What should I do about atrial fibrillation (AFib)?

Dozens of conditions can be associated with atrial fibrillation (AFib), but few patients have an identifiable cause of their atrial fibrillation.

Non-Cardiac Causes of AFib

These include:

• Age. The risk of getting AFib increases with age.
• Obesity. This condition ends up coating the heart with fat. Patients with more fat around the heart as seen on MRI scans get more AFib.
• Alcohol and caffeine. People who drink too much caffeine or alcohol are more prone to AFib, but the research on this remains controversial.
• Physical activity:  Too little exercise and ironically, too much exercise in endurance athletes, can predispose to AFib.
• Hyperthyroidism.  President George H. W. Bush famously got AFib while in the White House and was later found to have hyperthyroidism.

Cardiac Causes of AFib

Almost every disease of the heart can cause AFib. These include

• Hypertension
• Coronary disease
• Disease of the heart muscle
• Abnormalities of the heart valves
• Inflammation of the lining of the heart (pericarditis)

The questions and answers below offer more helpful information about AFib.

There are two main things we worry about when patients have atrial fibrillation. The first is a weakening of the heart that we call a cardiomyopathy. The second, which can be even more serious, is stroke.

Congestive Heart Failure

The weakening of the heart can occur when the heart beats very fast — in excess of 110 beats per minute — for weeks and months. The fast heartbeat is called tachycardia, and the resulting weakening called tachycardia-related cardiomyopathy. Patients with this condition can fill up with fluid, a condition called congestive heart failure. Fortunately, tachycardia-related cardiomyopathy will usually reverse and go away over a period of months after the heart rate is controlled.

Stroke

The most feared complication of AFib is disabling stroke. Stroke in AFib is caused by clot that forms in the left atrial appendage, which is like a windsock attached to the side of the left atrium. When one of these clots breaks loose, it flies out of the heart and can take a turn into the arteries that lead to the brain. The clot will plug up a brain artery and within a minute begins to kill a smaller or larger piece of brain. If the clot is small and dissolves quickly, it only causes brief symptoms of a mini-stroke (also called a TIA). If the damage is persistent, it will cause a stroke. If a patient is lucky and quickly goes to a hospital where he is given a clot busting drug like tPA, or if a neuroradiology specialist can extract the clot with a catheter, the stroke symptoms can be fully or partially relieved.

We use a risk score to evaluate the risk of stroke. It’s called CHADSVASc. Each letter stands for a condition which has a point score that we add up to assess the total risk:

• C=Congestive heart failure=1 point
• H=Hypertension=1 point
• A=Age 65-75=1 point or Age >75=2 points, Diabetes=1 point
• S=Stroke or TiA=2 points
• VA=Vascular disease of the heart, legs or brain arteries=1 point
• Sex Classification: Female Sex=1 point, Male Sex=0 point.

If your score is 3 points, you have enough risk to require blood thinners. 2 points, not counting sex, is also enough to justify blood thinners.

Aspirin is not a good enough blood thinner for patients with these high risk scores. Traditionally we have recommended Coumadin® (warfarin), but the newer blood thinners such as Eliquis®, Xarelto®, Savaysa®, and Pradaxa® have many advantages over Coumadin.

There are some patients who can’t take a blood thinner because they have had serious bleeding episodes, or because they engage in activities like cycling or skiing that make the use of blood thinners too risky.

Watchman® Device

Nearly all clots that cause strokes in atrial fibrillation come from the left atrial appendage. The left atrial appendage is like a windsock that is attached to the body of the left atrium. If the appendage is closed off, then clots stay bottled up in the appendage.

The appendage can be closed off in several different ways. It can be cut off and sewn over surgically, it can be closed with an external loop of suture tied around its base, and it can be plugged with a Gortex occluder. The Watchman® is the only Gortex method that has been studied extensively and approved by the FDA.

The Watchman is inserted through a vein and deployed though a catheter without the need for surgery. There is a small risk of complications during its insertion, and blood thinners are needed for several weeks after insertion, but in the long run, patients have as few strokes and far less bleeding than those on long-term blood thinners.

AFib seems to come and go when it pleases. Patients are always trying to find a cause and effect for each episode, usually without real success. Still, there are some factors that appear to be closely associated with AFib recurrences, and certain practices may cut down on your attacks:

• Avoid caffeine and alcohol
• Don’t drink ice-cold liquids
• If you are overweight, lose weight
  

The first order of business is to get the heart rate under control to a resting rate between 60 and 90 beats per minute. This can be done with three different classes of drugs. Each of these drugs regulate the rate at which electrical signals travel between the fibrillating atrium and the main pumping chambers, the ventricles. The beta blockers, the calcium blockers and digoxin all are effective in regulating the heartbeat, but some patients may need two or even three drugs for effective rate control.

• Beta blockers like metoprolol, bisoprolol, atenolol, and carvedilol may have some mild additional anti-arrhythmic effect as well as rate control, but some patients complain of tiredness on these drugs.
• Calcium blockers like diltiazem and occasionally verapamil are used to slow the heart rate, but some patients get swelling of the ankles and constipation from them.
• Digoxin is seldom if ever used by itself because while it slows the resting heart rate, it fails to control the heart rate during exercise. So digoxin is typically reserved as an add-on to a beta blocker or a calcium blocker.
  

