Atrial fibrillation: When the heart loses its rhythm

Content provided by the Faculty of the Harvard Medical School

Atrial fibrillation: When the heart loses its rhythm

You may not even feel it happening, but if the atria of the heart don’t beat correctly you could be in danger of a stroke.

Your heart has four compartments. The upper two are the atria; the larger two below are the ventricles. The atria are the anterooms of the cardiac pump house, each capable of holding just a few ounces of blood at a time.

The right atrium receives oxygen-depleted blood on its trip back to the heart from the rest of the body. The left one receives blood returning from the lungs after it has been freshly oxygenated and sends it to the powerful left ventricle. The left ventricle pumps blood out through the aorta to supply the whole body.

Normally, the atria and ventricles contract in a coordinated fashion at a nice steady clip of 60–80 times per minute. This rate is set by the sinoatrial node, a group of cells in the right atrium that serves as the heart’s natural pacemaker. The sinoatrial node generates a pulse of electrical activity that spreads across the muscle cells of the atria, causing them to contract. The electrical charge also travels to another cluster of cells in the middle of the heart called the atrioventricular node that acts like a gatekeeper, causing a brief delay of about a tenth of a second. As a result, your heartbeat marches in a two-beat rhythm: first the atria contract, then the ventricles, over and over again.

Why atrial fibrillation causes strokes

What goes wrong?

In atrial fibrillation, the regular surges of electrical activity become wild and random. Instead of moving in a predictable rhythm, the atria quiver and twitch — the medical term is fibrillate. As a consequence, the atria don’t pump blood efficiently. That also throws the ventricles off, because they don’t contract when they are most filled with blood. Blood pressure can drop, and the heart isn’t quite as effective in circulating the blood.

Who gets it?

Atrial fibrillation is one of the most common heart rhythm disorders in the United States. One in every four Americans age 40 and over will develop the condition at some time in his or her life, and the chances increase with age.

Atrial fibrillation can be viewed as a price we pay for our success in preventing and treating other conditions. More people survive heart attacks today than ever before. But if you survive a heart attack, you’re more vulnerable to developing atrial fibrillation. Demographic trends are also making it more common. As of 2005, about 2 million Americans have had atrial fibrillation. In the next 30–40 years, that number is expected to increase to 5 million as the baby boom bulge moves into its 70s and 80s.

What causes it?

Sometimes atrial fibrillation develops without any discernible underlying structural damage to the heart. Doctors call this lone atrial fibrillation, and it accounts for about a fifth of all instances of the condition. Patients with lone atrial fibrillation are typically younger and often male. They usually have a good prognosis.

More often, atrial fibrillation occurs because the atria — and the heart tissue more generally — have been damaged or strained in some way. That’s why heart attacks are a risk factor: they cause the death of heart muscle. Other precipitating conditions include diseases that affect the heart’s valves (rheumatic fever is perhaps the best known), an enlarged (and therefore weakened) heart, and congenital heart defects. High blood pressure is a major risk factor because it puts an extra strain on the walls of the left atrium.

There are several noncardiac causes, too. Too much thyroid hormone from an overactive thyroid gland seems to make atrial muscle cells excitable and jumpy and therefore prone to fibrillation. (The first President Bush developed atrial fibrillation because of an overactive thyroid.) The “holiday heart syndrome” is a polite way of talking about atrial fibrillation caused by excessive alcohol. Caffeine may cause a racing heart, which suggests a possible link to atrial fibrillation. Surprisingly, this connection hasn’t been proved experimentally.

What does it feel like?

Many people with atrial fibrillation don’t know they have it. Even after an episode is over and has been treated, atrial fibrillation may return without symptoms.

If there are symptoms, one of the most common is the fluttering sensation of a racing heart — what some people call palpitations. With or without that sensation, a person may become short of breath or suddenly feel tired. Some people feel lightheaded and may even faint during an episode.

Why is it important?

Usually one or two isolated episodes aren’t important. It’s persistent cases or going in and out of atrial fibrillation that is worrisome.

Atrial fibrillation can reduce the heart’s pumping capacity by about 20%. The ventricles of a robust heart can compensate for atria that aren’t contracting properly. But if the ventricles are weak, or the heart valves aren’t working properly, atrial fibrillation can produce or aggravate the symptoms of heart failure, including fatigue, shortness of breath, and swelling in the feet and ankles.

