform pre- and post-amputation exercise testing.

The New Oral Anticoagulants (NOACs), (DOACs—Direct Oral Anticoagulants) 

The FDA has approved several new blood thinners—dabigatran (brand name Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa) which are considered as effective or even more effective than warfarin without many of the accompanying problems of warfarin. 

Dabigatran (brand name Pradaxa) is a direct thrombin inhibitor, a newer type of medication. Thrombin is an enzyme that converts soluble fibrinogen into insoluble fibrin. Fibrin is a fibrous protein involved in the clotting of blood. It forms a mesh or clot over a wound.

Another new anticoagulant approved by the FDA Nov. 4, 2011 is rivaroxaban (Xarelto) which may work better for some patients than dabigatran. It is in a class of medications called Xa inhibitors (xabans). The FDA has approved another new anticoagulant apixaban (Eliquis) approved December 2012. “the results of large randomized trials indicate that bleeding remains a major concern even with the new agents. Studies with rivaroxaban, edoxaban and dabigatran showed that these drugs have incidences of severe bleeding comparable to those of enoxaparin and warfarin.”⁹

For more about the NOACs, see my July 2014 article: Warfarin vs. Pradaxa and the Other New Anticoagulants, and my report from the Boston AF Symposium 2013: The New Anticoagulants (NOACs).

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  Drug Therapies for A-Fib

There are two basic approaches to managing Atrial Fibrillation with medications: Rate Control drugs and Rhythm Control drugs.

Rate Control drugs try to control the heart rate (ventricular beats), but generally leave the heart in A-Fib. ¹⁰ Rhythm control drugs try to stop the A-Fib and make your heart beat in normal rhythm by using antiarrhythmic drugs.

  Method 1: Rate Control

Though rate control drugs slow the rate of the ventricles, they usually leave you in A-Fib. They usually don’t reduce A-Fib attacks. They may alleviate some A-Fib symptoms, but do not address the primary risks of stroke and death associated with A-Fib.¹¹ Their main purpose is to avoid rapid A-Fib rates whenever possible and practical. Over time, the heart can “wear out” if the rate is too fast for too long. An elevated heart rate for a long period of time (weeks to months) can cause ventricular dysfunction leading to heart failure. When using rate control drugs, you should aim for a resting heart rate below 110 beats.

Keep in Mind: Leaving patients in A-Fib overworks the heart and leads to remodeling and fibrosis which increase the risk of stroke.¹² Mellanie True Hills of StopAfib.org asks, “Should we leave folks in A-Fib long term, especially the non-elderly? Between the risk of heart failure, and fibrosis from long-term remodeling increasing stroke risk, could staying in A-Fib long-term be a death sentence?”¹³ If your doctors only prescribe rate control meds for your A-Fib, you should question them and probably get a second opinion. 

Categories of Rate Control Medications 

Medications used for rate control can be categorized as:

• Calcium-channel blockers
• Beta-blockers
• Cardiac Glycosides

1. Calcium channel blockers prevent or slow the flow of calcium ions into smooth muscle cells such as the heart and blood vessels. They slow heart rate and lower blood pressure. Calcium channel blockers are preferred if you have heart or lung disease. Common side effects are the heart beats too slowly, constipation, low blood pressure and heart failure.¹⁴ They also cause swelling in the legs. “Calcium channel blockers weaken the heart and can damage the liver,” according to Dr. Julian Whitaker in his Health & Healing newsletter of October 2015.

A study of nearly 3,000 women found that “women who took calcium-channel blockers for 10 years or longer had more than double the risk for breast cancer.” No risk was found for short-term use (less than 10 years).¹⁵ Calcium-channel blockers include: diltiazem (Dilt, Cardizem, Tilazem, Cartia XT) [the generic name of a medication is listed first, the Brand name is in parentheses] and verapamil (Calan, Isoptin).