Some patients’ heart rate cannot be controlled even with three drugs, and other patients are intolerant of the drugs. In these cases we consider a procedure called pace and ablate.

A pacemaker is placed to provide a “floor” to the patient’s heart rate, so it cannot go below a minimum rate of for example, 60 beats per minute. Then a radiofrequency catheter is used to permanently block (ablate) the electrical pathway between the atrium and the ventricle. The patient becomes dependent on the pacemaker to control the heart rate, and the atrial fibrillation no longer can excessively speed up the heart.
When the patient exercises, the pacemaker will speed up the heart normally by tracking the heart’s natural pacemaker as long as the patient is in normal rhythm. When the patient is in AFib, the pacemaker will speed up the heart using a built in sensor such as an accelerometer.

Trying to force the heart back into normal rhythm sounds like a good thing. If it could be done safely and effectively, it would be. Unfortunately the anti-arrhythmic drugs we have available are neither completely effective nor completely safe.

The standard-setting drug is amiodarone, but it is at best only 50-60% effective in preventing recurrent AFib over the first year. All the other drugs we have are even less effective.

In terms of safety, amiodarone’s side effects are more frequent with high doses and longer duration of treatment. For AFib, the dosing is usually pretty low, around 100-200 mg per day. But many patients on amiodarone develop over or underactive thyroid and excess skin sensitivity to sunlight. It’s very unusual, but some patients get severe side effects in the lung, liver or nerves, which sometimes are fatal. All the anti-arrhythmic drugs except amiodarone can cause life-threatening arrhythmias, especially among patients who have weak hearts or coronary artery blockages. At least amiodarone doesn’t do that.

In patients whose hearts are completely normal except for the atrial fibrillation, drugs like propafenone, sotalol, flecainide and others can be used with relative safety.

To summarize, anti-arrhythmic drugs can be used, but with all the issues surrounding them, there ought to be a very good reason to use such anti-arrhythmic drugs.

It wasn’t that long ago that specialists in electrical diseases of the heart discovered that almost all atrial fibrillation comes from a nearly hidden location in the left atrium. In the back of left atrium there are four pulmonary veins that drain all the oxygen-containing blood from the lungs into the heart. The left atrium has a cuff of muscle tissue that extends a short distance into each of the four pulmonary veins, and those cuffs of muscle are where the atrial fibrillation comes from in almost every case.

Electrophysiologists have figured out that if the area around the pulmonary veins is electrically isolated from the rest of the left atrium in a procedure called ablation, that 60-85% of patients will remain free of atrial fibrillation for at least a year.

As you may guess, atrial fibrillation ablation is not easy to do. A catheter is threaded up a vein from the groin, and it is passed through the wall between the right and left atrium. Once in the left atrium, radiofrequency energy or extreme cold can be used to create a ring of scar that encircle the pulmonary veins and isolate the atrial fibrillation, allowing normal rhythm to return.

After an ablation, it is not uncommon for there to gaps between adjacent scars that need to be touched up in a second procedure if the AFib returns.

Left atrial ablation is a wonderful procedure, but it is not without risks, some of which are life-threatening, like perforation of the heart, creation of a hole in the esophagus, stroke, and death. These are very infrequent, around 1 in 200, but the risk makes us hesitate to do this procedure in any but very symptomatic patients.

When a patient has his or her first episode of atrial fibrillation, and it doesn’t go away in a short time by itself, we call it persistent AF. We will often recommend that the patient be put to sleep for a couple of minutes and undergo electrical cardioversion.

Cardioversion involves delivering an electrical shock, about half the intensity of the ones use for cardiac arrest, in order to synchronize the electrical signals of the atrium and restore normal rhythm. It is effective around 90% of the time, but about half of patients will go back into AFib within a year. Results are best when the duration of the AFib is short, and worse when it’s been present for over 6 months.

We know that patients with AFib have worse outcomes that those in normal rhythm, and certainly the doctor and patient feel better when they see normal rhythm. But we have no good studies that show that cardioversion improves outcomes. Nonetheless, the consensus is that nearly everyone should get at least one shot at normal rhythm.

Cardioversion is generally considered quite safe. The risk of death is nearly zero, and the risk of stroke is very small since we insist on at least 3 weeks of blood thinners before the procedure to dissolve any clots. If the cardioversion must be done earlier, a transesophageal echocardiogram (TEE) is performed to inspect the left atrium to make sure there are no clots that could break loose and cause a stroke.

If a patient has had one or more attempts at cardioversion and has relapsed into atrial fibrillation, many times the best treatment is to avoid further efforts at restoring normal rhythm. There have been large studies comparing anti-arrhythmic therapy vs simple rate control which showed that trying force patients back into normal rhythm with drugs leads to more deaths and strokes. So at least for patients who have no or minimal symptoms, the best strategy may be to leave them alone.