By far the most serious consequence of atrial fibrillation is stroke. The traditional explanation: Because fibrillating atria don’t pump effectively, tiny stagnant pools of blood collect inside them. When blood doesn’t move, clots (thrombi) tend to form. And if a clot in the atrium breaks off, it can be carried in the blood and lodge in an artery supplying a vital organ. A stroke happens when these traveling clots (emboli) reach the brain and block an artery there.

Another school of thought is that atrial fibrillation is just a marker for atherosclerosis in the arteries and the clots come from there.

One scary statistic: Atrial fibrillation increases the risk of stroke by 400%. But the risk isn’t the same for all. Older people and those with other risk factors for stroke are at higher risk.

How is it treated?

Rhythm vs. rate control. After slowing down the heart with a beta blocker or another drug to make the patient comfortable, doctors have traditionally focused on trying to get the atria to beat normally again. The first step is usually administration of an anti-arrhythmia medication; many cardiologists currently favor a drug called amiodarone (Cordarone, Pacerone). People are sometimes hospitalized when they begin taking this or other anti-arrhythmia drugs so their doctors can watch for side effects.

If a drug doesn’t work, doctors will often boost the dose or try another one. If none of the medications work, the next step may be to “convert” the patient’s heart back to normal rhythm with an electrical shock to the chest. Sedatives are used, and the shock is mild, so it doesn’t hurt.

The logic of so-called rhythm control is appealing, but in practice it often doesn’t work out. Many patients must take anti-arrhythmia drugs indefinitely, and the medications often have side effects. Besides, they’re not all that effective. Up to 60% of the time atrial fibrillation comes back, often without symptoms, so people don’t know they’re in danger.

An alternative is rate control — slowing the heart down, instead of tackling the arrhythmia head-on. The drugs used for rate control are mainstream cardiovascular medications: beta blockers (atenolol, metoprolol), some calcium-channel blockers (verapamil, diltiazem), and, in heart failure patients, digoxin.

Several studies have compared rhythm and rate control. The two approaches came out about the same with respect to preventing stroke and other important outcomes. So many doctors now prefer rate to rhythm control because the drugs are easier to use, less expensive, and have fewer side effects. In 2003, the American College of Physicians and the American Academy of Family Physicians issued guidelines advising rate control for most patients with atrial fibrillation.

Some patients will have persistent symptoms (palpitations, lightheadedness, fainting spells, etc.) with rate control. Switching to an anti-arrhythmia regimen makes sense.

Preventing blood clots: Warfarin vs. aspirin. One consequence of the growing preference for treating atrial fibrillation by slowing down the heart rate is that more people need to take anticoagulation medications for an extended period to prevent clots.

Warfarin (Coumadin) is the main anticoagulant. In some studies, it cuts the stroke risk from atrial fibrillation by 70%. Finding the right dose is tricky, though. It has to be high enough to prevent blood clots, but low enough to avoid the risk of bleeding. People taking warfarin must have frequent tests to see if their blood is in that safe range and, if necessary, have the dose adjusted.

Aspirin would seem to be an attractive alternative. It also prevents blood clots, although in an entirely different way. It’s far simpler to use than warfarin because it doesn’t have the same bleeding risks. The problem is that, overall, it’s just not as effective.

But stroke risk from atrial fibrillation varies tremendously, depending on age, health of the heart, individual history of stroke, and various other factors. Low-risk patients may not need the heavy-duty protection of warfarin; aspirin may be good enough for them. Unfortunately, as of 2005, there’s no firm consensus on how to classify patients into high- and low-risk groups.

Experimental procedures. Doctors can treat several types of heart arrhythmias by destroying (ablating) tiny areas of heart tissue with high-frequency radio waves. The idea is to eliminate the tissue triggering the electrical activity that causes the irregular heartbeat.

But this approach hasn’t worked well for atrial fibrillation, probably because doctors haven’t been able to pinpoint the source of the trouble. There are high hopes, though, for a relatively new procedure that creates circles of scar tissue around pulmonary veins where they join the left atrium. The pulmonary veins are the big blood vessels that carry blood from the lungs to the heart. Some cases of atrial fibrillation may originate from unwanted electrical signals that develop in or near the pulmonary veins; the scar tissue is supposed to hem in that area. The doctors developing this procedure hope it will cure, not just treat, atrial fibrillation, but as of 2005 it’s an experimental treatment reserved for those who haven’t responded to other approaches.

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Last updated:	August 21, 2006