2. Beta-blockers, also called “beta-adrenergic blocking agents” “block” the action of adrenaline on beta receptors in the cells of heart muscle. They slow down conduction through the heart and make the AV Node less sensitive to A-Fib impulses. They also are said to reduce the frequency of premature beats which may trigger A-Fib. Because they lower adrenaline, they can help maintian sinus rhythm, but also cause fatigue and put you to sleep. Unlike antiarrhythmic drugs, they are not specifically designed to stop or reduce episodes of A-Fib but are generally safe.  

Beta-blockers are better for active or young people, because exercise reduces the effectiveness of Digitalis and Calcium-channel blockers. 

Beta-blockers can be roughly catagorized into two types:

1. 1.  Lipophilic (lipid-soluble). Be advised that they penetrate the blood-brain barrier and enter brain tissue. In addition to fatigue, they can cause mental dullness or “brain fog” in 10% to 20% of patients. They include the most commonly prescribed beta-blocker metoprolol succinate (Toprol XL) and metoprolol tartrate (Lopressor) as well as propranolol (Inderal) which has been linked to increased risk for depression and nightmares, and the newer beta-blocker carvedilol (Coreg) (also contains an alpha-blocker). If you are taking metoprolol, check with your doctor if you are experiencing tiredness, fatigue, and reduced energy. A newer beta-blocker, nebivolol (Bystolic) works by dilating (vasodilating) blood vessels, and may help you feel less tired..
   2. Hydrophilic (water soluble). Does not cross the blood-brain barrier. Includes atenolol (Temormin), bisoprolol (Zebeta, Concor), nadolol (Corgard), and betaxolol (Kerlone)

Common side effects of beta-blockers are: the heart beats too slowly, low blood pressure, tiredness, cold fingers and toes, thinning hair, erectile dysfunction, and loss of sex-drive.^16,17 Long-term side effects may include disorientation, short-term memory loss, emotional lability (rapid, extreme changes in mood), inability to concentrate or think clearly, and decreased performance on neuropsychological tests used to measure psychological function.

In many people, beta-blockers can reduce heart rate by 10 to 30 beats per minute.¹⁸ Beta-blockers like metoprolol can be particularly dangerous for older people (over 60) and cause symptoms similar to aging,¹⁹ Beta blockers also carry substantial risk for psychiatric side effects, particularly depression. When using beta blockers, a person’s psychiatric health should be monitored carefully.²⁰ They can also cause vivid dreams and insomnia, aggravate asthma, and impair blood sugar. “Beta-blockers are notorious for causing impotence, fatigue, and depression,” according to Dr. Julian Whitaker in his Health & Healing newsletter of October 2015.

Beta-blockers include: atenolol (Tenormin), metoprolol succinate (Toprol-XL, sustained timed release), metoprolol tartrate (Lopressor, immediate acting), esmolol HCI (Brevibloc), propranolol (Inderal), timolol, nadolol, pindolol, and the newer drugs carvedilol (Coreg), nebivolol (Bystolic) and Labetalol. (Propanolol and atenolol are often prescribed to help with A-Fib anxiety.)

Added: 5/18/22  Landiolol (INN) is an ultra short-acting intravenous adrenergic blocking agent which decreases heart rate effectively with less negative effect on blood pressure or myocardial contractility.

Note: A new study casts doubt on the effectiveness of most beta-blockers, because they promote fibrosis in the heart.

Beta-blockers “undermine the structure and function of the heart…Blocking the beta-receptor alone promotes cardiac remodeling via growth of cardiac fibroblasts induced by alpha-adrenergic receptor signaling. The growth of fibroblasts in the heart further damages the integrity and function of the heart.”) ²¹

Carvedilol (Coreg), however, targets both the beta- and alpha-adrenergic receptors on the heart muscle. “Beta-blockers (like carvedilol) which target both receptors “offer the most benefit to cardiac patients.” A study in 2003 showed that carvedilol produced a greater survival rate than metoprolol. (Thanks to Janet Brown for calling our attention to this research.)

Nebivolol (Bystolic) seems to eliminate most of the common bad side effects of beta blockers by dilating blood vessels through the release of nitric oxide. But it also only blocks Beta 1 receptors.

(Alpha-blockers) Like beta-blockers, they block the the effects of stress hormones on the body, but they also cause blood vessels to dilate, which can mitigate some of the bad effects of beta-blockers. The most widely prescribed alpha-blocker is doxazosin (Cardura).

3. Cardiac Glycosides slow down and control the heart rate by blocking the electrical conduction between the atria and ventricles. The most widely prescribed Glycoside is digoxin (a Digitalis [foxglove] compound, brand names Lanoxin, Digitek), but medical authorities consider it the least effective.²²

Digoxin is usually not prescribed as a first-line therapy. ²³

While Digoxin is a commonly used drug for rate control, it is only effective at controlling heart rate at rest, e.g. when you are in the doctor’s office. But when you leave, your heart rate may go too high. It’s not as effective at controlling heart rate during physical activity or when stressed (when the sympathetic nervous system is more active). Beta-blockers and calcium-channel blockers are generally more effective than Digoxin.²⁴

Caveat about digoxin: A 2013 study found that A-Fib patients “taking the heart drug digoxin were 35% more likely to suffer a cardiovascular-related death and 61% more likely to die due to an arrhythmia (irregular heartbeat) than A-Fib patients not taking digoxin.

In a 2014 study of veterans newly diagnosed with A-Fib, mortality rates were higher for digoxin-treated patients than for untreated patients. (This was a large retrospective study of 122,465 patients mostly male, with 28,679 receiving digoxin.) A-Fib patients treated with digoxin had a more than 20% increased risk of dying within about three years.²⁵

In a 2017 trial of A-Fib patients with heart failure, digoxin use was significantly associated with increased all-cause mortality, cardiovascular death, SCD, death caused by HF, and heart failure hospitalization.²⁶

According to 2017 results from the ARTISTOTLE trial, patients with A-Fib taking digoxin had an increased risk of death, whether or not they had heart failure. And this risk increased with higher levels of digoxin in the bloodstream (≥1.2 ng/mL). Patients not taking digoxin before the ARISTOTLE trial who began taking it over the course of the study had a 78 percent increase in the risk of death from any cause and a four-fold increased risk of sudden death after starting digoxin.

According to lead researcher Dr. Renato Lopes, “Digoxin should be avoided in patients with AFib, particularly if symptoms can be alleviated with other treatments.”²⁷

If you’re taking digoxin, talk to your doctor about switching to beta-blockers or calcium channel blockers to slow down fast heart rate. If you and your doctor conclude digoxin is the best drug for you, try to use the lowest possible dose and make sure you are closely monitored.²⁸

If using rate control drugs, be advised that you will still have A-Fib.

About All Rate Control Drugs

If you are using any of the above rate control drugs, please be advised that you will usually still have A-Fib. Only your lower heart (the ventricles) is controlled. You are still at risk of stroke and must continue taking anticoagulants.

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  Method 2: Rhythm Control

Rhythm control medications called antiarrhythmic drugs have been available for nearly 100 years and remain a mainstay in the management of atrial fibrillation. These drugs target a reduction in the frequency and duration of episodes of arrhythmia. But there hasn’t been any major advancement in rhythm control meds in decades. One major problem with these meds is that they usually are not specific for the atria but can affect the ventricles as well. Most rhythm control drugs have bad side effects. 

Many rhythm control drugs require you to be hospitalized for 3-4 days when they are initially administered, in order to monitor you for bad side effects. Some rhythm control meds can have a “pro-arrhythmic” effect on some people (people react differently to medications).

Keep in Mind: In general, current “antiarrhythmic” (anti irregular heart rhythm, rhythm control) drugs aren’t always effective and tend to have bad side effects such as pulmonary fibrosis and impaired liver function.²⁹‘³⁰‘³¹‘³²They also become less effective over time, with approximately half of the patients eventually developing resistance to them.³³ Up to 50% of patients experience a recurrence of A-Fib after 1-year of antiarrhythmic treatment, and up-to 85% experience a recurrence after 2-years.³⁴‘³⁵

If one rhythm control drug fails to control your A-Fib, it’s unlikely any of the others will work, with the possible exception of amiodarone, the most toxic and dangerous of the rhythm control drugs.

Antiarrhythmics are not a long-term solution for most people. Be aware that all antiarrhythmics may increase your risk of a life-threatening ventricular arrhythmia.

In addition, according to Heart Rhythm Society’s ‘General Approach to the Patient with AF’ Guidelines, “most patients managed using a rhythm control strategy also require medications for rate control”.

According to Drs. Irina Savelieva and John Camm of St. George’s University of London, “The plethora of antiarrhythmic drugs currently available for the treatment of A-Fib is a reflection that none is wholly satisfactory, each having limited efficacy combined with poor safety and tolerability.”³⁶

Classes of Antiarrhythmic Drugs

Antiarrhythmic drugs are grouped in “classes” according to how they work:

1. Class I are Sodium Channel Blockers which decrease the speed of electrical conduction in the heart muscle.

2. Class II are Beta-Adrenergic or Beta-Blockers which slow down conduction through the heart and make the AV node less sensitive to A-Fib impulses.

3. Class III are Potassium Channel Blockers which slow nerve impulses in the heart.

4. Class IV are Calcium Channel Blockers which prevent or slow the flow of calcium ions into smooth muscle cells such as the heart. This impedes muscle cell contraction, thereby allowing blood vessels to expand and carry more blood and oxygen to tissues.

Here is a list of the more commonly used antiarrhythmic drugs, based on an article by Dr. R. Falk of the Boston University School of Medicine:³⁷

Procainamide (Procan SR, Promine, Pronestyl, Procanbid): Slows nerve impulses in the heart and reduces the sensitivity of heart tissue. Not FDA approved for A-Fib. Long-term use associated with lupus. Generally not used as a first-time drug because of bad side effects. Less effective against A-Fib than the other Class 1A drugs Quinidine and Disopyramide.³⁸ (Class 1A drug) (Rerely used today because of high side effects.)

Quinidine (Quinaglute, Quinidine Glaconate, Quinidex): FDA approved for A-Fib but risk of death increases during long-term use. Generally not used as a first-time drug because of bad side effects such as increasing the heart rate and impairing the heart’s pumping efficiency. (Class 1A drug)

Disopyramide (Norpace): Not FDA approved for A-Fib. Strong negative inotropic effect (heart muscle contractions weakened). Generally not used as a first-time drug. Good for patients with nocturnal or post-prandial (after meals) vagal A-Fib.³⁹

Flecainide (Tambocor): Slows nerve impulses in the heart and makes the heart tissue less sensitive. Approved only for paroxysmal (occasional) A-Fib with structurally normal heart. Normally the first drug tried on otherwise healthy patients with new A-Fib. Not recommended after a heart attack or if you have a structural heart disease. Can cause headaches. Often used as a Pill-In-The-Poocket treatment. (Class 1C drug) Please be advised that flecainide has an FDA Black Box Warning which is the most serious the FDA issues. A Black Box Warning alerts doctors and patients that a drug has potentially dangerous effects.

(Andrew writes about his experience with flecainide “I had to rely on flecainide in order to keep my heart in rhythm [while I waited to have a catheter ablation].” “The flecainide made me feel awful [digestive problems, acid reflux].” “I’ve only been able to eat a very limited diet, losing about 28 pounds in the process. If I had been overweight to begin with, it wouldn’t have seemed so bad…My theory is that, because flecainide is used to calm the heart by inhibiting the cell sodium channels and therefore attenuating the overall strength of the heart muscle contraction, the other muscles in your body are also affected—including the lower esophageal sphincter, which would allow acid to leak upward from my stomach.”

“Flecainide also makes me feel extremely tired. I find that two or three hours after taking a dose, I feel an overwhelming tiredness that I cannot fight, I’m forced to take a sometimes two hour sleep in order to remedy. When i was initially admitted to the hospital, I was put on 100 mg of flecainide per day which slowed my heart to 30 beats per minute and put me in a half stupor where I couldn’t think clearly. I also had shaky legs, I kept falling asleep, and I felt irrationally unhappy…I’m currently taking 25 mg per day…which is considered a tiny dose.”)

Propafenone (Rhythmol and the newer version Rhythmol SR (Sustained Release)): Same limitations as flecainide. Can cause fatigue, dizziness, low heart rate, and a metallic taste in the mouth. Often used as a Pill-In-The-Pocket treatment. (Class 1C drug)

Sotalol (Betapace):  Not recommended (conversion from A-Fib to normal rhythm rate is low). Only approved in the US for ventricular arrhythmias. (Class II and class III drug—a beta-blocker with potassium channel blocking, antiarrhythmic effects). Should not be used in patients with severe heart failure or those with a long QT interval (see my article: Understanding the EKG Signal), because it may trigger a lethal cardiac arrhythmia (torsades de pointes ventricular tachycardia).⁴⁰Like beta-blockers, it may cause severe fatigue, low heart rate, dizziness, and exacerbate asthma. Patients starting Sotalol are usually monitored in a hospital for three days.

Dofetilide (Tikosyn): FDA-approved for conversion and maintenance. (Class III drug). Patients starting this medication must be monitored in a hospital for three days. Like Sotalol, must be monitored for a lethal cardiac arrhythmia (torsades de pointes ventricular tachycardia). Can cause headaches. 

Amiodarone (Cordarone, Pacerone): Not FDA-approved for A-Fib. Moderately effective for conversion from A-Fib to normal rhythm, but onset is slow. Good rate slowing in A-Fib. This is usually the last drug tried on patients because of its toxic side effects particularly in the lungs, thyroid, liver, and eyes. (Beware of any doctor starting you on amiodarone as a first-choice antiarrhythmic drug or putting you on it for a long time.) See https://a-fib.com/amiodarone-effective-but-toxic/. (Class III drug but it also blocks Sodium Channels like a Class I drug.)

Dronedarone (Multaq): FDA approved in 2009. Chemically similar to amiodarone, but without the iodine molecule. While not as effective as amiodarone, it has less toxic side effects. Not for patients with severe heart failure. Can cause GI (gastrointestinal) problems. 

Ibutilide (Corvert): Not for patients with low blood potassium, a prolonged QT interval (slow heart beat), or torsade de pointes (very irregular, fast ventricular heart beats). Effective in electrical cardioversion. Often used as an IV in place of Electrocardioversion (33% to 49% success rate) and is generally more effective in cases of Atrial Flutter than in A-Fib. (Class III drug)

The Class 1 drugs Quinidine, Procainamide, Disopyramide, Flecainide, and Propafenone should probably be avoided if you’ve had a heart attack or have structural heart disease. The Class III drugs Amiodarone, Sotatol, Dofetilide, and Azimilide appear to be safer to use if you have structural heart disease.⁴¹ In structurally normal hearts, Class IC drugs (Flecainide and Propafenone) cause less heart rhythm problems and are the least toxic.⁴²

Xanax (alprazolam): Xanax does seem to have beta-blocker properties, though it is primarily used to help panic attacks. But be advised that Xanax is a controlled substance and can be addictive. It isn’t recommended to take Xanax on a regular basis for more than 2-3 weeks because of the danger of addiction.

Sally writes that her A-Fib comes on at night and is very severe, preventing her from sleeping. “I get up and take Xanax 0.5 mg, and within 15 minutes or so, the A-Fib stops. And I can go to sleep.” 

Harlan writes that when in A-Fib, he takes 1 mg of Xanax and lies on his back in a darkened room. “Within 15 minutes I am in sinus rhythm.” Negative emotional stress is what primarily brings on his A-Fib, even from something as simple as watching an emotional or scary movie or TV show.

Janet writes that she has been taking Xanax occasionally for over 30 years to stop A-Fib attacks which happen often at night or during stressful situations, loud noises, or bright flashing lights. “It works every time in about 15 minutes.”

Abigail writes: For unknown and seemingly random reasons, I can feel my heart rate start to accelerate and feel like it’s on the cusp of going into A-Fib. I will then stop what I’m doing, drink a few glasses of ice-cold water, take 0.5 mg of Xanax, and try to lie down. In most instances, I can avoid a full-blown episode of A-Fib. I know it’s bad to be taking Xanax, but I think it’s better than constantly feeling anxious about another A-Fib attack.I recently did an experiment where I took 0.5 mg of Xanax each day at about 10 am. I noticed a much more steady heart rate all day, documented with my watch/phone.

Also, antiarrhythmic drugs become less effective over time, with approximately half of the patients eventually developing resistance to them.

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“Pill-in-the-Pocket” Treatment

Another treatment approach for A-Fib is to take an antiarrhythmic med at the time of an A-Fib attack.

For example, Leon writes that he takes 100 mg of flecainide three times at intervals of twenty minutes when he has an A-Fib attack. This often shortens the time of an A-Fib attack. “It (the Pill-In-The-Pocket treatment) has changed my life in that it reduces my time in A-Fib to usually a couple of hours as opposed to between 12 to 36 hours. It allows me to recover completely in a lot quicker time, because my heart hasn’t been going crazy for a day or more. And it also allows me to remain out of hospital, which has been fantastic.” (Leon, E-mail: sandman_oz (at) yahoo.com)

Marilyn writes she would take Rythmol 300 mg and Inderal 20 mg, wait three hours, then take Inderal 20 mg, wait three hours, then again start the Rythmol 300 mg and Inderal 20 mg, etc. Although she daily took a 325 mg coated aspirin, during a bout of A-Fib she would also chew an 81 mg baby aspirin. (Marilyn, E-mail: nmshook (at) sbcglobal.net)

(Leon and Marilyn were both later cured of A-Fib by Pulmonary Vein Ablations. You can read their stories and others; go to Personal Experiences/By Subject/Pill-In-The-Pocket)

Another treatment strategy is to take lower doses of an antiarrhythmic med on a regular basis, then take a higher dose during an A-Fib attack. A-Fib patient Reg writes he takes 300 mg of flecainide, and 2 hours later goes back into SR. He normally is on a loading dose of flecainide 100 mg in the morning and 50 mg in the afternoon. (Email: r.j.tooth (at) shu.ac.uk)

A-Fib patient Will writes that he takes Rhythmol SR 325 regularly. If he gets a break-through event of A-Fib, he takes 600 propafenone, immediate release. “This always gets me back in Sinus Rhythm, usually in 90 minutes.”

At best, the Pill-In-The-Pocket treatment is a stop gap measure rather than a “cure” of A-Fib. (See also in the FAQs/MineralDeficiencie/DrugTherapies Question 2: “Is the “Pill-In-The-Pocket” treatment a cure for A-Fib? When should it be used?)

 Conclusion

In general, don’t expect miracles from current medications. To date, the magic pill that will cure your A-Fib probably doesn’t exist. As heart rhythm specialist, Dr. Dhiraj Gupta says, “Drugs don’t cure A-Fib but merely keep it at bay.”

Additional Readings

♥ Frequently Asked Questions: Drug Therapies and Medicines
♥ Anticoagulant Therapy after Successful A-Fib Catheter Ablation: Is it Right for Me?
♥ Warfarin vs. Pradaxa and the Other New Anticoagulants
♥ Amiodarone: Most Effective and Most Toxic
♥ My Top 5 Articles About Warfarin Therapy, Associated Risks and Alternatives
♥ Watchman: the Alternative to Blood Thinners

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Return to Treatments for Atrial Fibrillation
Last updated: Saturday, February 18, 2023

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Mann, Samuel J. Is a Beta-Blocker Right for You? Bottom Line Personal, Volume 42, Number 17, September 1, 2021.

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